Sorghum Root and Stalk Rots - Agropedia

Sorghum Root and Stalk RotsA Critical ReviewProceedings of theConsultative Group Discussionon Research Needs and Strategies for Controlof Sorghum Root and Stalk Rot DiseasesBellagio, Italy27 N o v - 2 Dec 1983Sponsored byUSAID Title XII Collaborative Research Support Programon Sorghum and Pearl Millet(INTSORMIL)International Crops Research Institute for the Semi-Arid Tropics(ICRISAT)with Support from the Rockefeller Foundation1984

Correct citation: ICRISAT (International Crops Research Institute for the Semi-Arid Tropics). 1984.Sorghum Root and Stalk Rots, a Critical Review: Proceedings of the Consultative Group Discussion onResearch Needs and Strategies for Control of Sorghum Root and Stalk Rot Diseases, 27 Nov - 2 Dec1983, Bellagio, Italy. Patancheru, A.P. 502324, India: ICRISAT.Workshop Coordinator and Scientific EditorL. K. MughoghoPublication EditorGloria RosenbergThe International Crops Research Institute for the Semi-Arid Tropics (ICRISAT) is a nonprofit scientificeducational institute receiving support from donors through the Consultative Group on InternationalAgricultural Research. Donors to ICRISAT include governments and agencies of Australia, Belgium,Canada, Federal Republic of Germany, France, India, Italy, Japan, Mexico, the Netherlands, NewZealand, Nigeria, Norway, Sweden, Switzerland, United Kingdom, United States, and the followinginternational and private organizations: Asian Development Bank, European Economic Community, FordFoundation, International Bank for Reconstruction and Development, International DevelopmentResearch Centre, International Fertilizer Development Center, International Fund for Agricultural Development,the Leverhulme Trust, the Organization of Petroleum Exporting Countries, the RockefellerFoundation, and the United Nations Development Programme. Responsibility for the information in thispublication rests with ICRISAT or the individual authors. Where trade names are used this does notconstitute endorsement of or discrimination against any product by the Institute.

ContentsForewordVInaugurationOpening address and objectives of the meeting L.K. Mughogho 3Welcome from ICRISAT C.R. Jackson 5Welcome from INTSORMIL E.R. Leng 7Basic Disease ProblemsCharcoal rot of sorghum L.K. Mughogho and S. Pande 11Fusarium root and stalk disease complex N. Zummo 25Pythium root and seedling rots G.N. Odvody and G. Forbes 31Anthracnose stalk rot R.A. Frederiksen 37Periconia root rot G.N. Odvody and L.D. Dunkle 43Acremonium wilt R.A. Frederiksen 49Plant-parasitic nematodes affecting sorghum L.E. Claflin 53Spatial and temporal succession of fungal J.E. Partridge, J.E. Reed, 59species in sorghum stalks as affected by S.G. Jensen,environmentand G.S. SidhuSummary and synthesis L.K. Mughogho 73Discussion 74Physiological and Environmental Factorsin Root and Stalk Rot DiseasesRole of edaphic factors in disease development W.R. Jordan, R.B. Clark,81and N. SeetharamaThe association of plant senescence with root R.R. Duncan 99and stalk diseases in sorghumMorphological and physiological factors J.W. Maranville, and M.D. Clegg 111associated with stalk strengthRelation of senescence, nonsenescence, G.G. McBee 119and kernel maturity to carbohydratesand carbohydrate metabolism in sorghumSorghum sensitivities to environmental J.D. Eastin, C.Y. Sullivan, 131stressesJ.M. Bennett, A.M. Dhopte,T.J. Gerik, V.A. Gonzalez-Hernandez, K.-W.Lee,V. Ogunlela, and J.R. RiceSummary and synthesis D.F. Schoeneweiss 145Discussion 147

Experience with Root and Stem Rots of CropsOther than SorghumThe maize root rot, stalk rot, A.J. Pappelis 155lodging syndromeand J.N. BeMillerRoot and stalk rots caused by Macrophomina J.B. Sinclair 173phaseolina in legumes and other cropsSummary and synthesis J.E. Partridge 183Discussion 185Control of Sorghum Root and Stalk RotsThe role of fungicides in the control R.J. Williams and O. Nickel 191of sorghum root and stalk diseasesCultural and biological control of root B. Doupnik, Jr. 201and stalk rot diseases of sorghumBreeding for resistance to root D.T. Rosenow 209and stalk rots in TexasBreeding for stalk rot resistance as A.B. Maunder 219a component of acceptable agronomicperformanceLodging, stalk rot, and root rot in R.G. Henzell, R.L. Dodman, 225sorghum in AustraliaA.A. Done, R.L. Brengman,and P.E. MayersSummary and synthesis I R.W. Schneider 237Summary and synthesis II J.F. Scheuring 241Discussion 243Group Discussions and Recommendations 251Meeting Organization and Participants 265

ForewordDespite several decades of research, diseases remain a major constraint to sorghumproduction throughout the world. That was the reason ICRISAT and Texas A & MUniversity cosponsored the first international workshop on sorghum diseases, hostedby ICRISAT at Hyderabad, India, in December 1978. It was also the reason for asecond major international effort exactly 5 years later, by INTSORMIL and ICRISAT,to gain more understand ing for better control of these diseases. This took the form of ahighly specialized consultants' group meeting to make recommendations on theresearch needs and strategies for control of sorghum root and stalk rots.Root and stalk rots are a group of diseases that reduce crop stands in theemergence and seedling stages, or most commonly cause stalk lodging in thepostf lowering and grain-filling stages of plant development. The improved high-yieldpotentialvarieties and hybrids under good management tend to be particularlysusceptible to Iodging i nduced by root and stalk rot. Although good progress has beenmade against other diseases of sorghum, research for control of root and stalk rotshas been painfully slow. This is due to the complexity of the diseases themselves andthe paucity of intensive interdisciplinary research on them.ICRISAT and INTSORMIL are committed to supporting and conducting researchthat will provide the technology necessary for farmers to improve sorghum yields andhelp meet world food needs. Their joint sponsorship of the Consultative GroupDiscussion on Research Needs and Strategies for Control of Sorghum Root and StalkRot Diseases and the publication of these proceedings are important steps towardthis objective. The contents of the background papers, the discussions, and therecommendations contained in this book represent the combined experience andknowledge of 27 scientists in the disciplines of breeding, physiology, and pathology.We feel certain that if national, international, and other sorghum improvement programsfollow the various strategies and recommendations, significant progress willbe made in this field.ICRISAT expresses special appreciation to the scientists who participated in thismeeting, to INTSORMIL for its help in funding the conference, and to the RockefellerFoundation for hosting the meeting at its Study and Conference Center at Bellagio,Italy.L.D. SwindaleDirector General, ICRISATv

Inauguration

Opening Addressand Objectives of the MeetingL.K. Mughogho*It is with great pleasure that I welcome you all to this Consultative Group Discussionon Research Needs and Strategies for Control of Sorghum Root and Stalk RotDiseases. Our meeting here has been made possible by the encouragement andfinancial support of ICRISAT and INTSORMIL. We are most grateful to both institutions.We are also grateful to the Rockefeller Foundation for the use of their excellentconference facilities at this villa and the generous hospitality accorded to us. I wouldalso like to thank the organizing committee at ICRISAT Center and Dr. R.A. Frederiksenof Texas A & M University, USA, for everything they did to make this meeting areality.It may appear strange that we are meeting to discuss sorghum diseases in acountry not commonly known for sorghum production. Although this is not the rightseason to see sorghum, an examination of the FAO production figures for 1981shows that Italy produced 84000 tons of sorghum grain on 15000 ha at a yield of5600 kg/ha. This yield was eight times higher than the average of 700 k g / h a in thedeveloping countries of Africa and Asia, where the crop is a major cerealfood crop.Diseases, including root and stalk rots, are partly responsible for this yield gap.The idea to hold this discussion group meeting originated from a review inSeptember 1980 of the ICRISAT sorghum charcoal rot research project. The discussionsat that review emphasized the need for a multidisciplinary research thrustinvolving pathologists, physiologists, and breeders for effective control of the disease.As a starting point, we felt that a meeting of scientists familiar with the problemshould be held to make recommendations for future research. During the planningstage other root and stalk rot diseases were included for discussion in order toprovide a comprehensive and overall picture of the role and importance of variousroot and stalk rot pathogens.Although a number of pathogens are implicated as causal agents of root and/orstalk rots in sorghum, little is known about (a) the etiology and epidemiology of thediseases they cause, (b) the plant physiological and environmental factors thatpredispose sorghum to infection and favor disease development, (c) host resistanceand techniques to identify and utilize host resistance in breeding projects, and (d)*Workshop Coordinator and Principal Plant Pathologist Sorghum Improvement Program,ICRISAT,3

the effect of various crop management practices on disease incidence. Effectivecontrol measures have not yet been devised, largely because of lack of or incompleteknowledge and understanding of the diseases concerned.This meeting has three objectives: (a) to assess present knowledge and researchactivity, (b) to determine where gaps in knowledge exist, and (c) to plan and makerecommendations for future research and strategies for effective control of root andstalk rot diseases of sorghum. The participants here include pathologists, physiologists/nutritionists,biochemists, and breeders with valuable experience in sorghumresearch. These disciplines represent the four major areas in which joint research isrequired that would eventually lead to the understanding and control of thesediseases. We also have participants with research experience on similar diseases inmaize and legumes.Finally, I would like to emphasize that from this consultative group discussion weexpect positive, realistic, and practical recommendations that can be taken up bynational, regional, international, and other sorghum improvement programs for theeventual benefit of the sorghum grower. The wide experience and expertiseassembled here will no doubt achieve this objective. We look forward to fruitfuldiscussions and a pleasant stay at Bellagio.4

5Welcome from ICRISATCurtis R. Jackson*You have my sincere apologies and personal regrets that I cannot be with you for thisimportant conference. I have asked John Scheuring, our principal breeder in Mali, toread this short message for me on behalf of ICRISAT.Sorghum is ICRISAT's most promising grain crop at this time, and we have 18principal scientists working on this crop in Asia, Africa, and Latin America.The traditional rainfed sorghum crops in the semi-arid tropics have yields rangingfrom 200 to 1000 kg/ha. But in good years we can easily obtain on-station yieldsexceeding 3.5 t/ha using F 1 hybrids or exotic inbreds with so-called high yieldpotential. Yet, as a general rule, the higher the yield potential under optimal conditionsthe greater susceptibility to stalk rot under stress conditions. In Mali we have seenCSH-5 yield over 4t/ha. We have also seen it fall 100% to charcoal rot. We've pickedout excellent ICRISAT varieties one year only to watch them buckle under stalk rot thenext year.One might argue that even grain from lodged plants can still be harvested. In factwe've salvaged yields exceeding 2t/ha from completely lodged fields. But the grain isvirtually worthless as food. Food grain, unlike feed grain, must have the quality toassure long term-on-farm storage, processing with minimal bran loss and acceptablefood taste, texture, and keeping quality.It is not by accident that local tropical sorghum cultivars are photoperiod-sensitive,with flowering usually at 75 to 100 days. Dry matter accumulation comes slowly intropical latitudes compared to temperate latitudes. During the rainy season, nighttemperatures are relatively high and daylengths are 1 to 3 hours shorter than those intemperate latitudes. The higher night-time temperatures and shorter days translateinto limited source size and accentuated source stress in high-yield-potentialvarieties.In brief, the lessons we learn about stalk rots in temperate latitudes certainly cantake us far in understanding stalk rots in the tropics. But let us take care to recognizethe distinct differences of the plant environment and the grain uses between temperateand tropical sorghums. We may very well find that resistance mechanisms andcritical source-sink thresholds are entirely different for temperate and tropicalsorghums.*Director of International Cooperation, ICRISAT.

6Let us remember that the clientele of INTSORMIL and ICRISAT are farmers in thesemi-arid tropics and that when it comes to sorghums growing in the tropics, particularlybelow 20° latitudes, most of us—breeders, physiologists, and pathologists alike— are only at the beginning of description, much less understanding.There is no guru (master) among us. So let us be prudent and brief in our commentsand let us carefully consider the comments of others.Hopefully this collaborative exchange of ideas will lay the groundwork for solidcollaborative research between scientists in temperate and tropical areas.But collaborative research or no collaborative research—we must address thestalk rot question if we are to raise sorghum yield levels in the tropics.We are pleased to have you here as our guests and guests of our near relative,INTSORMIL I hope you will have a productive and rewarding meeting. Please give usyour best thoughts and actions.Thank you.

Welcome from INTSORMILEarl R. Leng*INTSORMIL is pleased to be a cosponsor of this important group discussion. Ourstated mission is to conduct collaborative research on topics likely to be significantfor enhancing sorghum and millet production in the developing world. There is nobetter way to insure collaboration than to bring together, as this meeting is doing,most of the world's experts on a particular problem.Stalk rots remain one of the major detrimental influences on production of largestemmedcereals such as sorghum, maize, and to some extent pearl millet. Manyyears ago, researchers were confident that problems with stalk rot would be quicklysolved, largely by selection for genetic resistance. This hope has proved to be anillusion. Stalk rots of various types are with us almost everywhere, and solutionsappear to be less near than we thought some thirty years ago.For this reason, a group discussion such as this is really needed, since from it weshould have a chance to focus research better, and maybe to make faster progress.Some may feel that stalk rots are more of a problem for developed than fordeveloping countries, since they present particular difficulties for machine harvesting.But, probably no one in this group needs to be told what severe yield losses canresult from stalk rot attacks, no matter how the crop is harvested. Therefore, it isclear that you will be dealing with a problem of major concern to the developingworld.To repeat, INTSORMIL is happy to have the opportunity to cosponsor this conferenceand to participate in its deliberations. We really hope that out of it will grow moreproductive research on the problem, which in turn will lead to improved sorghumproduction and a better life for sorghum-using peoples of the world.*Program Director, INTSORMIL, University of Nebraska, Lincoln, NE 68583-0723.7

Basic Disease Problems

Charcoal Rotof Sorghum

Charcoal Rot of SorghumL.K. Mughogho and S. Pande*SummaryCharcoal rot of sorghum caused by the fungus Macrophomina phaseolina is a root and stalk rotdisease of great destructive potential in most sorghum-growing regions. Improved, highyieldingcultivars under good management tend to be very susceptible to the disease. M.phaseolina is a common soilborne, nonaggressive, and plurivorous pathogen that attacksplants whose vigor has been reduced by unfavorable growing conditions. Drought stress is theprimary factor that predisposes sorghum to charcoal rot. In diseased roots and stalks, M.phaseolina is often associated with other fungi, suggesting that the disease is of complexetiology. Control by fungicides, cultural practices, and host resistance are briefly discussed,and priority areas for future research are listed.Charcoal rot, caused by Macrophomina phaseolina(Tassi) Goid., is the most common and probablyalso the most important root and stalk rotdisease of sorghum. Reviews by Tarr (1962), Dhingraand Sinclair (1977, 1978), and Sinclair (theseproceedings) provide comprehensive informationon the biology of M. phaseolina and the epidemiologyand control of the diseases it causes in manyplant species. Several papers in these proceedings(Sessions III, IV, and V) discuss in detail the physiologicaland environmental factors that influencecharcoal rot and its control by fungicides, culturalpractices, and host resistance. In this review,emphasis will therefore be on those aspects of thepathogen and disease that have or may haveimportant implications in disease control andmanagement.Occurrence andGeographical DistributionCharcoal rot is a worldwide disease: it has beenreported from all the ecologically diverse areas ofsorghum culture in the tropics, subtropics, andtemperate regions (Tarr 1962, ICRISAT 1980).When inoculum is present, the occurrence of charcoalrot in a particular area is greatly influenced,like most plant diseases, by environmental conditions.It may be widespread in some years andlocalized or even absent in others. In India thedisease occurs on sorghums growing in both red(Alfisol) and black (Vertisol) soils. In general theworldwide distribution of the disease would indicateits occurrence on many different soil types.SymptomsA variety of symptoms are associated with charcoalrot. These include root rot, soft stalks, lodgingof plants, premature drying of stalks, and poorlydeveloped panicles with small inferior-quality grain(Hsi 1956, Uppal et al. 1936),The most striking and usually first indication ofthe disease is lodging of plants as they approachmaturity. Lodging is due to the weakened conditionof the stalk, caused by the disintegration of the pithand cortex by the pathogen, leaving the lignifiedfibrovascular bundles suspended as separate*Principal Plant Pathologist and Plant Pathologist, ICRISAT.International Crops Research Institute for the Semi-Arid Tropics. 1984. Sorghum Root and Stalk Rots, a CriticalReview: Proceedings of the Consultative Group Discussion on Research Needs and Strategies for Control ofSorghum Root and Stalk Rot Diseases, 27 Nov - 2 Dec 1983, Bellagio, Italy, Patancheru, A.P. 502 324, India:ICRISAT.11

12strands in the hollow stalk; hence "hollow stalk ofsorghum" as the disease was first named by Uppalet al. (1936). The vascular bundles are profuselycovered with tiny black sclerotia of the pathogen,which give the charcoal appearance to theaffected area. Thus the name "charcoal rot" describesthe appearance of the disease insideinfected roots and stalks.Sometimes charcoal rot symptoms are not easilynoticeable. Harris (1962) reported that in Nigeriathe disease escaped attention because symptomswere inconspicuous. Affected plants lookedhealthy but had much thinner stalks than normaland had very small panicles.M. phaseolina may also infect seedlings, causingseedling blight or damping-off symptoms undermoist and high temperature conditions (Uppal et al.1936). There is also one report of the pathogencausing leafspot symptoms in sorghum (Raut andBhombe 1972). Very little is known about these twophases of the disease.Economic ImportanceIn order to determine the research needs andstrategies for control of charcoal rot, a realisticdefinition of the problem with reference to croplosses is required. The literature contains manyreports on the destruction of sorghum crops bycharcoal rot, but sound and reliable quantitativedata on yield losses are not given. Uppal et al.(1936) determined that the disease was of "sufficienteconomic importance" on postrainy-seasoncrops in Maharashtra State, India. Harris (1962)reported that in Kano, Nigeria, charcoal rot caused"considerable loss in yield." In nearby CameroonS.B. King and D. Barry (Major Cereals in AfricanProject, Samaru, Nigeria, 1970; unpublished reportof a trip to Cameroon and Chad) saw severe symptomsof charcoal rot in farmers' fields and estimatedyield losses of over 50%. Similarly "seriouslosses" in several states in the USA were reported,but no quantitative data on crop loss were given(Leukel et al. 1951).In spite of the lack of data on field crop losses, thedestructive potential of charcoal rot in susceptiblecultivars is unquestionable. Four types of croplosses may be recognized: (1) loss in grain yieldand quality due to stunted plants, smaller stalksthan normal, and premature drying; (2) poor cropstands due to seedling blight; (3) complete loss ofyield in lodged plants where mechanical harvestingof grain is practiced, and where harvesting is manual,destruction of lodged plants by termites orother animal pests before the grain or fodder iscollected; (4) loss in quality and quantity of fodderdue to infection and destruction of the stalk.Under experimental conditions we haveobtained 100% lodging and grain yield losses of 23to 64% in CSH-6 hybrid at three locations in Indiaand one in Sudan (Table 1). In these experimentsnatural charcoal rot infection of plants was inducedby subjecting them to drought by withdrawing irrigationat different growth stages; grain yield wasdetermined from both lodged and standing plants.Although drought alone must have contributed tosome yield reduction, the combined effects ofdrought and charcoal rot that caused plants tolodge must have greatly increased the level of yieldTable 1. Lodging and yield of charcoal-rot-infected CSH-6 sorghum under four moisture stress treatments atfour locations in 1981.Locations, lodging (%), and plot yield (kg/18 m 2 )ICRISAT Center (India) Dharwar (India) IMandyal (India) Wad Medani (Sudan)Moisture stresstreatments Lodging (%) Yield Lodging (%) Yield Lodging (%) Yield Lodging (%) Yieldirrigation to grain maturity 8 2.2Loss in yield (%) aIrrigation to 50% anthesis 42 2.2Irrigation to boots swollen 46 1.8Irrigation to ligule visible 55 1.6SE±3.54 0.08277 3.3 1 3.086 2.5 2 2.0100 2.1 36 1.7100 1.7 47 1.11.92 0.10 3.51 0.1748 643 2.15 1.956 1.973 1.63.13 0.1023a.Irrigation to grain maturity - irrigation to ligule visible x 100Irrigation to grain maturity

13loss. At Dharwar a 35% reduction in 1000-grainweight was recorded when this technique wasused. Similarly Anahosur and Patil (1983) reported15-55% loss in grain weight in their experimentsconducted at Dharwar. These data on grain yieldlosses clearly show the economic importance ofthe disease when it occurs as plants approachmaturity. However, there is still need for more data,particularly on the various types of losses describedabove from surveys in farmers' fields.Improved, high-yielding cultivars tend to be ultrasusceptibleto charcoal rot. Improved varieties andhybrids that revolutionized sorghum production inIndia in the 1970s (Rao 1982) have proved verysusceptible to the disease, with 100% lodging insevere cases (Nagarajan et al. 1970, Anahosur andRao 1977, Avadhani and Ramesh 1979). In WestAfrica high-yielding exotic cultivars tend to be verysusceptible to charcoal rot (J.F. Scheuring, ICRI-SAT/Mali Program, personal communication, Feb1983). The susceptibility of improved cultivars tocharcoal rot poses a serious problem for sorghumimprovement programs worldwide, and a solutionmust be found that would enable farmers to.benefitfrom the use of improved cultivars.Causal OrganismThe causal organism of charcoal is a commonsoilborne fungus often known by its imperfect stateMacrophomina phaseolina (Tassi) Goid. (Domschet al. 1980). The perfect state is called Sclerotiumbataticola Taub. Eight synonyms that may beencountered in the literature are: Macrophominaphaseoli (Maubl.) Ashby, Macrophomina PhilippinesPetr., Macrophomina crochori Sawada,Macrophomina cajani Syd. & Butl., Macrophominasesami Sawada, Rhizoctonia bataticola (Taub.)Butl., Rhizoctonia lamellifera Small, and Dothiorellacajani Syd. & Butl. (Holliday and Punithalingam1970).Association with Other FungiIn diseased roots and stalks with conspicuoussigns of charcoal rot, fungal isolations usuallyreveal the association of M. phaseolina with otherfungi. In Texas, USA, both M. phaseolina and Fusariummoniliforme were obtained in cultures of diseasedstalks (Tullis 1951). Similar observationswere made in Georgia, USA (Luttrell 1950), and inIndia(ICRISAT1983). In Argentina, where F.moniliformewas the predominant fungus isolated fromlodged plants, 40% of the isolations were M. phaseolina.Other fungi isolated included unidentifiedFusarium spp, Rhizoctonia solani, Helminthospohumsativum, and Nigrospora sphaerica (Frezziand Teyssandier 1980). Similarly, in New SouthWales, Australia, systematic surveys to assess therelative importance of fungi associated with rootand stalk rots revealed that, although F. moniliformewas predominant, M. phaseolina and N.sphaerica were regularly isolated simultaneouslyfrom diseased roots and stalks (Trimboli and Burgess1982).Data cited above show clearly that in most casesof charcoal rot, M. phaseolina is not the sole causeof the disease under natural field conditions, butacts in combination with other pathogens to produceit. In other words, what is visually identified ascharcoal rot is a sign of one fungus among severalin a disease of complex etiology. Wadsworth andSieglinger (1950) suggested that the several fungiassociated with stalk rots attack in some orderlysequence, with M. phaseolina being the last andmost conspicuous of the sequence. Leukel et al.(1951) also suggested that root and stalk invasionby M. phaseolina is preceded by F. moniliforme. P.Mayers (Department of Primary Industries,Queensland, Australia; personal communication,Aug 1983) has suggested that temperature influencesthe dominance of a particular pathogen in thedisease complex. F. moniliforme is the dominantfungus under low soil temperatures, whereas M.phaseolina predominates at high soil temperatures.The pathological significance of the involvementof several fungi in causing root and stalk rot isnot known and must be investigated.Host Range andPhysiological SpecializationM. phaseolina is a plurivorous pathogen of over 75different plant families and about 400 plant species(Dhingra and Sinclair 1977). Among these areimportant food crops, such as cereals (maize,sorghum, and finger millet), legumes (cowpea,groundnut, soybean, pigeonpea, and chickpea),vegetables (cabbage, tomato, and pumpkin), andfruits (apple, pear, orange, and banana). As its widehost range suggests, M. phaseolina is a highly variablepathogen in both its pathogenicity and myco-

logical characteristics. Some isolates of thepathogen are host specific (Hildebrand et al. 1945),while others can attack a wide range of hosts (Holidayand Punithalingam 1970). Physiological raceshas been reported for isolates of some crops suchas jute (Ahmed and Ahmed 1969), and variability incultural characteristics and pathogenicity of isolatesfrom different parts of the same plant hasbeen reported in soybean (Dhingra and Sinclair1973).Pathogen variation and physiological specializationare important factors that require considerationin disease control programs using hostresistance, In the case of charcoal rot of sorghum,it would be useful to know (a) if sorghum is susceptibleto isolates of the pathogen from other plantspecies and (b) whether physiological races existamong sorghum isolates of the pathogen. Unfortunatelysuch information is not available in theliterature.Biology and EpidemiologyMost of our knowledge of the biology of M. phaseolinais derived from results of research with isolatesfrom crops other than sorghum. It is assumed thatthe general biology of sorghum isolates is similar tothat of isolates from other crops, although thepathosystem may be different. As stated in ourintroduction, only those aspects of the biology thatinfluence the pathosystem will be reviewed.Source and Survival of InoculumM. phaseolina is a root-inhabiting fungus (Garrett1956), with little or no saprophytic growth in eithersoil or dead host cells of infected plants (Norton1953, Edmunds 1964). In the absence of hostplants, it survives or overseasons predominantly assmall black sclerotia in diseased root and stemdebris or in soil after decay of the plant material inwhich they were formed (Smith 1969a, Bhattacharyaand Samaddar 1976). Thus the primary sourceof inoculum is sclerotia in the soil. Cook et al. (1973)reported that after 16 months in soil, 23% of sclerotiafrom sorghum stalks germinated. Sclerotia fromother plant hosts are known to survive for severalyears (Dhingra and Sinclair 1977).Populations of sclerotia in a maize field rangedfrom zero to more than 1000/g of soil (Papavizasand Klag 1975). This great variation in inoculumdensity in soil is one of the factors responsible forthe highly variable incidence of charcoal rot in thefield. According to Meyer et al. (1973), inoculumdensity increased in soil with continuous croppingof a susceptible crop of soybeans. This has implicationsin disease management strategies, whichwill be discussed later.Root Penetration and the Effectsof Drought Stress on Host Colonizationand Disease DevelopmentThe process and mechanisms by which M. phaseolinapenetrates roots and colonizes sorghumroots and stalks are not clearly known or understood.It is assumed from the work of Smith (1969b)with pine and Bhattacharya and Samaddar (1976)with jute that sorghum root exudates stimulate thegermination of sclerotia in the soil. What happensnext is still being debated. Reports in the literaturecan be summarized into two views. The first view isthat mycelia from germinating sclerotia penetraterootlets at any time, but no further growth or colonizationtakes place until the plants are droughtstressed, when the pathogen grows extensivelyand colonizes roots and stalks (Norton 1958). In thesecond view, exemplified by the work of Odvodyand Dunkle (1979), root penetration does not occuruntil plants are drought stressed. Whatever thetruth is with regard to time of penetration, it is clearfrom the literature that colonization of root and stalktissue and charcoal rot development occur onlywhen plants are drought stressed during the grainfillingstage (Edmunds 1964, Edmunds and Voigt1966, Odvody and Dunkle 1979).Drought causes harmful physiological or metabolicchanges in the plant. It reduces plant vigor;plants so affected are predisposed to attack bynonaggressive pathogens such as M. phaseolina(Schoeneweiss 1978). From a review of stalk rotproblems in maize and sorghum and the associatedenvironmental factors, Dodd (1977, 1980)developed a "photosynthetic stress-translocationbalance" concept to explain the predisposition ofsorghum to charcoal rot. According to thishypothesis:a. sorghum plants are predisposed to charcoalrot as the root cells senesce because of areduction of carbohydrates to maintain metabolicfunctions, including resistance;14

. the availability of carbohydrate to the roottissue is influenced by the environmentalstresses affecting photosynthesis and bycompetition for carbohydrate by the developinggrain;c. if the combination of photosynthetic stress andtranslocation balance reduces carbohydrateto root tissue, root cells and also those of thelower part of the stalk senesce and lose resistanceto the charcoal rot pathogen;d. the charcoal rot pathogen invades and destroysroot tissue, and subsequently rots thestalk, reducing its strength. This frequentlyresults in lodging.Although many environmental factors reduce photosynthesis,and hence assimilate (photosynthate)supply, drought stress at grain filling is the primaryfactor that triggers events that eventually lead tocharcoal rot disease and plant lodging.Dodd's hypothesis implies that the interaction ofdrought stress and pathogens causes stalk rotsand lodging. Direct evidence for this has been providedby P. Mayers (Department of Primary Industries,Queensland, Australia; personal communication,Aug 1983), who reported as follows:In field experiments Fusarium stalk rot (F.moniliforme) and subsequent lodging developedwhen plant moisture stress and highinoculum density interacted. Minimal andsevere moisture stress were obtained byusing irrigation and rain excluding shelters.In the presence of inoculum, stress accentuatedstalk rot 13.5 fold. Natural and very lowlevels of Fusarium inoculum were achievedby soil fumigation with dazomet. Fumigationdecreased stalk rot from 59.3% to 1.3% in themost susceptible hybrid. Mean stalk rot percentagewas below 2.8% in non-stressedplots irrespective of inoculum level and wasbelow 1.7% on fumigated plots irrespectiveof stress level. Extensive stalk rot developedonly in non-fumigated, moisture stressedplots.Henzell and Gillieron (1973) and Chamberlin(1978), on the other hand, hold the view that plantlodging under drought stress is a purely physiologicalproblem. Drought stress reduces assimilatesupply to the lower part of the stalk for maintenancerespiration. This results in senescence, disintegrationof pith cells, and hence lodging. These twoviews on the causes of lodging are fully discussedby Henzell et al. (these proceedings). It is acknowledgedthat drought stress alone can cause lodgingwithout assistance from pathogens where inoculumis absent. However, where pathogens arepresent, drought-stressed plants are invariablyinvaded by them, and this leads to increased damageof plants. It is possible that low or intermediatelevels of drought stress may be tolerated by theplant except when combined with the pathogen.There is an obvious need for further research toclarify these issues.Cultural Practices and Charcoal RotNitrogen fertilization and plant densities have beenreported to influence charcoal rot. In India the highlevels of nitrogen fertilization needed to maximizethe yield potential of improved cultivars increasethe severity of charcoal rot (Avadhani et al. 1979,Mote and Ramshe 1980). Patil et al. (1982) reportedcultivar differences in the effect of plant density oncharcoal rot. While charcoal rot incidence was significantlyhigher in the hybrid CSH-8R at 180 000plants/ha than at 45000 plants/ha, no differenceswere detected in the varieties SPV 86, SPV 265, andM 35-1. In a factorial experiment using line-sourceirrigation, we obtained highly significant positivecorrelations between drought stress, plant density,and nitrogen level (Table 2). It appears that highplant density increases plant competition for availablesoil moisture and that this competitionincreases with drought. The effect of nitrogen inincreasing charcoal rot is probably due to its indirecteffect on the ratio of root-to-shoot growth.Nitrogen promotes luxuriant shoot growth, and rootdevelopment suffers. Under drought stress, thelack of a sufficient root system reduces the ability ofa plant to obtain moisture, while at the same time itswater requirement is increased by the luxuriantgrowth (Ayers 1978).Systems of crop management that reduce pathogeninoculum and increase conservation of soilwater decrease the incidence of charcoal rot.Sorghum grown under minimum tillage (ecofallow)in a winter wheat-sorghum-fallow rotation had 11%stalk rot, compared to 39% in conventional tillage(Doupnik and Boosalis 1975).Sorghum grown in a mixed crop situation hasalso been reported to suffer less charcoal rot damagethan sole crop sorghum (Khume et al. 1980),15

Table 2. Percent lodging in CSH-6 sorghum at three levels of nitrogen and three plant populations subjected toten different moisture stress levels with line source irrigation at ICRISAT Center.Percent lodgingPlant density andNitrogen levels amoisture stress N 1 N 2 N 3 MeanD 1b7.57 3.83 6.38 5.93Stress-1 c 0.00 1.98 5.24 2.41Stress-2 1.08 1.09 3.26 1.81Stress-3 0.36 0.84 2.44 1.21Stress-4 1.57 1.39 2.09 1.68Stress-5 0.69 0.64 0.76 0.70Stress-6 0.00 0.69 0.00 0.23Stress-7 9.83 7.09 8.76 8.56Stress-8 21.52 11.64 14.18 15.78Stress-9 14.35 6.97 11.03 35.35Stress-10 26.30 5.94 16.00 16.08D2 13.91 18.40 18.76 17.02Stress-1 1.01 5.88 3.00 3.30Stress-2 0.55 1.42 7.58 3.18Stress-3 2.93 3.03 9.85 5.27Stress-4 2.25 6.73 3.24 4.07Stress-5 4.43 12.69 7.97 8.36Stress-6 7.63 11.24 6.78 8.55Stress-7 13.33 23.59 18.21 18.38Stress-8 30.13 37.78 30.64 32.85Stress-9 37.77 36.43 45.73 39.98Stress-10 39.03 45.19 54.76 46.33D3 29.40 37.00 36.17 34.19Stress-1 1.95 4.54 7.34 4.61Stress-2 4.83 6.12 10.73 7.23Stress-3 4.43 8.26 10.35 7.68Stress-4 9.35 9.48 13.12 10.65Stress-5 17.68 31.72 28.83 26.08Stress-6 24.37 49.76 38.12 37.42Stress-7 43.34 63.07 49.34 51.92Stress-8 51.62 58.45 55.16 55.08Stress-9 65.14 69.97 71.77 68.96Stress-10 71.30 68.62 76.92 72.28Mean 16.96 19.74 20.44 19.05SE (±) Density 2.73 2.35 3.09 1.58SE (±) Stress 3.05 2.46 3.17 1.68SE (±) Stress x density 5.29 4.26 5.49 2.91a.N 1 = 20 kg nitrogen/haN 2 = 60 kg nitrogen/haN 3 =120 kg nitrogen/hab. D 1 = 66675 plants/haD 2 = 133350 plants/haD 3 =266700 plants/hac. Stress-1 = Nearest to line source (minimum moisture stress level).Stress-10 = Farthest from line source (maximum moisture stress level).16

Anatomical and PhysiologicalFactors Associated with ResistanceSeveral anatomical and physiological plant charactershave been associated with resistance tocharcoal rot and suggested as selection criteria inresistance screening programs. Maranville andClegg (these proceedings) discuss the correlationof "stalk strength" with resistance to charcoal rot.Although much variation exists in the stalk anatomyof genetically diverse sorghum lines (Schertz andRosenow 1977), there is no experimental evidenceyet of this variation being associated withresistance.Maunder et al. (1971) reported that in a charcoalrot nursery where plants were drought stressedfrom the boot stage to maturity, "bloomless plants"had 38.4% more disease than those with the waxybloom on the stalk internodes. They suggested thatbloomless plants were more predisposed to charcoalrot than "bloomed plants," Further research isneeded to confirm this.The most promising plant character that is positivelycorrelated with charcoal rot resistance, and isincreasingly used as a selection criterion, is nonsenescence.Rosenow (1980) reported significantcorrelations between nonsenescence, lodging resistance,and charcoal rot resistance in Texas, USA.Selection for charcoal rot resistance is based onthe degree of nonsenescence exhibited by plantsunder drought stress during the late grain developmentstage. Both Duncan and Rosenow (theseproceedings) provide more detailed descriptions ofthe nonsenescence character and its utilization inselection and breeding for charcoal rot resistance.In India we also found significant positive correlationsbetween charcoal rot resistance and plantnonsenescence (Table 3). However, multilocationaltesting for stability of the nonsenescencecharacter showed that lines nonsenescent at onelocation were not necessarily nonsenescent atanother location (Table 4), indicating the locationspecificity of the character. This would beexpected from variations in pathogen inoculumdensity and in the level of drought stress to whichplants are subjected during evaluation at differentlocations. Stability of nonsenescence would mostprobably depend on the level of drought stress. Upto a specific level of stress, a genotype would showstability in nonsenescence at several locations, butbeyond that it may not. Further research is obviouslyneeded to elucidate this.Disease Rating ScaleSeveral disease rating scales have been used toevaluate sorghum lines for resistance to charcoalrot or stalk rots in general. The most commonlyused is a 1 -to-5 scale based on the percentage oflodged plants, where 1 = no lodged plants and 5 =over 20% plants lodged (Frezzi and Teyssandier1980). The main disadvantage of this method ofdisease evaluation is that it excludes infectedplants that have not lodged. It is not uncommon in acharcoal rot nursery to see standing plants that areinfected by the disease. Where toothpick inoculationis carried out, a rating scale based on thegrowth of the pathogen up the stem from the pointof inoculation is used (Rosenow 1980). As discussedearlier under "Resistance screening technique,"this method of inoculation and evaluation isepidemiologically unsound since infection isthrough the root system in nature. In the ICRISATcharcoal rot research project we have developed arating scale that takes into account roof infection,soft stalk of infected plants that do not lodge, andlodged plants. This scale is laborious to use whenTable 3. Correlation coefficients among parameters of charcoal rot disease scores under depleting soil moisturecondition at four locations in India (Patancheru, Dharwar, Nandyal, and Madhira).Disease Lodging Soft stalk Mean no. of Mean score a Leaf andparameter (%) (%) nodes crossed for root infection plant death aLodging (%) 0.96** 0.88** 0.57** 0.65**Soft stalk (%) 0.88** 0.52** 0.60**Mean no. of nodes crossed 0.47** 0.52**Mean score for root infection 0.92**Leaf and plant deathCorrelation coefficient at 5% = 0.288, at 1% = 0.372 (**significant at 1%).a. Based on three locations (Patancheru, Dharwar and Nandyal).18

Table 4. Days to flowering, plant height (m), leaf and plant death, grain weight, percent lodging, percent softstalk, mean number of nodes crossed, and mean score for root infection of six sorghum genotypes(rated as nonsenescent) at four locations in India during 1981 postrainy season.Leaf a 1000- Mean Mean bDays to Plant and grain Percent no. of score of50% height plant weight Percent soft nodes rootGenotype Location flowering (m) death (g) lodging stalk crossed infectionIS-108 Patancheru 56 0.85 2.50 29.87 0.00 0.00 0.50 3.00Dharwar 47 1.62 4.42 19.94 44.62 37.50 1.17 4.00Nandyal 53 1.60 4.50 27.68 40.00 55.00 2.00 4.50Madhira 55 1.75 2.27 23.82 10.22 3.55 0.31 2.25IS-176 Patancheru 70 1.25 4.00 26.48 25.00 40.00 0.70 4.50Dharwar 59 1.75 4.55 17.10 43.17 62.50 1.67 4.50Nandyal 71 1.19 2.40 34.17 5.00 5.00 0.05 3.00Madhira 65 1.35 3.36 25.53 0.00 0.00 0.43 1.50IS-2954 Patancheru 67 1.10 4.50 25.90 20.00 50.00 1.10 5.00Dharwar 60 1.35 3.60 24.81 2.38 5.00 0.15 2.00Nandyal 71 1.00 2.60 30.66 0.00 15.00 0.80 1.95Madhira 65 1.25 4.00 27.67 30.00 61.85 1.53 4.00IS-3927 Patancheru 61 0.75 4.30 50.97 55.00 55.00 1.95 5.00Dharwar 57 1.12 2.95 34.44 26.25 15.00 0.35 2.00Nandyal 60 1.05 3.55 40.66 45.00 50.00 2.80 4.00Madhira 59 1.25 2.80 45.74 0.00 13.35 0.33 2.50IS-10722 Patancheru 65 1.15 3.60 31.88 25.00 25.00 0.55 4.50Dharwar 60 1.20 3.22 24.32 22.80 35.00 0.75 2.50Nandyal 71 0.95 2.90 46.36 10.00 20.00 0.85 3.25Madhira 66 1.40 4.07 19.82 48.75 48.75 2.00 4.00CSH-6 Patancheru 62 1.15 4.79 26.95 78.75 85.00 2.65 4.73Dharwar 62 1.57 4.70 25.62 57.41 72.18 2.32 4.87Nandyal 67 1.25 4.08 25.22 100.00 100.00 4.70 5.00Madhira 56 1.34 4.91 26.36 83.67 92.36 5.41 4.93SE for cultivar (±) 2.16 2.05 0.26 2.12 9.21 8.91 0.69 0.46SE for location (±) 0.46 0.44 0.056 0.45 1.97 1.91 0.15 0.14a. Nonsenescence ratings based on leaf and plant death scores on 1 -5 scale, where 1 = completely green and 5 = dead.b. Root infection score on 0-5 scale, where 0 = no discoloration and infection; and 5 = more than 50% roots showing infection anddiscoloration.large numbers of material are to be evaluated.Nevertheless it is essential that the differentphases of the disease are considered in a resistancescreening program. Since leaf and plantdeath (senescence) are positively correlated withcharcoal rot infection, a leaf and plant death scoringscale would be most useful for disease evaluationof large numbers of plants.Resistance SourcesAttempts to find sources of resistance to charcoalrot for breeding programs were started in the USAin the 1940s, In one of the most comprehensivetesting programs Hoffmaster and Tullis (1944)screened 232 sorghum lines of diverse geneticbackground at 4 locations for 4 years. Althoughthey found differences in the susceptibility of theselines to charcoal rot, data showed no stability in theperformance of the lines from year to year. Theythus concluded, "it is impossible from the dataavailable to recommend certain varieties for localitiesin which Macrophomina dry rot is a limitingfactor."In the ICRISAT charcoal rot research project wehave also found inconsistencies in the reaction tothe disease of a large number of germplasm lines.19

This lack of stability is due, as explained earlier, todifferent levels of drought stress and hence differentlevels of predisposition to the disease. However,one line, E 36-1, has consistently shownresistance to lodging at several locations in 3 yearsof testing. The plants were infected, as shown byfungal isolations from roots and stalks, but theinfection was not severe enough to cause lodging(ICRISAT 1982).In the USA the line New Mexico-31 released byMalm and Hsi (1964) as resistant to charcoal rothas been used extensively in breeding programs.In recent years Rosenow (1980) identified 13 nonsenescentlines as good sources of resistance tocharcoal rot. The stability of resistance of theselines outside Texas is not known. They should betested for use in other countries where charcoal rotis a problem.The need for stable and better sources of resistanceis obvious. Most of the large (over 20000lines) ICRISAT sorghum germplasm collection hasnot been screened, and it is conceivable thatamong these (especially among lines fromdrought-prone areas) are lines resistant to charcoalrot. However, the priority should be to developa reliable screening technique that can be used todistinguish resistant from susceptible lines undergraded levels of drought stress.Crop ManagementThe ideal and most effective control strategy forcharcoal rot is to prevent drought stress from predisposingplants to infection. In other words, resistanceto predisposition would be the best method ofcontrol. This can be done by proper managementof the soil-plant-water system. Except wheresorghum is grown under irrigation, farmers have nocontrol over the variability of rainfall in mostsorghum-growing areas. Cultural practices thatreduce pathogen inoculum in soil and that increasewater availability and use by plants (e.g., plant density,rate of nitrogen fertilization, use of varietieswith different rooting characteristics, and crop rotation)have been suggested as possible measuresof reducing drought-stress-related diseases (Cookand Papendick 1972). Such measures have beensuccessful in controlling fusarium foot rot of wheat(Cook 1980). Whether similar crop husbandrypractices would be effective and practicable forcontrol of charcoal rot awaits investigation.Drought resistance as an indirect method ofcharcoal rot control raises the obvious and importantquestion: will genotypes that resist droughtalso resist charcoal rot? We are unable to answerthis question because we have insufficient knowledgeof the interactions of drought stress, the charcoalrot pathogen, and the host. The onlyproposition we can offer is that certain levels ofdrought stress may be resisted by plants in theabsence of the pathogen. Where the pathogen ispresent, such plants may be infected; the pathogenthen destroys roots, which contributes to furtherdrought stress. Therefore breeding for drought resistancealone may not provide the answer to thecharcoal rot problem.Priorities forFuture ResearchThis review will have shown that in spite of itsimportance, research on charcoal rot has been'largely superficial. Wide gaps still exist in the biologyof the pathogen and epidemiology of the disease,and in particular, the process ofpathogenesis and how it is influenced by environmentaland plant physiological factors. The technicalproblems of working with a soilborne,root-infecting pathogen are partly responsible forthese deficiencies. However, techniques are nowavailable that could profitably be used in charcoalrot research.Following are some of the areas that needresearch attention in the future:1. Crop loss. Quantitative crop loss data areneeded that distinguish between direct effectsof drought and indirect effects through croppredisposition and subsequent damage bycharcoal rot. Under what conditions are indirecteffects more important than directeffects?2. Pathogenesis. Root rot precedes stalk rot.When, in the growth stage of the plant, andunder what conditions are roots penetrated bythe pathogen? What conditions favor root andstalk colonization?3. Interactions with other pathogens. Since M.phaseolina does not infect plants alone, thereis need for basic studies on the interactionsamong the different pathogens involved. Whatis the sequence of infection? Is there synergismin host-parasite interaction?20

4. Pathogen variation and physiological specialization.In view of the wide host range ofM. phaseolina, it would be useful for control ofthe disease to know (a) if sorghum is susceptibleto pathogen isolates from other hosts, and(b) whether physiological races exist amongthe sorghum isolates.5. Predisposition by drought stress and plantgrowth stage. What level of drought stress(plant water potential) is optimum for predisposingplants to infection? Is there a varietaldifference in this? Can charcoal rot occur inplants at all growth stages if sufficientlypredisposed?6. Predisposition and plant water potential. Inscreening for resistance, can we actuallyrelate predisposition of plants to actual measurementsof plant water potential? Gradedlevels of soil moisture supply, and hence predisposition,can be provided by the line-sourceirrigation technique.7. Sink. Improved high-yielding varieties andhybrids tend to be ultrasusceptible to charcoalrot. Is it sink size or other factors that makesuch cultivars vulnerable to the disease? Canwe identify the conditions under which a givensize of sink is likely to indirectly predisposeplants to infection?8. Association of nonsenescence and diseaseresistance. Study the physiological basis ofnonsenescence, its stability under differentenvironmental conditions, and its relationshipto charcoal rot resistance.9. Correlation between drought resistanceand charcoal rot resistance. Since droughtstress is the primary factor that predisposesplants to charcoal rot, would drought-resistantplants also resist charcoal rot?10. Development of a reliable field screeningtechnique. This is essential for success inbreeding for resistance.Answers to most of the questions raised abovewould require interdisciplinary and collaborativeresearch efforts between pathologists, physiologists,breeders, and soil scientists. We hope thatthe proceedings of this meeting will help to bringforth this essential cooperation for the understandingand eventual control of charcoal rot of sorghum.ReferencesAHMED, N., and AHMED, Q.A. 1969. Physiological specializationin Macrophomina phaseoli (Maubl.) Ashbycausing root rot of jute, Corchorus species. Mycopathologiaet Mycologia Applicata 39:129-138.ANAHOSUR, K.H., and PATIL, S.H. 1983. Assessment oflosses in sorghum seed weight due to charcoal rot. IndianPhytopathology 36:85-88.ANAHOSUR, K.H., PATIL, S.H., and HEGDE, R.K. 1983.Evaluation of PCNB against Macrophomina phaseolina(Tassi) Goid. causing charcoal rot of sorghum. Pesticides17:11-12.ANAHOSUR, K.H., and RAO, M.V.H. 1977. A note on theepidemic of charcoal rot of sorghum in the regionalresearch station, Dharwar. Sorghum Newsletter 20:22.AVADHANI, K.K., PATIL, S.S., MALLANAGOUDE, B., andPARVATICAR, S.R. 1979. Nitrogen fertilization and itsinfluence on charcoal rot. Sorghum Newsletter 22:119-120.AVADHANI, K.K., and RAMESH, K.V. 1979. Charcoal rotincidence in some released and pre-released varietiesand hybrids. Sorghum Newsletter 21:37-38.AYERS, P.G. 1978. Water relations of diseased plants,Pages 1 -60 in Water deficits and plant growth (ed. T.T.Kozlowski). New York, New York, USA: Academic Press.323 pp.BHATTACHARYA, M., and SAMADDAR, K.R. 1976.Epidemiological studies on jute diseases. Survival ofMacrophomina phaseoli (Maubl.) Ashby in soil. Plant andSoil 44:27-36.CHAMBERLIN, R.J. 1978. The physiology of lodging ofgrain sorghum (Sorghum bicolor L Moench). Ph.D. thesis,University of Queensland, Australia.COOK, G.E., BOOSALIS, M.G., DUNKLE, L.D., andODVODY, G.N. 1973. Survival of Macrophomina phaseoliin corn and sorghum stalk residue. Plant Disease Reporter57:873-875.COOK, R.J. 1980. Fusarium foot rot of wheat and itscontrol in the Pacific Northwest. Plant Disease 64:1061 -1066.COOK, R.J., and PAPENDICK, R.I. 1972. Influence ofwater potential of soils and plants on root disease. AnnualReview of Phytopathology 10:349-374.DHINGRA, O.D., and SINCLAIR, J.B. 1973. Location ofMacrophomina phaseoli on soybean plants related toculture characteristics and virulence. Phytopathology63:934-936.DHINGRA, O.D. and SINCLAIR, J.B. 1977. An annotatedbibliography of Macrophomina phaseolina 1905-1975.Vicosa, Brazil: Imprensia Universitaria, Universidade Federalde Vicosa. 244 pp.21

DHINGRA, O.D., and SINCLAIR, J.B. 1978. Biology andpathology of Macrophomina phaseolina, Vicosa, Brazil:Imprensia Universitaria, Universidade Federal de Vicosa.166 pp.DODD, J.L. 1977. A photosynthetic stress-translocationbalance concept of corn stalk rot. Pages 122-130 In Proceedingsof the 32nd Annual Corn and SorghumResearch Conference (eds. H.D. Loden and D. Wilkinson).Washington, D.C., USA: American Seed TradeAssociation.DODD, J.L. 1980. The photosynthetic stresstranslocationbalance concept of sorghum stalk rots.Pages 300-305 In Sorghum Diseases, a World Review:Proceedings of the International Workshop on SorghumDiseases, sponsored jointly by Texas A&M University(USA) and ICRISAT. Patancheru, A.P. 502 324, India:ICRISAT.DOMSCH, K.H., GAMS, W., and ANDERSON, T.H. 1980.Compendium of soil fungi. 2 vols. London, U.K.: AcademicPress. 859 and 405 pp.DOUPNIK, B., and BOOSALIS, M.G. 1975. Ecofallowreduces stalk rot in grain sorghum. Phytopathology65:1021-1022.EDMUNDS, L.K. 1964. Combined relation of plant maturity,temperature, and soil moisture to charcoal stalk rotdevelopment in grain sorghum. Phytopathology 54:514-517.EDMUNDS, L.K., and VOIGT, R.L. 1966. Role of seedproduction in predisposition of sorghum to charcoal rot.Phytopathology 56:876 (abstract).EDMUNDS, L.K., VOIGT, R.L., and CARASSO, F.M. 1964.Use of Arizona climate to induce charcoal rot in grainsorghum. Plant Disease Reporter 48:300-302.FREZZI, M., and TEYSSANDIER, E.E. 1980. Summary andhistorical review of sorghum diseases in Argentina. Pages11-15 in Sorghum Diseases, a World Review: Proceedingsof the International Workshop on Sorghum Diseases,sponsored jointly by Texas A&M University (USA) andICRISAT. Patancheru, AP. 502 324, India: ICRISAT. 469PP.GARRETT, S.D. 1956. Biology of root-infecting fungi. London,U.K.: Cambridge University Press. 293 pp.HARRIS, E. 1962. Diseases of guineacorn. Samaru TechnicalNotes 2:1-13.HENZELL, R.G., and GILLIERON, W. 1973. Effect of partialand complete panicle removal on the rate of death ofsome Sorghum bicolor genotypes under moisture stress.Queensland Journal of Agricultural and Animal Sciences30:291-299.HILDEBRAND, A.A., MILLER, J.J., and KOCH, LW. 1945.Some studies on Macrophomina phaseoli (Maubl.) Ashbyin Ontario. Scientific Agriculture 25:690-706.HOFFMASTER, D.E., and TULLIS, E.C. 1944. Susceptibilityof sorghum varieties to Macrophomina dry rot (charcoalrot). Plant Disease Reporter 28:1175-1184.HOLLIDAY, P., and PUNITHALINGAM, E. 1970. Macrophominaphaseolina. No. 275 in CMI (CommonwealthMycological Institute), Descriptions of pathogenic fungiand bacteria. Kew, Surrey, U.K.: CMI.HSI, D.C.H. 1956. Stalk rots of sorghum in eastern NewMexico. Plant Disease Reporter 40:369-371.ICRISAT. 1980. Sorghum Diseases, a World Review: Proceedingsof the International Workshop on Sorghum Diseases,sponsored jointly by Texas A&M University (USA)and ICRISAT. Patancheru, A.P. 502 324, India: ICRISAT.469 pp.ICRISAT. 1983. Annual Report 1982. Patancheru, A.P.502 324, India: ICRISAT.KHUNE, N.N., SHIWANKAR, S.K., and WANGIKAR, P.D.1980. Effect of mixed cropping on the incidence of charcoalrot of sorghum. Food Farming and Agriculture12:292-293.KRIKUN, J., ORION, D., NACHMIAS, A., and REUVENI, R.1982. The role of soilborne pathogens under conditions ofintensive agriculture. Phytoparasitica 10:247-258.LEUKEL, R.W., MARTIN, J.H., and LEFEBVRE, C.L. 1951.Sorghum diseases and their control. Farmers' Bulletin No.1959. Washington, D.C., USA: U.S. Department of Agriculture.50 pp.LUTTRELL, E.S. 1950. Grain sorghum diseases in Georgia.Plant Disease Reporter 34:45-52.MALM, N.R., and HSI, D.C.H. 1964. New Mexico 31: acharcoal rot-resistant grain sorghum line. New MexicoAgricultural Experiment Station Research Report 93. LasCruces, New Mexico, USA: New Mexico State University.MAUNDER, A.B., SMITH, D.H., and JUDAH, B.W. 1971.Bloom and bloomless isogenics as related to charcoal rotand diffusive resistance. Sorghum Newsletter 14:20-21.MEYER, W.A., SINCLAIR, J.B., and KHARE, M.N. 1973.Biology of Macrophomina phaseoli in soil studied withselective media. Phytopathology 63:613-620.MOTE, U.N., and RAMSHE, D.G. 1980. Nitrogen applicationincreases the incidence of charcoal rot in rabisorghum cultivars. Sorghum Newsletter 23:129.MUGHOGHO, L.K. 1982. Strategies for sorghum diseasecontrol. Pages 273-282 in Sorghum in the Eighties: Proceedingsof the International Symposium on Sorghum,sponsored by INTSORMIL, ICAR, and ICRISAT. Patancheru,A.P. 502 324, India: ICRISAT.NAGARAJAN, K., SARASWATHI, V., and RENFRO, B.L.1970. Incidence of charcoal rot (Macrophomina phaseoli)on CSH-1 sorghum. Sorghum Newsletter 13:25.22

NORTON, D.C. 1953. Linear growth of Sclerotium bataticolathrough soil. Phytopathology 43:633-636.NORTON, D.C. 1958. The association of Pratylenchushexincisus with charcoal rot of sorghum. Phytopathology48:355-358.ODVODY, G.N., and DUNKLE, L.D. 1979. Charcoal stalkrot of sorghum: effect of environment on host-parasiterelations. Phytopathology 69:250-254.PAPAVIZAS, G.C., and KLAG, N.G. 1975. Isolation andquantitative determination of Macrophomina phaseolinafrom soil. Phytopathology 65:182-187.PATIL, R.C., DESHAMANE, N.B., and PANDHARE, T.M.1982. Effect of plant density and row spacing on charcoalrot incidence in four cultivars of sorghum. Sorghum Newsletter25:110.RAJKULE, P.N., CHAUHAN, H.L., and DESAI, K.B. 1979.Chemical control of charcoal rot. Sorghum Newsletter22:120.RAO, N.G.P. 1982. Transforming traditional sorghums inIndia. Pages 39-59 in Sorghum in the Eighties: Proceedingsof the International Symposium on Sorghum, sponsoredby INTSORMIL, ICAR, and ICRISAT. Patancheru,A.P. 502 324, India: ICRISAT.RAUT, J.C., and BHOMBE, B.B. 1972. Leaf spot ofsorghum caused by Rhizoctonia bataticola. Indian Phytopathology25:586-587.ROSENOW, D.T. 1980. Stalk rot resistance breeding inTexas. Pages 306-314 in Sorghum Diseases, a WorldReview: Proceedings of the International Workshop onSorghum Diseases, sponsored jointly by Texas A&M University(USA) and ICRISAT. Patancheru, A.P. 502 324,India: ICRISAT.SCHERTZ, K.F., and ROSENOW, D.T. 1977. Anatomicalvariation in stalk internodes of sorghum. Crop Science17:628-631.SCHOENEWEISS, D.F. 1978. Water stress as a predisposingfactor in plant disease. Pages 61-99 in Vol. 5,Water deficits and plant growth (ed. T.T. Kozlowski). NewYork, New York, USA: Academic Press. 323 pp.SMITH, W.H. 1969a. Comparison of mycelial and sclerotialinoculum of Macrophomina phaseoii in the mortality ofpine seedlings under varying soil conditions. Phytopathology59:379-382.SMITH, W.H. 1969b. Germination of Macrophomina phaseolisclerotia as affected by Pinus lambertiana root exudate.Canadian Journal of Microbiology 15:1387-1391.TARR, S.A.J. 1962. Diseases of sorghum, sudan grassand broom corn. Kew, Surrey, U.K.: CommonwealthMycological Institute. 380 pp.TRIMBOLI, D.S., and BURGESS, L.W. 1982. The fungiassociated with stalk and root rot of grain sorghum in NewSouth Wales. Sorghum Newsletter 25:105-106.TULLIS, E.C. 1951. Fusarium moniliforme, the cause of astalk rot of sorghum in Texas. Phytopathology 41:529-535.UPPAL, B.N., KOLHATKAR, KG., and PATEL, M.K. 1936.Blight and hollow-stem of sorghum. Indian Journal ofAgricultural Science 6:1323-1334.WADSWORTH, D.F., and SIEGLINGER, J.B. 1950. Charcoalrot of sorghum. Oklahoma Agricultural ExperimentStation Bulletin No. B-355. Stillwater, Oklahoma, USA:Oklahoma A&M College and U.S. Department of Agriculture.7 pp.WATANABE, T., SMITH, R.S., Jr., and SNYDER, W.C.1970. Populations of Macrophomina phaseoli in soil asaffected by fumigation and cropping. Phytopathology60:1717-1719.Q u e s t i o n sMaunder:Should your reference to high-yield cultivars beingsuper susceptible, referring to hybrids, not be betterstated as first-cycle hybrids? The breeder has atendency to place yield ahead of lodging, and thiswill be more dramatic in initial transition to hybrids.But in the case of U.S. sorghum history, after thefirst 8-10 years the problem with charcoal rot wasgreatly reduced.Pande:Yes, hybrids under Indian conditions are quite susceptiblewhen planted in the postrainy season.Schoeneweiss:You stated that Macrophomina phaseolina doesnot grow in dead plant cells. Are you saying that thefungus does not grow as a saprophyte on organicmatter derived from sorghum?Pande:Yes.Vidyabhushanam:It was stated that lodging is not the only criterion formeasuring charcoal rot intensity. Is there any alternatemeasurement possible to know the level ofincidence of the disease? Has any correlationbetween root and stalk rot infection beenestablished?23

Pande:Lodging is the first apparent symptom of charcoalrot, and to confirm charcoal rot one has to split theplants to see the fungal colonization. Probably thetwo are necessary to assess the clear picture ofcharcoal rot.Vidyabhushanam:It is established that predisposition to droughtstress is essential for charcoal rot. Is it clearlyunderstood what stage and intensity of droughtstress is required for the disease to manifest itself?Pande:I suppose moisture stress is the most importantpredisposing factor for charcoal rot infection anddevelopment. We do not know exactly at whatstage the stress is effective. It seems stress at 50%flowering that continues up to maturity gives goodcharcoal rot expression.24

Fusanum Root andStalk DiseaseComplex

Fusarium Root and Stalk Disease ComplexN. Zummo*SummaryThis paper presents a brief review of a fusarium root and stalk disease complex of sorghum.The Fusarium species involved in this disease complex may occur wherever sorghum is grownworldwide and may also affect maize, millet, rice, and sugarcane. There are indications thatcertain cultural practices, such as maximum cultivation, high fertility levels, and high plantdensities, may increase the prevalence of this disease complex. A better understanding of thesymptomology, etiology importance, and means of control is necessary. This is especiallyimportant in some of the less developed areas of the world where short, high-yielding sorghumsare being introduced to replace local native varieties.Fusarium moniliforme, one of the most cosmopolitanof plant pathogens, is found in soils whereversorghum can be grown. The fungus persists onplant residues that remain in the soil and on itssurface. Mycelia, conidia, and—in the perfect state(Gibberella fujikuroi)—ascospores may be producedon or in plants or the soil at any time duringthe growing season, and secondary infection ofhost tissues may occur whenever environmentalconditions are favorable for disease development.F. moniliforme may also be a serious pathogen onmaize, millet, rice, and sugarcane (Bolle 1927,Bolle 1928, Dickson 1956, Bourne 1961, Sheldon1904, Ullstrup 1936, and Voorhies 1933). F. moniliformeaffects sorghum plants at all stages ofgrowth and can cause seedling blight, root andstalk rot, pokkah boeng, seed mold, and headblight.The FungusAccording to Booth (1971), Dickson (1956), Tarr(1962), and Saccas (1954), the Fusarium spp associatedwith root and stalk rots in sorghum include:1. Gibberella fujikuroi (Saw.) Wr.[G. moniliformis (Sheld.) Wine,]F. moniliforme Sheld. Conidial stage.2. G. fujikuroi (Saw.) Wr, var. subglutinans Ed.F. moniliforme Sheld. var. subglutinans Woll. &Reink.3. G. zeae (Schw.) Petch[G. saubinetti (Mont.) Sacc]F. graminearum Schw.G. roseum f. cerealis (Cke.) Snyder & HansenF. roseum f. cerealis (Cke.) Snyder & Hansenvar. graminearumOther Fusarium spp associated with sorghumroots and stalks, but for which pathogenicity is stillquestionable, include:F. culmorum (W.G. Sm.) Sacc.F. equiseti (Cda.) Sacc.F. oxysporum SchlechtF. sambucinum Fck.F. scirpi Lambotte & Fantr.F. solani (Mart.) Appel et Wr.F. tricinctum Cda.*Research Plant Pathologist, USDA-ARS, and Adjunct Professor of Plant Pathology, Mississippi State University, P.O.Drawer PG, Mississippi State, MS 39762, USA.International Crops Research Institute for the Semi-Arid Tropics. 1984. Sorghum Root and Stalk Rots, a CriticalReview: Proceedings of the Consultative G r o u p Discussion on Research Needs and Strategies for Control ofS o r g h u m Root and Stalk Rot Diseases, 27 Nov - 2 Dec 1983, Bellagio, Italy. Patancheru, A.P. 502 324, India:ICRISAT.25

Part of the problem in working with fusarial rootand stalk rots is that F. moniliforme often does notproduce macroconidia in culture. Tullis (1951)attributed stalk rot of sorghum in Texas to F. moniliformebut noted that it produced only microconidia.Leonian (1929), in a very comprehensive study of220 cultures of Fusarium spp on various culturemedia, found that conidial production by F. moniliformeand three subspecies was markedly affectedby 2 and 3% tartaric acid in the medium. F. monilhforme var. subglutinans produced no macro- ormicroconidia at all when 2 or 3% tartaric acid waspresent in the medium. On malt extract agar at25°C, one strain of F. moniliforme failed to producemacroconidia and four others did so onlyoccasionally.Bourne (1961) discussed the identity of whiteand purple strains of Fusarium occurring in associationwith cane stalk rots and pokkah boeng diseasein Florida. The fungus was found to beidentical with F. moniliforme (Sheld.) Snyd. et Hans.Subsequent to publication of these data, the purplestrain of F. moniliforme was maintained in pureculture for 4 years. After this period the isolate stillproved highly pathogenic to cane cuttings andgrowing stalks. However, this strain completely lostthe ability to produce septate macroconidia orchromogenic substances when transferred frequentlyon nutrient potato dextrose agar at 23°Cafter 2 years in culture. Wineland (1924) found thatcertain strains of F. moniliforme in culture producedmacroconidia in abundance at first, lost this characterafter a time, and afterwards produced onlymycelia and microconidia.Seedling BlightYoung sorghum plants in the one-to-three leafstage can be severely affected by F. moniliformeduring periods of prolonged cloudy humid weather.The first symptoms on these plants are tan-brownred-purple-blackirregular lesions on the leaves.The tips of the leaves wither first, and later theentire leaf dies. Because young sorghum plants arerather delicate and grow slowly, infected plants areoften killed if cloudy humid weather persists for anextended period (Zummo 1980). If conditionsfavorable for plant growth resume, the sorghumplants will apparently overcome the disease.Where the disease is severe and the environmentremains unfavorable for rapid seedling growth, thecrop may have to be replanted. It may be assumedthat a percentage of Fusarium infected/infestedseed will give rise to infected seedlings or spreadthe disease in some other manner.Root RotFusarium root rot on sorghum typically involves thecortical tissues first, then the vascular tissues of theroots. Newly formed roots may exhibit distinctlesions of various sizes and shapes. Root rot isprogressive, so older roots are often destroyed,leaving little plant anchorage. When sorghum rootrot is extensive, the plants are often easilyuprooted.Stalk RotFusarium stalk rot is usually accompanied by rootdamage. Under irrigation and heavy nitrogen fertilization,root damage may not result in abovegroundchanges in plant appearance before thestalks begin to rot. Stalk rot may reduce seed fill,resulting in seed weight losses as high as 60%(Edmunds and Zummo 1975).Fusarium stalk rot has become increasinglycommon in recent years as a root/stalk rot diseaseof sorghum in many areas of West Africa (Saccas1954, Tarr 1962, Zummo 1980). In the UnitedStates, the disease is generally found in the areaswhere charcoal rot occurs, particularly on the HighPlains from Texas to Kansas (Edmunds andZummo 1975). Like charcoal rot, fusarium stalk rotapparently requires some predisposing conditionsfor disease development as plants approachmaturity. Unlike charcoal rot, which is most injuriousduring periods of moisture stress, fusariumstalk rot is usually most damaging during cool, wetweather following hot, dry weather.Trimboli and Burgess (1983) reproduced basalstalk rot and root rot on grain sorghum plants grownin the greenhouse in Fusarium moniliforme infestedsoil at optimal soil moisture until flowering, thensubjected the plants to a gradual development ofsevere moisture stress between flowering and themiddough stage, followed by rewetting. Stalk rot didnot develop, and root rot was not severe in plantsgrown to maturity at optimal soil moisture, althoughmany of these plants were infected by F. moniliforme. Stalk and root rot developed in the majorityof stressed plants grown in soil initially uninfestedbut contaminated by F. moniliforme after planting.26

Reed et al. (1983), in Nebraska, studied the associationof soil fungi with the roots and stalks ofsorghum throughout the growing season. Theyfound that F. moniliforme was the most prevalentspecies isolated from stalks and F. equiseti wasmost commonly isolated from roots. Other Fusariumspp that were isolated included F. graminearum,F. tricinctum, F. oxysporum, and F. solani. F.moniliforme was rarely isolated from roots beforethe flag-leaf stage of plant development, but byanthesis it was recovered from 30% of the samples.F. oxysporum end F. solani combined were almostas common as F. equiseti early in the season, butthe frequency of these two species declined toalmost zero by the end of the season. In contrast,the isolation frequency of F. equiseti, althougherratic, remained high throughout the season.Recommendationsfor Future Research1. Probably the most important need in researchon the fusarium root and stalk disease complexis to determine the amount of damagebeing done by it in particular sorghum-growingareas. This assessment should take into considerationvarietal reaction to the disease;source of and carryover of inoculum; effect ofenvironment, with particular emphasis onmoisture stress; soil type and fertilizer, andcultural practices employed.2. The use of resistant varieties offers promisefor the control of some or all of this Fusariumdisease complex. However, unlike charcoalrot and anthracnose, good sources of resistanceto the entire disease complex have notyet been identified. Some sorghum varieties,especially among the sweet sorghums andsome of the tall landraces from Africa, appearto be resistant to certain elements of the Fusariumdisease complex but may be susceptibleto other components of it.3. Further work is also needed in order to morefully understand the mode of infection, sourceof and carryover of inoculum, effect of environment,soil fertility, and cultural practices ondisease severity, and the role of insects andnematodes on disease spread.ReferencesBOLLE, P.C. 1927. Een onderzoek naar de oorzaak vanpokkahboeng en toprot [An investigation into the cause ofpokkahboeng and toprot]. Archief SuikerindustrieNederlands-lndie III, 35:589-609.BOLLE, P.C. 1928. Verdere onderzoek ingen over pokkahboengen toprot [Further investigations in pokkahboengand toprot]. Archief SuikerindustrieNederlands-lndie I, 36:116-129.BOOTH, C. 1971. The genus Fusarium. Kew, Surrey, U.K.:Commonwealth Mycological Institute. 237 pp.BOURNE, B.A. 1961. Fusarium sett or stem rot. Pages187-202 in Vol. I, Sugar-cane diseases of the world (eds.J.P. Martin, E.V. Abbott, and C.G. Hughes). New York, NewYork, USA: Elsevier Publishing Co.DICKSON, J.G. 1956. Diseases of field crops. New York,New York, USA: McGraw Hill Book Co. 517 pp.DOUPNIK, B., Jr., and BOOSALIS, M.G. 1980.Ecofallow—a reduced tillage system—and plant diseases.Plant Disease 64:31 -35.DOUPNIK, B., Jr., BOOSALIS, M.G., WICKS, G.A., andSMIKA, D. 1975. Ecofallow reduces stalk rot in grainsorghum. Phytopathology 65:1021-1022.EDMUNDS, L.K., and ZUMMO, N. 1975. Sorghum diseasesin the United States and their control. U.S. Departmentof Agriculture Handbook No. 468. Washington, D.C.,USA: U.S. Government Printing Office. 47 pp.GOURLEY, L.M., ANDREWS, C.H., SINGLETON, L.L, andARAUJO, L. 1977. Effects of Fusarium moniliforme onseedling development of sorghum cultivars. Plant DiseaseReporter 61:616-618.LEONIAN, L.H. 1929. Studies on the variability and dissociationin the genus Fusarium. Phytopathology 19:753-868.NORTH, D.S. 1932. Pokkah boeng. Bulletin No. 100, Proceedingsof the Fourth Congress of the InternationalSociety of Sugar Cane Technologists, San Juan, PuertoRico. New York, New York, USA: Elsevier Publishing Co.REED, J.E., PARTRIDGE, J.E., and NORDQUIST, P.T.1983. Fungal colonization of stalks and roots of grainsorghum during the growing season. Plant Disease67:417-420.SACCAS, A.M. 1954. Les champignons parasites dessorghos (Sorghum vufgare) et des penicillaries (Penniseturntyphoidum) en Afrique Equatorial Francaise. AgronomieTropicale Nogent 9:135-173, 263-301, 647-686.SHELDON, J.L. 1904. A corn mold (Fusarium moniliformen. sp.). Nebraska Agricultural Experiment Station AnnualReport (1903)17:23-32.TARR, S.A.J. 1962. Diseases of sorghum, sudan grass28

and broom corn. Kew, Surrey, U.K.: CommonwealthMycological Institute. 380 pp.TRIMBOLI, D.S., and BURGESS, L.W. 1983. Reproductionof Fusarium moniliforme basal stalk rot and root rot ofgrain sorghum in the greenhouse. Plant Disease 67:891 -894.TULLIS, E.C. 1951. Fusarium moniliforme, the cause of astalk rot of sorghum in Texas. Phytopathology 41:529-535.ULLSTRUP, A.J. 1936. The occurrence of Gibberella fujikuroivar. subglutinans in the United States. Phytopathology26:685-693.VOORHIES, R.K. 1933. Gibberella moniliforme on corn.Phytopathology 23:368-378.WAKKER, J.H., and WENT, F.A.F.C. 1896. Overzicht vande ziekten van het suikerriet op Java [An overview ofsugarcane diseases in Java]. Archief SuikerindustrieNederlands-lndie IV, pp. 425-435.WINELAND, G.O.1924. An ascigerous stage and synonymyfor Fusarium moniliforme. Journal of AgriculturalResearch 28:909-922.ZUMMO, N. 1972. External Fusarium moniliforme var.subglutinans associated with right angle bending andtwisting of sweet sorghum stalks. Phytopathology 62:800(abstract).ZUMMO, N. 1980. Fusarium disease complex of sorghumin West Africa. Pages 297-299 in Sorghum Diseases, aWorld Review: Proceedings of the International Workshopon Sorghum Diseases, sponsored jointly by Texas A&MUniversity (USA) and ICRISAT. Patancheru, A.P. 502 324,India: ICRISAT.Q u e s t i o n sleft with 100% correlation of association but nocontrols.Pappelis:Are you saying that F. moniliforme in the root cortexis not a disease of the root?Zummo:Any plant may harbor organisms—sometimesparasitic on other plants—on the roots. Justbecause these organisms have been isolated is notproof of parasitism until Koch's postulates havebeen carried out on them.Clark:Pokkah boeng appears in symptomology similar toCa deficiency. What are your comments relating tothis?Zummo:I believe that pokkah boeng is a disease incited byF. moniliforme var. subglutinans. I'm aware of thecalcium deficiency symptoms on maize that mimicpokkah boeng but still feel that we are dealing witha parasitic disease, not a deficiency symptom.Maranville:Relating to the Ca++ implication, isn't it likely thatthe organism could cause disruption in Ca++metabolism, which then appears as the symptom?In essence then, the problem may actually be withCa++, although triggered via metabolism disruption,rather than a true lack of soil Ca++.Zummo:It is possible, but I don't think so.Partridge:In your pokkah boeng greenhouse studies, could F.moniliforme var. subglutinans be recovered fromanywhere on the surface of nondiseased plants oron the "healthy" controls?Zummo:It was sometimes isolated from healthy plants—butsporadically.Partridge:Realizing the difficulty of preventing F. moniliformevar. subglutinans from spreading—apparentlythrough the air—to "uninfected'' plants, one still is29

Pythium Root andSeedling Rots

Pythium Root and Seedling RotsG.N. Odvody and G. Forbes*SummaryPythium spp cause a root and mesocotyl rot of sorghum seedlings in cold, wet soils and a rootrot of mature sorghum in warm, wet soils. Identity of the causal species is incomplete for severalreasons, including changing and variable nomenclature, isolate variability, and differences ininterpretation of fungal structures in culture. Pythium can cause death of seedlings and matureplants, and although disease incidence and severity are influenced by several environmentalfactors, temperature and moisture are most important. Seed treatments with most fungicidesare generally ineffective in controlling seedling disease, but new, specific systemic fungicidesneed to be evaluated for efficacy against pythium seedling disease and pythium root rot ofmature plants. There is host plant resistance against both, but better characterization of theresistance is needed. More knowledge is needed concerning the mechanism of pathogensurvival, initial inoculum, initial infection, and the influence of specific host-pathogenenvironmentinteractions.In the literature of the past several decades,numerous reports describe identified and unidentifiedPythium spp occurring on sorghum roots, andmost are discussed either in the review by Tarr(1962) or the publication by Pratt and Janke (1980).Most published information concerning Pythium asa sorghum pathogen is fraught with confusionbecause of errors in isolation, inoculation, speciesidentification, and establishment of particular isolatesas actual causal agents of observed diseasein the field (Pratt and Janke 1980). AlthoughPythium arrhenomanes is a true root pathogen ofsorghum, its erroneous, long-term acceptance asthe causal agent of milo disease (Elliott et al. 1937)until 1948 (Leukel 1948) has cast further doubt onmany earlier reports. The great majority of reportsof Pythium on sorghum refer to its occurrence onyoung seedlings in the field, but there are somereports of its occurrence on mature plants (Frederiksenet al. 1973, Pratt and Janke 1980). Thereported susceptibility of sorghum seedlings toPythium isolates from other hosts provided nobeneficial information, because the resultsobtained under controlled environmental conditionswere never related to disease occurrence infield-grown sorghum (Pratt and Janke 1980). Difficultiesin species identification, nomenclaturalchanges, and disagreement about either the characteristicsof species or their synonomy furtherconfuse earlier reports.Seedling Disease and Damping-offPoor stand establishment of sorghum may involveinteractions of several biotic and abiotic factors,but in the United States environment has oftenbeen considered the most important through thedirect, detrimental effects of low soil temperature,saturated soil, and soil crusting (Leukel and Martin1943). The involvement of fungal pathogens in preandpostemergent damping-off of sorghum was*Plant Pathologist/Assistant Professor, Texas A&M University Agricultural Research and Extension Center, Rt.2, P.O.Box 589, Corpus Christi, TX 78410; and graduate student, Department of Plant Pathology and Microbiology, Texas A&MUniversity, College Station, Texas 77843, USA.International Crops Research Institute for the Semi-Arid Tropics. 1984. Sorghum Root and Stalk Rots, a CriticalReview: Proceedings of the Consultative Group Discussion on Research Needs and Strategies for Control ofSorghum Root and Stalk Rot Diseases, 27 Nov - 2 Dec 1983, Bellagio, Italy. Patancheru, A.P. 502 324, India;ICRISAT.31

first studied extensively by Leukel and Martin(1943), who distinguished between seedborne andsoilborne pathogens attacking seeds and seedlingsin soil. They tried to determine the effect ofpathogens on germination, emergence, and subsequentgrowth of the seedling. Research by Leukeland Martin (1943) and others demonstrated thatfungicide seed treatments reduced preemergentdamping-off associated with several seed-rottingfungi (e.g., species of Aspergillus, Rhizopus, Penicillium,and Fusarium), which rapidly colonizeunprotected seed primarily in cold, wet soils.Sometimes Penicillium and Fusarium spp proceedto parasitize the host tissue and cause postemergentdamping-off. However, Pythium is the fungusmost frequently isolated from diseased seedlingsgrown in cold, wet soil, and Leukel and Martin(1943) demonstrated that Pythium spp isolatedfrom root and mesocotyl lesions of sorghum seedlingswere highly virulent to sorghum planted insoils with high moisture and low temperature(15°C). Standard fungicide treatments do not protectagainst infection by Pythium attack, probablybecause either the site of parasitic attack is distal tothe seed or the fungicide (captan or thiram) has nosignificant effect on Pythium.Symptoms on seedlings are either brown or graywater-soaked roots or root tips, or lesions on roots(Forbes 1983) that become flaccid and necrotic(Edmunds and Zummo 1975). Lesions also occuron the plumule and mesocotyl (Leukel and Martin1943, Forbes et al. 1983), and the mesocotyl producessomewhat more pigment in response to thepathogen than do the roots (Odvody, unpublishedobservation, 1983). However, the lesion pigmentationis less than that induced by other soilbomepathogens, e.g., Fusarium (Edmunds and Zummo1975). Plants succumbing to postemergentdamping-off usually wilt rapidly and die, but oftenmany stunted plants remain alive despite the lossof most leaves and Pythium damage to the rootsand mesocotyl (Odvody, unpublished observation,1983; Edmunds et al. 1970). However, there is usuallywide variation in plant height and spacingthroughout affected fields, and many plants may beadversely affected throughout subsequent development(Edmunds et al. 1970).Root Rot of Mature PlantsThe occurrence of Pythium spp on roots of matureplants was first reported in 1937, when P. arrhenomaneswas erroneously considered the cause of"milo disease" in Texas and other areas of theUnited States where this disease occurred (Elliot etal. 1937). Severe root rot in the North Texas HighPlains in 1971-72 (Frederiksen et al. 1973) wascaused by a species of Pythium identified as P.graminicola (Pratt and Janke 1980). Symptoms onthe large adventitious (or buttress) roots are darkenedand blackened roots (Frederiksen et al.1973) and sunken red-brown to black root lesions,and sometimes at root death the entire lesion orroot has a tan color (Pratt and Janke 1980). Fusariumspp and other fungi may rapidly follow attackby Pythium spp (Odvody, unpublished observation,1982) and cause greater pigmentation of lesionsthan Pythium alone (Edmunds and Zummo 1975).Once established, these secondary fungi are moreeasily isolated (Frederiksen et al. 1973) than theprimary pathogenic Pythium.In 1972, stalk rots (caused primarily by Fusariumspp) followed development of the pythium root rotand were important causes of subsequent stalklodging (Frederiksen et al. 1973). Isolates ofPythium obtained from roots of mature plants werehighly virulent on sorghum seedlings (Frederiksenet al. 1973, Pratt and Janke 1980), but the occurrenceof similar Pythium strains in seedling infectionsin the field is unknown. On the North TexasHigh Plains, root infections of sorghum began toincrease at the boot stage or later when largenumbers of adventitious roots were being producedin irrigated fields (high soil temperature andhigh soil moisture conditions) (Odvody, unpublishedobservation, 1983). Pratt and Janke (1980)demonstrated that P. graminicola from roots couldcause stalk rot when plants were inoculated atmaturity, but it is probably not the cause of stalk rotin the field. At one South Texas location, Pratt andJanke (1980) isolated P. myriotylum and P. periplocumfrom insect-damaged roots and stalks ofmature sorghum. Only the former was pathogenicon sorghum seedlings inoculated in the greenhouse.Because only one site was investigated, theextent of the natural occurrence of P. myriotylumon mature sorghum roots is unknown.Taxonomy of PathogensThe changes in Pythium taxonomy during the pastfew decades present both problems and benefits inunderstanding the occurrence of this pathogen onsorghum. Hendrix and Campbell (1973) proposed32

that P. graminicola and P. arrhenomanes form acomplex in which isolates have characteristics thatconstitute a continuum between the two typespeciesand that other similar complexes exist.This helps clarify some of the older literature andmay lend more support for the pathogenic activitiesof Pythium reported in 1937, despite its erroneousidentification with milo disease (Elliott et al. 1937).The Pythium spp attacking seedlings also remaininsufficiently characterized. Forbes (1983) demonstratedthat a majority of isolates from infectedseedlings grown in a field soil in the greenhouseproduced lobulate sporangia but only 50% of thoseproduced oospores in culture. The characteristicsof these latter isolates were most similar to P.arrhenomanes as described by Drechsler (1936).Etiology and InfectionPythium spp pathogenic to sorghum probably survivein soil as oospores (Hendrix and Campbell1973). Saprophytic growth may be of minor importancebecause Pythium is a poor competitor thatapparently colonizes tissue only when other organismsare either absent or relatively inactive due toenvironmental factors (Hendrix and Campbell1973). Other data (Hendrix and Campbell 1973)indicate that oospores of Pythium spp pathogenicto sorghum germinate in response to host seed androot exudates in wet soil—either directly by producinggerm tubes or indirectly by producing zoosporesthat encyst and then germinate. Thepathogen then rapidly penetrates host cells andtissues that lack secondary wall thickenings (Hendrixand Campbell 1973). Although numerousenvironmental factors influence these germinationand infection processes by the pathogen, temperatureand moisture (especially in combination) arethe two most important ones (Hendrix and Campbell1973, Leukel and Martin 1943), probablybecause of their additional effect on the host plantand associated soil microflora. Under cold, wet soilconditions, germination of seed and growth ofseedlings are slowed such that emergence isdelayed, primary root growth is reduced, and inolder seedlings, new roots are slow to establishfrom the mesocotyl and crown. The transitory rootsystem of emerging seedlings is especially vulnerableto attack in cold, wet soils (Edmunds andZummo 1975), and the delay in production of thepermanent root system from the crown is probablyone of the greatest factors involved in postemergentdamping-off. We have often observed theprimary root system and mesocotyl of 2-week-oldseedlings being killed by Pythium, but without postemergentdamping-off because a healthy, permanentcrown root system was established in thewell-drained upper soil layer.Pythium pathogens isolated from seedlings mayhave an optimum growth temperature in culturemuch different from the environment in which theyare normally pathogenic (Hendrix and Campbell1973). Thus, the pathogen's competitive ability inthe soil-plant environment may be more importantthan its ability to grow in a noncompetitive culturalenvironment. However, the Pythium root rot thatoccurs on mature plants in warm, wet (floodirrigated)soil of the North Texas High Plains correlateswell with the high optimum temperaturereported for P. graminicola (Waterhouse andWaterston 1964a) and P. arrhenomanes (Waterhouseand Waterston 1964b). Infection in thesemature plants appeared to occur on roots of allsizes and ages, but initial infections may haveoccurred earlier in root development (Odvody,unpublished observation, 1983).For both pythium seedling disease and matureplant root rot, nothing is known about either thelevels of inoculum or the increase and secondaryspread of the pathogen. In maize, oospores andsporangia of Pythium are rapidly formed in infectedtissues (Nyvall 1981), and oospores, sporangia,and coenocytic mycelia have been observed inroots of infected sorghum seedlings (Forbes et al.1983). However, the role of these sporangia andzoospores in the infection of proximal, healthy rootsof the same and different plants is not known.The influence of previous crops and of tillage andcultural practices on Pythium diseases in sorghumis not known, but these variables are conjectured tohave some effect, especially in relation to initialinoculum and soil moisture and soil temperature(Leukel and Martin 1943, Hendrix and Campbell1973). The incidence and severity of pythium rootrot on mature sorghum may be directly affected byirrigation and irrigation frequency.Potential Controlwith FungicidesMost fungicides applied to sorghum seed are noteffective in controlling damping-off caused byPythium (Leukel and Martin 1943), but some newsystemic fungicides, like metalaxyl and fosetyl-A1,33

may provide the previously lacking protection oftissues distal to the seed. The additional cost ofseed treatment must be compared with the potentialfor pythium seedling diseases in the plantingarea. There is a continued need for additional fungicideslike captan to control the principal seedrottingfungi, because most of the potentiallyeffective systemic fungicides are specific forPhycomycetes.Potential Control ThroughHost Plant ResistanceHost plant resistance to Pythium attack in the seedlingstage is not well defined, but most germplasmis thought to be susceptible in disease-conducivecold, wet soil. In general, varieties are more susceptiblethan hybrids, and plants from either old orlow-quality seed are more susceptible than thosefrom either young or high-quality seed. Althoughsome cultivars were less affected by Pythiumcaused damping-off in the field (Forbes et al. 1983),the reason for and consistency of the reduceddamage is not known. The multiplicity of factorsinvolved with stand establishment in the fieldnecessitates evaluations in controlled environmentsto determine major factors responsible forincreased stand establishment. For a particulargenotype, the increased stand in cool, wet soilscould be due either to resistance to Pythium or tophysiological and physical factors like continuedgermination and growth under these conditions,rapid establishment of a permanent root system,and secondary thickening of cell walls in outer roottissues. Any stress factor that delays establishmentof the permanent root system from the coleoptileand upper nodes probably increases the potentialfor Pythium caused seedling damage or dampingoffin cool, wet soils. Varieties are likely more susceptibleto Pythium damage because of theirreduced vigor. They are generally slower to germinate,emerge, and establish a permanent root system.Plants from old seed of hybrids (and varieties)are more susceptible than plants from young seedbecause their reduced vigor is especially apparentin cool, wet soils. Plants from either nontreated ordamaged seed are also more susceptible to seedlingdisease, not only because Pythium can attackmore readily, but also because other seed-rottingfungi additionally reduce vigor and delay emergenceand plant establishment (Leukel and Martin1943).The Pythium disease syndrome on mature plantsis incompletely characterized, but some genotypes(e.g., Tx 2751, Tx 2737) demonstrate more lateseasonplant death associated with Pythium thando others. However, other pathogens and factorsmay either promote Pythium attack or contribute toplant death. Root wounding by nematodes andinsects may be a contributing factor (Frederiksenet al. 1973), as might primary and secondary infectionsby other root pathogens like Fusarium andPericonia. Additionally, genotypes may differ intheir tolerance to similar amounts of root losscaused by Pythium (Odvody, unpublished observation,1983).Research Needs1. Better characterization of Pythium species orspecies complexes that are pathogenic tosorghum roots.2. Determination of geographical and local variationin Pythium spp pathogenic to sorghum.3. Improved understanding of initial inoculum,germination stimuli, type of germination (director indirect), type of infective propagules (oospores,sporangia, or zoospores), site of infections),and importance of secondary spreadof the pathogen.4. Improved knowledge of environmental factorsnecessary for disease development and howthey interact with the pathogen, soil microflora,and host to cause disease.5. Development of meaningful screening techniquesto identify resistant genotypes and todetermine mechanisms of field resistance orsusceptibility.6. Determination of the effects of croppingsequence, tillage, and cultural practices(especially irrigation in relation to mature-plantroot rot) on disease incidence and severityand on increase in soilborne inoculum.7. Investigation of other edaphic and biotic factorsthat influence disease incidence andseverity.8. Evaluation of new systemic fungicides for abilityto control Pythium on seedlings and maturesorghum.34

ReferencesDRESCHLER, C. 1936. Pythium graminicolum and P.arrhenomanes. Phytopathology 26:676-684.EDMUNDS, L.K., FUTRELL, M.C., and FREDERIKSEN,R.A. 1970. Sorghum diseases. Pages 200-234 inSorghum production and utilization (eds. J.S. Wall andW.M. Ross). Westport, Connecticut, USA: AVI PublishingCo.EDMUNDS, L.K., and ZUMMO, N. 1975. Sorghum diseasesin the United States and their control. U.S. Departmentof Agriculture Handbook No. 468. Washington, D.C.,USA: U.S. Government Printing Office. 47 pp.ELLIOTT, C., MELCHERS, L.E., LEFEBVRE, C.L., andWAGNER, F.A. 1937. Pythium root rot of milo. Journal ofAgricultural Research 54:797-834.FORBES, G.A. 1983. Development of a technique forscreening seedlings of Sorghum bicolor (L.) Moench forresistance to seedling disease. M.Sc. thesis, Texas A&MUniversity, College Station, Texas, USA.FORBES, G.A., COLLINS, S.D., ODVODY, G.N., andFREDERIKSEN, R.A. 1983. Seedling disease in SouthTexas in 1983. Sorghum Newsletter 26:124-125.FREDERIKSEN, R.A., ROSENOW, D.T., and TULEEN, D.1973. Pythium root rot of sorghum on the Texas HighPlains 1972. Sorghum Newsletter 16:137-138.HENDRIX, F.F., Jr., and CAMPBELL, W.A. 1973. Pythiumsas plant pathogens. Annual Review of Phytopathology11:77-97.Mycological Institute) Descriptions of plant pathogenicfungi and bacteria Kew, Surrey, U.K.: CMI. 2 pp.QuestionsPartridge:You indicated Fusarium follows Pythium infection.Is there a predominant Fusarium that is isolatedfrom roots following Pythium?Odvody:We didn't routinely identify these Fusarium speciesexcept to determine their presence, becausePythium was so predominantly isolated.Partridge:Do cold-tolerant sorghums tend to be resistant?Odvody:Not in the limited number observed in the field, butmore research is needed to clarify this importantaspect of seedling disease.LEUKEL, R.W. 1948. Periconia circinata and its relation tomilo disease. Journal of Agricultural Research 77:201 -222.LEUKEL, R.W., and MARTIN, J.H. 1943. Seed rot andseedling blight of sorghum. U.S. Department of AgricultureTechnical Bulletin 839. 26 pp.NYVALL, R.F. 1981. Diseases of com (Zea mays L).Pages 55-86 In Field crop diseases handbook. Westport,Connecticut, USA: AVI Publishing Co.PRATT, R.G., and JANKE, G.D. 1980. Pathogenicity ofthree species of Pythium to seedlings and mature plantsof grain sorghum. Phytopathology 70:766-771.TARR, S.A.J. 1962. Diseases of sorghum, sudan grassand broom corn. Kew, Surrey, U.K.: CommonwealthMycological Institute. 380 pp.WATERHOUSE, G.M., and WATERSTON, J.M. 1964a.Pythium graminicola. No. 38 in CMI (CommonwealthMycological Institute), Descriptions of plant pathogenicfungi and bacteria, Kew, Surrey, U.K.: CMI. 2 pp.WATERHOUSE, G.M., and WATERSTON, J.M. 1964b.Pythium arrhenomanes. No. 39 in CMI (Commonwealth35

Anthracnose Stalk Rot

Anthracnose Stalk RotR.A. Frederiksen*SummaryAnthracnose persists as one of the most destructive diseases of sorghum. The pathogen,Colletotrichum graminicola, affects the foliage and inflorescence (including grain), as well asthe stalks. Losses of up to 50% are not uncommon. The use of host resistance has reducedlosses, but shifts in populations of the pathogen in many areas where the disease is prevalenthave limited the effectiveness of resistance. Factors reducing inoculum, utilization of blendedsources of resistance, and levels of resistance that reduce the spread of the pathogen arerecommended as means of reducing disease losses.Anthracnose, caused by the fungus Colletotrichumgraminicola (Cesati) Wilson, is one of the mostdamaging diseases of sorghum, particularly inwarm humid sorghum-growing areas (Tarr 1962).These areas include many regions in the semi-aridtropics and temperate regions with warm humidsummers, as well as the humid tropics. The commonfactor among these sorghum-growing regionswith prevalent anthracnose is frequent rainfall, particularlyduring the later stages of plant growth.DistributionAnthracnose has been reported from essentially allof the sorghum-growing regions of the world(Pastor-Corrales and Frederiksen 1980). It is farmore important in the more humid regions or duringrainy seasons. Anthracnose is the most importantsorghum disease in Brazil and is a major threat inmost of the Latin American countries (Nakamura1982, Pastor-Corrales and Frederiksen 1979). InIndia anthracnose can be very damaging in UttarPradesh (L.K. Mughogho, ICRISAT; personal communication,Nov 1983), and it can be widespread inregions of West Africa (N. Zummo, USDA; personalcommunication).SymptomsThree phases of anthracnose are recognized in theevaluation of host resistance or extent of damage(Harris et al. 1964, Harris and Fisher 1973, Lohmanet al. 1951). These disease symptoms include afoliar phase, stalk rot, and colonization of the panicleincluding the grain.Foliar anthracnose can be recognized by a rangeof symptoms including an "oval leaf spot," diffuseor patchy foliar colonization, and midrib infection.The range in foliar symptoms may be caused byvariation in the pathogen, host resistance (Pastor-Corrales 1980), or physiologic status of the hostfollowing infection. Weakened, chlorotic, stressed,or senescent leaves of susceptible cultivars arerapidly colonized by the pathogen.Infection and colonization of the panicle frequentlyresult in losses in both quality and quantityof grain (Reyes et al. 1969). Differences in theextent of colonization of the rachis appear to beinfluenced greatly by host genotype, specifically bywhether the rachis tissues senesce naturally duringmaturation or are genetically susceptible. Manysorghums with moderately high levels of foliar resistancereadily succumb to colonization in thepanicle. Frequently, sorghum grains may be colon-*Professor of Plant Pathology, Department of Plant Pathology and Microbiology, Texas A&M University, College Station,TX 77843, USA.International Crops Research Institute for the Semi-Arid Tropics. 1984. Sorghum Root and Stalk Rots, a CriticalReview: Proceedings of the Consultative Group Discussion on Research Needs and Strategies for Control ofSorghum Root and Stalk Rot Diseases, 27 Nov - 2 Dec 1983, Bellagio, Italy. Patancheru, A.P. 502 324, India:ICRISAT.37

ized by the anthracnose fungus (Pastor-Corrales1980); these grains have concentric rings or stripesof black acervuli from the stylar region.Anthracnose stalk rot, occasionally referred toas red rot, develops after the other phases andultimately results in lodging. Symptoms of stalk rotcan be diagnosed by their irregularly mottled ormarbled pattern of colonization. These symptomsare diagnostic during colonization of tissues of leafmidveins, panicle and rachis branches, and stalks.The marbling may result from either multiple infectionsor colonization of stalk tissue from a singleinoculation site. Le Beau et al. (1951) describedthese symptoms in detail, noting an absence ofmycelium in the pale areas surrounded by pigmented,sparsely colonized areas. Variation in pigmentand rate of colonization are related tohost-plant color and susceptibility to anthracnose.The PathogenC. graminicola has been recognized as the causeof anthracnose for about seven decades. Otherreviewers have adequately covered the earlierconfusion as to species identification (see Tarr1962). Problems arose, however, when Arx(1957)attempted to combine the falcate-spored Colletotrichums(C. graminicola and C. falcatum Went)within the species Glomerella tucumanenis (Speg.)Arx and Muller.Le Beau (1950) demonstrated a high degree ofhost specificity when he compared isolates fromsorghum, johnsongrass, and sugarcane. He studied593 isolates from 18 grass species, from geographicallyseparated regions. He concluded thatisolates of C. falcatum from sugarcane were pathogenicto sugarcane but that C. graminicola isolatesfrom sorghum were specific for sorghum. Sutton(1968), using size and shape of appressoria of C.graminicola from both maize and sorghum and C.falcatum from sugarcane, was able to differentiatethree groups of isolates. Huguenin et al. (1982)separated these three groups of falcate-sporedColletotrichum spp on the basis of electrophoreticpatterns. Politis (1975) also provides evidence forthe separate speciation of these fungi with theidentification of the perfect stage, Glomerella graminicolaPolitis. He obtained an isolate of C. graminicolafrom infected maize that was pathogenic tomaize. Wheeler et al. (1974) found an isolate frommaize that attacked both sorghum and maize. Perhapssome isolates of C. graminicola are virulenton both grass species, but apparently these isolatesare rarely observed.Physiologic SpecializationC. graminicola is a highly variable species. Evidencefor races exists from observations made inthe United States and from other regions of theworld (Harris and Johnson 1967, Foster and Frederiksen1979, Pastor-Corrales 1980, Nakamura1982). These and other reports clearly demonstratedifferences in pathogenicity of isolatesbetween and within locations. Gradual erosion ofresistance is recognized by the changes in reactionof resistance of Tx2536 and other sorghumlines in Georgia and Puerto Rico. Uniquely differentpopulations of C. graminicola are suggested by thedifferential reaction of sorghum entries in the InternationalSorghum Anthracnose Virulence Nursery(ISAVN) from Nigeria, Brazil, and the USA (King andFrederiksen 1976). Nakamura (1982) identified fiveraces of C. graminicola using five differential cultivarsof sorghum. These races were classified from1983 single spore isolates gathered from a numberof diseased plants throughout Brazil. Nakamura'swork confirms the supposition of many workers thatseveral physiological forms of C. graminicola arepresent not only within an area, but between locationsas well. Workers in Brazil have adopted a setof differential cultivars derived in part from theISAVN. Other races of C. graminicola are probablypresent in India because all of the sorghums in theISAVN were susceptible to anthracnose at Pantnagarin north India (L.K. Mughogho, ICRISAT; personalcommunication). Fortunately, other sorghumcultivars screened at Pantnagar are resistant inIndia. The significance of these observations isobvious: first the species is dynamic and affectedby directional selection pressure by host resistancegenes, and secondly, profoundly differentraces exist in different regions of the world. Thesefacts present challenging problems when usinghost resistance as the sole measure of control inareas with severe anthracnose.Anthracnose Stalk Rotand Yield LossesThe extent of damage or loss due to stalk rot is areflection of: (a) the host's susceptibility to anthrac-38

39nose, (b) the environment, (c) the aggressivenessof the pathogen, and (d) the physiologic state of thehost. In Texas a new high-yielding commercialhybrid introduced in 1965 was abandoned in 1968because of anthracnose (Reyes et at 1969). Inregard to environment, some sorghum hybridsvigorously attacked in Georgia are moderately resistantin Texas. Pastor-Corrales (1980) demonstratedthe influence of the environmentexperimentally by growing identical sorghumentries in a nursery where overhead sprinklers simulatedperiodic rainfall and in naturally rainfed nurseries.In his trials, sprinkling greatly enhanceddisease. In regard to the aggressiveness of thepathogen, the qualitative differences (virulence) ofColletotrichum spp have been amply recognized;but as with most other pathogens, efficiency inproduction of disease (aggressiveness) is also recognized.One may justifiably suspect that isolatesfrom India and Brazil are more aggressive thanthose from other regions. Finally host cell maturityor senescence is extremely important: Duncan(these proceedings) described "normal" sorghumsenescence as sequential from the bottom up. Thissequential senescence appears to be a factor infoliar anthracnose. Both physically and physiologically,lower leaves are more subject to colonizationby C. graminicola. But as leaves senesce from thebottom up, stalks mature from the top down.Anthracnose stalk rot in general follows this route.Panjcles, rachis branches, and heads are veryvulnerable to colonization in some sorghumgrowingregions but not others (Pastor-Corrales1980). In Texas, the peduncle is often the first partof the host affected by anthracnose under fieldconditions, followed by colonization of the rachisbranches.Studies on sequential anthracnose development,under natural or experimental conditions,have rarely been reported. Such studies may bevery useful in determining the effect of levels ofresistance on anthracnose stalk rot. Harris andFisher (1973) provided some data on the rate ofdisease development by their periodic evaluationof anthracnose on 49 commercial hybrids. Theyobtained negative correlations between diseaseratings and yield of hybrids, and these correlationsdecreased over time. Their data provide evidenceof slow development of anthracnose on somehybrids. Analysis of disease progress curves foreach cultivar would be of value in interpreting thesedata.Arguments in favor of a relationship betweenhost senescence and stalk rot are strongly supportedby a number of investigators (Dodd 1980,Katsanos and Pappelis 1969). Bockholt et al.(1971) and L. Reyes (Texas A&M University;unpublished data) observed massive yield loss andlodging because of anthracnose in sorghum at 1and 2 weeks after the normal harvest date. Allplants were affected at the time of harvest. Lossesresulted from lower test weight and from lodging.More recently Ferreira and Warren (1982) estimatedgrain losses caused by anthracnose toreach as high as 88.7% in the highly susceptiblecultivar IS-4255; RS-671 had yield losses of 42%,whereas resistant material such as IS-9189 andIS-9569 were essentially free from losses.Breeding and Genetic ProgressSources of resistance to anthracnose in sorghumhave been reported by many workers over the pastdecades (Harris and Johnson 1967, Le Beau andColeman 1950, Rosenow and Frederiksen 1982).These resistant sorghums have been used as parentsin breeding programs or as replacements forsusceptible cultivars. Coleman and Stokes (1954)determined that separate but linked genes conditionedresistances to stalk rot (LsLs) and foliaranthracnose (LL) in the sweet sorghum cultivarSart. The appearance of new races of C. graminicolaattacking some of these originally resistantsorghums suggests that other alleles must beinvolved. Harris and Johnson (1967) found a positivecorrelation between head and foliar ratings(r=0.50) and between head and stalk ratings(r=0.03). Nevertheless, Pastor-Corrales (1980)argues that environment plays a major role in theinterpretation of the genetics of resistance. In hiswork the stalk rot phase developed under conditionsless favorable for disease than did the foliarphase. Jones (1979) found that resistance toanthracnose was conditioned by one dominantgene for one parent and perhaps as many as threedominant genes for another. Jones also noted thatthe genetic background of the parents affected thelevel of disease susceptibility ratings in their progeny.She also noted that environmental factorshad a great influence on disease ratings.The ProblemWhere sorghum is grown and anthracnose commonlyappears, yield losses are likely to occur,

particularly in seasons in which harvesting isdelayed because of wet weather. Host resistancereduces the amount of disease, but in the presenceof abundant inoculum and a maturing host, lossesmay not be avoided. Furthermore, effective hostresistance is lost because of the frequent occurrenceof new races of the pathogen. Consequently,anthracnose control will depend on managementof the host resistance genes, utilization of lessvulnerable host phenotypes, manipulation of thehost-parasite environment, and reduction in sourcesof inoculum (i.e., destruction of debris or susceptiblecollateral weed hosts [weed hosts of C.graminicola important in its spread include Echinochloacolonum, Digitaria sanguinalis, and Dactylocteniumaegyptum; ICRISAT Annual Report1982]).To date, genetic management in sorghum hasbeen in response to the genetic changes of thepathogen—a practice that encourages shifts in thepathogen population. When many discrete populationsof pathogens are present, one tends to predominateon a genetically uniform host population.Host mixtures, blends, or multilines, however,reduce these tendencies of pathogen uniformity(Wolfe and Barrett 1980). Another type of host resistancemay be quantitative (horizontal), permittinga slower rate of disease development. Data fromHarris and Fisher (1973) suggest that this type ofresistance exists. Reevaluating their data, usingdisease progress curves, may demonstrate theeconomic value of moderately resistant cultivars.Reduced rates of resistance or even host mixturesmay not be adequate in seasons with extensiverainfall at host maturity.Chemical control has been economically practicalunder experimental conditions in Columbia(K.F. Cardwell de Castillo, Instituto ColombianoAgropecuario, La Libertad, Colombia; personalcommunication, 1982) but would be unacceptablewhere the crop is grown for food.It appears to me that stalks on most tall (i.e., 2 mor above) sorghum cultivars escape (are resistantto ?) direct invasion by C. graminicola. Taller sorghums,or tall photoperiod-sensitive sorghums, thatmature during the dry season escape diseaseBergquist (1973) suggested that taller stalks havean advantage in being physically farther from theinoculum in the soil and that the leaf-stripping characterof some tall sorghums also gives them anadvantage against anthracnose. Bergquist et al.(1974) also described a closed floret trait duringanthesis as a possible exclusion mechanism forreducing anthracnose infection in sorghum heads.The presence of C. graminicola as a grain moldand grain-weathering fungus only adds to the totaldestructiveness of this pathogen.Recommendationsfor Future Research1. Continue to identify sources of resistance andthe extent of pathogen variability.2. Examine the epidemiology of C. graminicola tofurther clarify the spread of the pathogen fromone part of the plant to another and from plantto plant.3. Determine the rate of disease developmentand spread of the pathogen in various genotypesand phenotypes of sorghum (e.g., theeffect of plant height, cultivar mixtures, or plantdensities) on the rate of disease development.4. Determine the method and length of survival ofinoculum under natural conditions as a meansof predicting the disease on a location basis.ReferencesARX, J.A. 1957. Die arten der gattung ColletotrichumCorda. Phytopathologische Zeitschrift 29:413-468 (inGerman).BERGQUIST, R.R. 1973. Cotietotrichum graminicola onSorghum bicolor in Hawaii. Plant Disease Reporter57:272-275.BERGQUIST, R.R., ROTAR, P., and MITCHELL, W.C.1974. Midge and anthracnose head blight resistance insorghum. Tropical Agriculture 51:431-435.BOCKHOLT, A.J., TOLER, R.W., and FREDERIKSEN, R.A.1971. Measuring the effect of disease on grain sorghumperformance. Pages 13-16 in Proceedings of the SeventhBiennial Grain Sorghum Research and Utilization Conference,sponsored by the Grain Sorghum Producers' Association(GSPA) and Sorghum Improvement Conferenceof North America, Lubbock, Texas. Available from GSPA,Abernathy, Texas, USA.COLEMAN, O.H., and STOKES, I.E. 1954. The inheritanceof resistance to stalk red rot in sorghum. Agronomy Journal44:41-43.DODD, J.L. 1980. The role of plant stresses in developmentof corn stalk rots. Plant Disease 64:533-537.FERREIRA, A.S., and WARREN, H.L. 1982. Resistance of40

sorghum to Colletotrichum graminicola. Plant Disease44:773-775.FOSTER, J., and FREDERIKSEN, R.A. 1979. Anthracnoseand other sorghum diseases in Brazil. Pages 76-79 inProceedings of the Eleventh Biennial Grain SorghumResearch and Utilization Conference, sponsored by theGrain Sorghum Producers' Association (GSPA) andSorghum Improvement Conference of North America.Available from GSPA, Abemathy, Texas, USA.HARRIS, H.B., and FISHER, C.D. 1973. Yield of grainsorghum in relation to anthracnose expression at differentdevelopmental stages of host. Pages 44-46 in Proceedingsof the Eighth Biennial Grain Sorghum Research andUtilization Conference, sponsored by the Grain SorghumProducers' Association (GSPA) and Sorghum ImprovementConference of North America, Lubbock, Texas.Available from GSPA, Abemathy, Texas, USA.HARRIS, H.B., JOHNSON, B.J., DOBSON, J.W., Jr., andLUTTRELL, E.S. 1964. Evaluation of anthracnose on grainsorghum. Crop Science 4:460-462.HARRIS, H.B., and JOHNSON, J.B. 1967. Sorghumanthracnose symptoms, importance and resistance.Pages 48-52 in Proceedings of the Fifth Biennial GrainSorghum Research and Utilization Conference, GrainSorghum Producers.' Association (GSPA) and SorghumImprovement Conference of North America, Lubbock,Texas. Available from GSPA, Abemathy, Texas, USA.HUGUENIN, B., LOUR, D.M., and GEIZER, J.P. 1982.[Comparison between isolates of Colletotrichum falcatumand Colletotrichum graminicola on the basis of theirmorphological, physiological and pathogenic characteristics.]Phytopathologische Zeitschrift 105:293-304 (inFrench).ICRISAT. 1983. Annual Report 1982. Patancheru, A.P.502 324, India: ICRISAT.JONES, E.M. 1979. The inheritance of resistance to Colletotrichumgraminicola in grain sorghum, Sorghum bicolor.Ph.D. thesis, Purdue University, West Lafayette, IN 47907,USA.KATSANOS, R.A., and PAPPELIS, A.J. 1969. Relationshipof living and dead cells to spread of Colletotrichum graminicolain sorghum stalk tissue. Phytopathology 59:132-134.KING, S.B., and FREDERIKSEN, R.A. 1976. Report on theInternational Sorghum Anthracnose Virulence Nursery.Sorghum Newsletter 19:105-106.LE BEAU, F.J. 1950. Pathogenicity studies with Colletotrichumfrom different hosts on sorghum and sugarcane.Phytopathology 40:430-438.LE BEAU, F.J., and COLEMAN, O.H. 1950. The inheritanceof resistance in sorghum to leaf anthracnose.Agronomy Journal 42: 33-34.LE BEAU,F.J., STOKES, I.E., and COLEMAN, O.H. 1951.Anthracnose and red rot of sorghum. U.S. Department ofAgriculture Bulletin 1035.LOHMAN, M.L., STOKES, I.E., and COLEMAN, O.H. 1951.Anthracnose and red rot of sorgo in Mississippi, PlantDisease Reporter 28:76-80.NAKAMURA, KAZUIOSSE. 1982. Especializacao fisiologicaem Colletotrichum graminicola (Ces.) Wils. (sensuArx, 1957) agente causal da anthracnose do sorgho(Sorghum spp). Doctoral thesis, Universidade EstadualPaulista, Jaboticabal, Brazil. 143 pp.PASTOR-CORRALES, M.A. 1980. Variation in pathogenicityof Colletotrichum graminicola (Cesati) Wilson andin symptom expression of anthracnose of Sorghum bicolor(L.) Moench. Ph.D thesis, Texas A&M University, CollegeStation, Texas, USA. 122 pp.PASTOR-CORRALES, M.A., and FREDERIKSEN, R.A.1979. Anthracnose and other sorghum diseases in Brazil.Pages 76-79 in Proceedings of the Eleventh BiennialGrain Sorghum Research and Utilization Conference,sponsored by the Grain Sorghum Producers' Association(GSPA) and Sorghum Improvement Conference of NorthAmerica. Available from GSPA, Abernathy, Texas, USA.PASTOR-CORRALES, M.A., and FREDERIKSEN, R.A.1980. Sorghum anthracnose. Pages 289-294 in SorghumDiseases, a World Review: Proceedings of the InternationalWorkshop on Sorghum Diseases, sponsored jointlyby Texas A&M University (USA) and ICRISAT. Patancheru,A.P. 502 324, India: ICRISAT. 469 pp.POLITIS, D.J. 1975. The identity and perfect state of Colletotrichumgraminicola. Mycologia 67:56-62.REYES, L, FREDERIKSEN, R.A., and WALKER, H.J. 1969.Anthracnose incidence on grain sorghum in the southTexas coastal bend area in 1968. Pages 8-9 in Proceedingsof the Sixth Biennial Grain Sorghum Research andUtilization Conference, sponsored by the Grain SorghumProducers' Association (GSPA) and Sorghum ImprovementConference of North America. Available from GSPA,Abemathy, Texas, USA.ROSENOW, D.T., and FREDERIKSEN, R.A. 1982. Breedingfor disease resistance in sorghum. Pages 447-455 inSorghum in the Eighties: Proceedings of the InternationalSymposium on Sorghum, sponsored by INTSORMIL,ICAR, and ICRISAT. Patancheru, A.P. 502 324, India:ICRISAT.SUTTON, B.C. 1968. The appressoria of Colletotrichumgraminicola and C. falcatum. Canadian Journal of Botany46:873-876.TARR, S.A.J. 1962. Diseases of sorghum, sudan grassand broom corn. Kew, Surrey, U.K.: CommonwealthMycological Institute. 380 pp.41

42WHEELER, H., POLITIS, D.J., and PONELEIT, C.G. 1974.Pathogenicity, host range/and distribution of Colletotrichumgraminicola on corn. Phytopathology 64:293-296.WOLFE, M.S., and BARRETT, J.A. 1980. Can we lead thepathogen astray? Plant Disease 64:148-155.QuestionsSeetharama:It is difficult to induce (cause) anthracnose before6th leaf stage. Is this related to the supply of seedreserves to younger leaves? If so, we can manipulatethe food supply to the young leaves and try tocause infection.Frederiksen:Dhurrin is higher in sorghum seedlings and hasbeen suggested as the reason sorghum seedlingsare more resistant to some pathogens.

Periconia Root Rot

Periconia Root RotG.N. Odvody and L.D. Dunkle*SummaryMilo disease, or periconia root rot, threatened to curtail cultivation of milo and milo derivativesorghums in several USA plains states in the 1920s and 1930s. Resistant germplasm fromother sources and from among surviving resistant mutants alleviated the problem by the early1940s. Periconia circinata was not identified as the causal agent of milo disease until 1948.Virulent isolates of P. circinata produce a host-specific toxin (tox+); host susceptibility to thepathogen and sensitivity to the toxin are conferred by a semidominant allele at the pc locus.Most strains of P. circinata in the milo disease nursery at Garden City, Kansas, cannot producetoxin (are tox-). In the Texas and Kansas milo disease nurseries, both tox* and tox- isolates ofP. circinata were obtained from roots of susceptible cultivars, but only tox- isolates wereobtained from resistant cultivars. In the 1970s, root rots associated with P. circinata werereported on resistant sorghum cultivars in the United States and Australia. No isolate of P.circinata from resistant cultivars at any location has produced a demonstrable toxin activeagainst any cultivar. In the absence of susceptible cultivars, P. circinata is apparently either asaprophyte or a low-virulence pathogen with a basic level of aggressiveness and is restrictedalmost exclusively to sorghum.Historical Occurrenceof Milo DiseaseMilo disease, or periconia root rot, is caused by theimperfect fungus Periconia circinata (Mang.) Sacc.The disease was first reported in Texas (Chillicothe)in 1924 and then in 1926 in Kansas (GardenCity) (Tarr 1962, Leukel 1948, Elliott et al. 1937). Inthe 1920s and 1930s, this disease threatened tocurtail production of susceptible sorghums in thestates of Texas, Kansas, Oklahoma, New Mexico,Nebraska, Arizona, and California (Elliott et al 1937,Tarr 1962). Resistant germplasm was availablefrom other sorghum types and was also selectedfrom among surviving resistant mutants in the fieldand increased (Melchers and Lowe 1943, Karper1949, Tarr 1962). By the late 1930s and early1940s, resistant sorghums had largely alleviatedthe milo disease problem (Tarr 1962, Quinby andKarper 1949), but the original milo disease nurseriesat Chillicothe and Garden City are still beingmaintained. They have provided a continuing, valuableresource for evaluating resistance of sorghumgermplasm and for other research purposes.SymptomsA summary of milo disease symptoms from severalpublications is contained in the book by Tarr(1962). Milo disease was initially described as aroot, crown, and shoot rot (Elliott et at. 1932). Sus-*Plant Pathologist/Assistant Professor, Texas A&M University Agricultural Research and Extension Center, Rt.2, P.O.Box 589, Corpus Christi, TX 78410; and Research Plant Pathologist/Associate Professor, USDA-ARS, Department ofBotany and Plant Pathology, Purdue University, West Lafayette, IN 47907, USA.International Crops Research Institute for the Semi-Arid Tropics. 1984. Sorghum Root and Statk Rots, a CriticalReview: Proceedings of the Consultative Group Discussion on Research Needs and Strategies for Control ofSorghum Root and Stalk Rot Diseases, 27 Nov -2 Dec 1983, Bellagio, Italy. Patancheru, A P . 502 324, India:ICR1SAT.43

ceptible cultivars, growing in soils with apparentlyhigh levels of inoculum, began showing symptomssimilar to drought stress within a few weeks ofplanting. Leaves on these plants wilted, drooped,and became slightly rolled, and older leaves turnedyellow with leaf tips and margins becoming desiccatedand necrotic. The youngest leaves were usuallythe last to become discolored and die. Plantswere generally stunted, and they often died withoutproducing a head. Under conditions of lower inoculumpotential and an environment less favorable fordisease expression, susceptible cultivars showedinitial symptoms at a later stage of growth, andalthough plant growth was more vigorous, headswere few and poorly filled. In some soils, plantsappeared normal or nearly normal throughout theseason, but roots were attacked and crowns wereinternally reddened. Milo disease was commonlyidentified by splitting open crowns to reveal thisdark-red discolored tissue.Because leaf symptoms were mediated throughroot damage, the latter were attacked prior toappearance of foliar symptoms (Tarr 1962, Wagner1936), Roots of infected seedlings showed a watersoaked,reddish discoloration of the cortical andvascular tissues. As the plant aged and the diseasedeveloped, smaller roots were destroyed andlarger ones became dark red or brown, especiallyin the stelar tissue, and finally disease symptomsprogressed into the crown.PathogenThe causal agent of milo disease proved elusive toinitial investigators, who probably isolated saprophytesand other primary and secondary pathogensfrom the roots of dead and dying plants. In1937, Elliott et al. provided evidence that Pythiumarrhenomanes was the pathogen causing milo disease.However, they and subsequent workers(Ezekiel 1938, Melchers 1942, Tarr 1962) determinedthat P. arrhenomanes killed resistant as wellas susceptible cultivars in the greenhouse and wasunable to reproduce symptoms of the disease infield-grown plants. In 1947, Leukel and Pollacksuggested Periconia circinata as the causal agentbecause of its frequent isolation from roots ofinfected plants. The definitive work of Leukel(1948) firmly established P. circinata as the causalagent of milo disease more than 10 years after theadvent of resistant sorghums (Quinby and Karper1949).P. circinata was first described from roots ofwheat in France (Mangin 1899). According to Leukel(1948), the mycelium of P. circinata fromsorghum is slender (2-6 µ), branched, and dirtywhiteto mouse-gray on potato dextrose agar(PDA), but turns black upon sporulation. The aerialconidiophores, single or in groups of two or three,are dark brown to black, thick-walled, and 6-8 µ x150-250 y . They are typically curved or circinatenear the apex, with a slightly swollen apical cellbearing generally three sporogenous cells thatundergo division, to form more sporogenous cells.Spherical conidia are borne on these cells inbasipetal succession, sometimes in short chains.The conidia are dark brown to black, 15-27 µ diam,and verrucose-spiny when mature.Another species, Periconia macrospinosa,(Lefebvre et al. 1949) often occurs on diseased orsenescent sorghum roots and can be easily mistakenfor P. circinata. Compared to P. circinata, theconidiophores of P. macrospinosa are longer andmore erect, and the conidia have much largerspines. Lefebvre et al (1949) demonstrated that P.macrospinosa was not a pathogen of eithersorghum or other grasses.Leukel (1948) had suggested that a pathogenproducedtoxin might be involved in milo diseasedevelopment, and Scheffer and Pringle (1961)demonstrated the production of a host-specifictoxin by P. circinata that was active only againstsusceptible cultivars. All symptoms of milo diseaseare induced by this toxin in the absence of thepathogen (Scheffer and Pringle 1961). Wolpert andDunkle (1980) demonstrated that the toxin of P.circinata was composed of two toxic lowmolecular-weight,acidic compounds containingaspartic acid and one or more residues of apolyamine. The latter is apparently responsible forselective biological activity. Host susceptibility to P.circinata and sensitivity to its toxin are conferred bya semidominant allele at the pc locus (Schertz andTai 1969). Homozygously recessive (pcpc) plantsare resistant; heterozygous plants (Pcpc) are intermediate;and homozygous dominant plants (PcPc)are fully susceptible (Schertz and Tai 1969). The Pcallele of the gene is relatively unstable, and mutationsof Pc to pc occur in one of approximately 8000gametes (Schertz and Tai 1969). This geneticinstability was probably responsible for the frequentappearance of resistant plants among thoseof susceptible genotypes and contributed to rapiddevelopment of isogenic resistant sorghum lines(Quinby and Karper 1949, Schertz and Tai 1969),44

Conidia and theInfection ProcessLeukel (1948) noted the abundance of conidia producedby P. circinata, but he and others (Pringleand Scheffer 1963, Oswald 1951) rarely observedtheir germination. These studies utilized eithermycelial or single conidiophore isolates. Dunkle etal. (1975) demonstrated that conidia of P. circinatafrom culture germinated on PDA at higher rates(50-70%) when subjected to a heat shock (45-48°C for 10 min) and at variable rates when nottreated (2-54%). Conidia produced on inoculatedand field-infected roots responded in a similarmanner (Dunkle et al. 1975, Odvody et al. 1977).Conidia of P. circinata adjacent to sorghum roots indistilled water had a higher germination rate (88%)than in either distilled water alone (0%) or on PDA(15%) (Odvody et al. 1977). Conidial germination inconcentrated root exudates from root washingswas greater (22%) than in distilled water alone (6%)(Odvody et al. 1977). On roots in liquid nutrientculture, conidia germinated at a high frequency,forming conidial germ tubes and appressoria-likestructures within 48 hours and small, red, corticallesions within 3-5 days (Odvody et al. 1977). P.circinata was easily re-isolated from corticallesions incited by any isolate on roots of anycultivar.Characterization of PericoniaCircinata in Milo Disease NurseriesThe pathogenic (toxin-producing, tox+) strains ofP. circinata have been perpetuated in nurseries atGarden City, Kansas, and Chillicothe, Texas, bycontinuously growing susceptible cultivars (primarilyS Colby milo) for more than 50 years. Despitethis monoculture, only 13% of the P. circinataisolates from the soil in the Garden City nurserywere tox+ (Odvody et al. 1977). In this samenursery, only 34% of the P. circinata isolates frominfected roots of a susceptible cultivar were tox+(Odvody et al. 1977). Although this demonstratedsome selection for tox+ strains (34% vs 13%), thepredominant strain in the soil population is apparentlyunable to produce toxin (is tox-). The predominanceof tox- isolates on susceptible cultivars maybe explained by growth of these isolates in toxinaffectedtissue near lesions caused by the tox+strain (Odvody et al. 1977). Oswald (1951) alsoobtained several tox- isolates of P. circinata fromroots of susceptible cultivars in California.Only tox- isolates were obtained from roots ofresistant cultivars growing in the Garden Citynursery (Odvody et al. 1977). If tox+ and toxstrainsdiffered only in toxin-producing ability, thenwe would expect isolates from resistant cultivars atGarden City to reflect the proportions existing in thesoil population (i.e., 13% tox+). Although we did notevaluate soil populations in the Chillicothenursery,we obtained only tox- isolates from resistant cultivars,and the proportion of tox+:tox- isolates fromsusceptible cultivars was similar to that obtained atGarden City (Odvody and Dunkle, unpublisheddata, 1981-1982).In laboratory pathogenicity tests, conidia fromtox+ and tox- isolates germinated on roots andincited cortical lesions on roots of both resistantand susceptible cultivars, but extensive vascularlesions and seedling death occurred only on susceptibleplants inoculated with tox+ isolates(Odvody et al. 1977). These results, consideredtogether with the absence of tox+ isolates fromresistant cultivars, indicate that the increase oreven maintenance of tox+ isolates in soil is unlikelywithout regular presence of susceptible cultivars.Odvody et al. (1977) postulated that prior to theintroduction of sorghum, P. circinata existed inNorth America as a soil saprophyte or weak parasiteof native plants. Several factors influencedincidence and severity of milo disease in specificyears, but disease severity apparently increasedwith continuous sorghum cropping (Elliott et al.1937, Quinby and Karper 1949). This suggests thattox+ strains comprised a minute proportion of thesoil population of P circinata until monoculture ofsusceptible cultivars selected for and increasedthe tox+ strain to a threshold level where damagewas apparent (Odvody et al. 1977). It is unlikely thatthe ability of P. circinata to produce a pathotoxinwas the result of a recent mutational eventbecause milo disease developed over a wide geographicalarea in a very short time (Odvody et al.1977). Suggested methods of pathogen dispersal(Quinby and Karper 1949) cannot account for thesporadic and sometimes localized occurrence ofmilo disease (Odvody et al. 1977).Periconia Problemsin Resistant SorghumsIn the early 1970s, there were several reports of P.circinata associated with root rots of cultivars pre-45

viously known to be resistant (Rosenow and Frederiksen1972, Troutman and Voigt 1971, Odvody etal. 1977, Dunkle 1979). Plants of these cultivarshad poorly developed heads and root systems,necrotic roots, and root lesions, with P. circinatapresent either before or after incubation in thelaboratory (Odvody et al. 1977, Rosenow andFrederiksen 1972, Troutman and Voigt 1971). Previouslyunreported on sorghum outside the UnitedStates, P. circinata was reported on sorghum rootsof resistant cultivars in Australia (Mayers 1976).However, in Australia and the United States, isolatesof P. circinata from resistant cultivars haveneither produced a demonstrable toxin activeagainst either resistant or known susceptible cultivarsnor reproduced the above field diseasesymptoms on inoculated plants (Odvody et al.1977; Odvody and Dunkle, unpublished data;Rosenow and Frederiksen 1972; Troutman andVoigt 1971; Burns 1974). However, Odvody et al.(1977) demonstrated that the tox- isolates theytested were all low-virulence pathogens on roots ofsusceptible and resistant cultivars in the laboratory.P. circinata was also observed on roots ofapparently healthy sorghum plants with well developedheads and root systems (Odvody et al. 1977).Pythium graminicola was demonstrated to be theprimary cause of the root rot in North Texas (Frederiksenet al. 1973; Pratt and Janke 1980; andOdvody, unpublished data), but P. circinata wasubiquitous on (or always isolated from) senescentand dying roots and caused numerous small corticallesions on buttress roots similar to those producedon seedling roots in the laboratory (Odvodyet al. 1977).The reported periconia root rot problems in Arizonaand California are not yet resolved (R.L. Voigt,University of Arizona; personal communication,1983). Partial control of the disease through treatmentof soil with benomyl (Burns 1974) implicatedinvolvement of a fungal pathogen (including P. circinata)in the Arizona root rot problem. Many elementsof the disease syndrome are similar totypical milo disease, including greater damage inlate summer plantings, foliar stress symptoms, andstunting (Burns 1974). Genetic studies in Arizonademonstrated that reaction to the root disease wascontrolled by a single, semidominant major factorfavoring susceptibility (Burns 1974). Dunkle (1979)showed that a shattercane (feral Sorghum bicolor)source in Nebraska was heterogenous in reactionto the known Periconia toxin and tox+ isolates.Dunkle (1979) suggested that these reactionsimplicated additional genetic factors beyond thetwo known alleles (Pc and pc). The susceptibility ofsuch standard resistant cultivars as Redlan in Arizona(Troutman and Voigt 1971, Burns 1974)necessarily focused more attention on potentialchanges in the pathogen (Voigt 1972). However, notoxin production was demonstrated (Troutman andVoigt 1971), and root damage was confined primarilyto the cortical tissue (Burns 1974), unlike thedistinct red stele so characteristic in roots of plantswith milo disease.Most evidence suggests that P. circinata is alow-virulence root pathogen restricted primarily tosorghum. Except for its original description onwheat (Mangin 1899) and the reports by Glynne(1939) and Mayers (1976), P. circinata is almostexclusively reported on sorghum, and we have notencountered it as a pathogen or saprophyte onroots of any other crop. Odvody (unpublished data,1978) isolated from wheat straw in Nebraska asaprophytic species of Periconia that had somecharacteristics similar to P. circinata, but its conidiophoreswere more circinate and the culture morphologywas different. This Periconia speciesproduced no demonstrable toxins against eithersusceptible or resistant sorghum cultivars, did notincite cortical lesions, and had other dissimilarcharacteristics that were distinct from P. circinata.All isolates (tox- and tox+) of P. circinata incited atleast cortical lesions on all sorghum cultivars evaluated(Odvody et al. 1977). The true saprophyte P.macrospinosa does not incite lesions, and we haveobserved it on roots of other crops (e.g., maize).ConclusionsDespite fragmentary data and unresolved root rotproblems, some conclusions can be drawn aboutP. circinata as a pathogen of sorghum. The hostspecifictoxin of P. circinata is not required for initialinfection of root tissue and early lesion developmentseen on both resistant and susceptible cultivars.But toxin is required for P. circinata to furthercolonize and kill extensive areas of root tissue onsusceptible cultivars. Similar root system damageon susceptible cultivars in the field results in thestem and foliar symptoms commonly associatedwith milo disease.Soil populations of P. circinata are probably composedpredominantly of tox- strains that are weaklyvirulent pathogens of sorghum but contain aninitially undetectable proportion of tox+ strains46

47capable of increasing when susceptible cultivarsare grown in monoculture.If other host-specific tox+ strains exist as recurring,minute proportions of the Periconia soil population,the past 50 years of growing resistant (pcpc)sorghums should have allowed sufficient time forselection and increase of any strains specific tothese sorghums. Although we expect a predominanceof tox- isolates from resistant plants, thecomplete absence of tox+ isolates from resistantplants negates the disease involvement of a toxinidentical to the one already known. Postulating thatwe have not yet developed proper production anddetection methods for these toxins is to assumeunrealistically that there are different nutritionalrequirements for toxin production and even a radicallydifferent toxin. The lack of differential virulenceamong tox- isolates and their inability toreproduce major field disease symptoms on anysorghum argue not only against toxin involvementbut against long-term selection of more virulenttox- strains.The small, cortical lesions incited by tox- strainsof P. circinata on sorghum roots in the field mayeither allow the pathogen an advantage in pioneercolonization of dead or dying roots, or, with stressinducedphysiological changes, the pathogen maymore easily parasitize root tissue. Such a hypothesisis not inconsistent with the normal pathogenicassociation where tox+ P. circinata grows extensivelyonly in susceptible tissue affected by toxin.The role of P. circinata as a soilborne pathogenand saprophyte of sorghum roots is probablyinterrelated with several factors of the soil environment,including microflora and other rootpathogens.Suggestions for Research1. Use of chemicals, soil fumigation, and manipulationof environmental variables in the fieldand laboratory to determine the actual role ofP. circinata in the Arizona root rot problem andwherever P. circinata is implicated as asorghum root pathogen.2. Use of a mixture of isolates of P. circinata inpure culture inoculations to facilitate detectionof a virulent toxin producer.3. Evaluation of the Periconia population in Arizonasoils and in other soils around the world,especially where milo types either originatedor are grown.4. Determination of genetic relationshipsbetween the Pc locus and disease reaction inArizona and California utilizing crossesbetween TX09 (resistant in Arizona), Redlan(susceptible in Arizona), and the isogenic linesof S and R Colby that are susceptible (PcPc)and resistant (pcpc), respectively, to knowntox+ isolates of P. circinata.ReferencesBURNS, M. 1974. Inheritance and etiology of an undescribedroot disease in Sorghum bicolor(L.) Moench. Ph.D.thesis, University of Arizona, USA. 49 pp.DUNKLE, L.D. 1979. Heterogenous reaction of shattercaneto Periconia circinata and its host-specific toxin.Phytopathology 69:260-262.DUNKLE, L.D., ODVODY, G.N., and JONES, B.A. 1975.Heat activation of conidial germination in Periconia circinata.Phytopathology 65:1321-1322.ELLIOTT, C., MELCHERS, L.E., LEFEBVRE, C.L., andWAGNER, F.A. 1937. Pythium root rot of milo. Journal ofAgricultural Research 54:797-834.ELLIOTT, C., WAGNER, F.A., and MELCHERS, L.E. 1932.Root, crown, and shoot rot of milo. Phytopathology22:265-267.EZEKIEL, W.N. 1938. Sorghum root and crown rot. TexasAgricultural Experiment Station Annual Report 15:118-119.FREDERIKSEN, R.A., ROSENOW, D.T., and TULEEN, D.1973. Pythium root rot of sorghum on the Texas HighPlains 1972. Sorghum Newsletter 16:137-138.GLYNNE, M.D. 1939. Fungal invasion of the roots ofhealthy wheat plants. Transactions of the British MycologicalSociety 23:210.KARPER, R.E. 1949. Registration of sorghum varieties, V.Agronomy Journal 41.536-540.LEFEBVRE, C.L., JOHNSON, A.G., and SHERWIN, H.S.1949. An undescribed species of Periconia. Mycologia41:416-419.LEUKEL, R.W. 1948. Periconia circinata and its relation tomilo disease. Journal of Agricultural Research 77:201-222.LEUKEL, R.W., and POLLACK, F.G. 1947. Periconia circinata(Mangin) Sacc. as a possible causal factor in "milodisease." Phytopathology 37:440.MANGIN, M.L. 1899. Sur le pietin ou maladie du pied duble. Bulletin de la Societe Mycologique de France 15:210-239,

48MAYERS, P.E. 1976. The first recordings of milo diseaseand Periconia circinata on sorghums in Australia. AustralianPlant Pathology Society Newsletter 5:59-60.MELCHERS, L.E. 1942. On the cause of the milo disease.Phytopathology 2:640-641.MELCHERS, LE., and LOWE, A.E. 1943. The developmentof sorghums resistant to milo disease. Kansas AgriculturalExperiment Station Bulletin 55. 24 pp.ODVODY, G.N., DUNKLE, L.D., and EDMUNDS, L.K.1977. Characterization of the Periconia circinata populationin a milo disease nursery. Phytopathology 67:1485-1489.OSWALD, J.W. 1951. The relation of Periconia to milo rootrot in California. Phytopathology 41:28 (abstract).PRATT, R.G., and JANKE, G.D. 1980. Pathogenicity ofthree species of Pythium to seedlings and mature plantsof grain sorghum. Phytopathology 70:766-771.PRINGLE, R.B., and SCHEFFER, R.P. 1963. Purification ofthe selective toxin of Periconia circinata. Phytopathology53:785-787.QuestionsPartridge:You indicated the toxin produced all symptoms ofthe disease. You also presented a slide showinglodged plants. My question is: Is there a stalkdecomposition or degeneration due to Periconiainfection or application of its toxin?Odvody:I stated that the toxin produced nearly all symptomsof disease, but even this is based on statements ofother researchers. To my knowledge researchershave subjected only seedlings to toxin by itself, so Ican't directly comment on stalk degeneration.However, plants succumbing to milo disease normallydid not lodge in the field.QUINBY, J.R., and KARPER, R.E. 1949. The effect of milodisease on grain and forage yields of sorghum. AgronomyJournal 41:118-122.ROSENOW, D.T., and FREDERIKSEN, R.A.1972. Lodgingin the Texas high plains. Sorghum Newsletter 15:133-134.SCHEFFER, R.P., and PRINGLE, R.B. 1961. A selectivetoxin produced by Periconia circinata. Nature 191:912-913.SCHERTZ, K.F., and TAI, Y.P. 1969. Inheritance of reactionof Sorghum bicolor (L) Moench to toxin produced byPericonia circinata (Mang.) Sacc. Crop Science 9:621 -624.TARR, S.A.J. 1962. Diseases of sorghum, sudan grassand broom corn. Kew, Surrey, U.K.: CommonwealthMycological Institute. 380 pp.TROUTMAN, J.L, and VOIGT, R.L. 1971. Root rot problemsassociated with sorghum in Yuma, Arizona. Pages22-23 in Proceedings of the Seventh Biennial GrainSorghum Research and Utilization Conference, sponsoredby the Grain Sorghum Producers' Association(GSPA) and Sorghum Improvement Conference of NorthAmerica. Available from GSPA, Abernathy, Texas, USA.VOIGT, R.L. 1972. A potential new strain of milo disease.Sorghum Newsletter 15:3.WAGNER, FA. 1936. Reaction of sorghums to the root,crown, and shoot rot of milo. Agronomy Journal 28:643-654.WOLPERT, T.J., and DUNKLE, L.D. 1980. Purification andpartial characterization of host-specific toxins producedby Periconia circinata. Phytopathology 70:872-876.

Acremonium Wilt

Acremonium WiltR.A. Frederiksen*SummaryAcremonium wilt has become an important disease of sorghum in part because of thecultivation of recently developed high-yielding cultivars. The pathogen Acremonium strictumGams appears to invade the foliage and colonize vascular tissues. Symptoms include vascularbrowning and both foliar and stalk wilt. The disease is widespread and probably best controlledby avoiding cultivation of unusually susceptible cultivars.Acremonium wilt is one of the more recently describeddiseases of sorghum (Natural et al. 1982). InEgypt El-Shafey et al. (1979) and Salama (1979)have described a wilt of sorghum caused byCephalosporium acremonium Cord. Gams (1971)reduced this species to synonymy with Acremoniumstrictum Gams. In this paper both diseasesare presumed to be caused by the same pathogen,and differences between the diseases will bementioned.In the USA, acremonium wilt was observed whenwilted plants of BTx423, BTx622, and BTx425developed a vascular wilt at Plainview, Lubbock,and Chillicothe, Texas (Frederiksen et al. 1980).Subsequently, the disease was reported in Argentina(Forbes and Crespo 1982) and Venezuela(Silva et al. 1983), and I observed it in Mexico,Sudan, and Honduras. The disease probablydevelops in susceptible sorghums wherever theenvironment favors infection.Symptoms and EtiologySymptoms of acremonium wilt involve foliar desiccationand vascular browning of lateral leaf veins.Initially only vascular browning is evident, but asthe disease progresses, large areas of wilted tissuedevelop on an axis of a leaf on either or both sidesof the midvein. Vascular plugging continuesthrough the leaf sheath and into vascular bundlesof the stalk. Wilted leaves can be distinguishedfrom other pathological or physiological wilt by thevascular browning. In wilted plants free from stalkrottingorganisms, browning of vascular bundlescan be followed vertically in the stalk. Infection andcolonization from the roots appears to be theexception.In Egypt, reports suggest that the pathogen issoilborne and colonizes the roots prior to invadingvascular tissue (El-Shafey and Refaat 1978).Observations in Texas suggest that infectiondevelops from foliar invasion. Root dipping, soilamending, and hypodermic injection in sorghumwhorls with conidia of A strictum all cause infectionand wilt; however, many cultivars treated in thismanner wilt more severely than under natural conditions(Frederiksen et al. 1981). The cultivars Red-Ian (BTx378), Martin (BTx398), and Wheatland(BTx399) are examples of field-resistant cultivarssusceptible to root inoculations. In the Nile deltanear Numberia, Egypt, I have observed diseasedevelopment in the field from foliar infection.According to Salama (1979), wilting occurs commonlyin regions of upper Egypt. It may be one ofEgypt's most important sorghum diseases. Acremoniumwilt is not a stalk rot, because A. strictumacts like a true vascular parasite. However, stalk-*Professor of Plant Pathology, Department of Plant Pathology and Microbiology, Texas A&M University, College Station,TX 77843, USA.International Crops Research Institute for the Semi-Arid Tropics. 1984. Sorghum Root and Stalk Rots, a CriticalReview: Proceedings of the Consultative Group Discussion on Research Needs and Strategies for Control ofSorghum Root and Stalk Rot Diseases, 27 Nov - 2 Dec 1983. Bellagio, Italy. Patancheru, A P . 502 324, India:ICRISAT.49

50rotting fungi often develop in wilted plants; in thisrespect A. strictum acts as a predisposing agent.A. strictum acts as a saprophyte on dead organicmaterial and is probably a poor colonizer in soilslow in organic matter. Sources of primary inoculumand environmental conditions conducive to infectionin the field remain unclear. Information onepidemiology may resolve differences betweeninfection patterns in Egypt and elsewhere.In a recent study (H.J. Kim and J.K. Mitchell,Department of Plant Pathology and Microbiology,Texas A&M University; personal communication,May 1983), blending conidia with steamed soil atplanting failed to cause disease, but disease diddevelop when seedlings were transplanted intoinfested soil, indicating that root wounding may benecessary for infection. Kim and Mitchell alsofound differences in pathogenicity between twoisolates of A.strictum based on symptoms anddetermined that their isolates infected maize, pearlmillet, and oats in greenhouse studies. They wereunable to infect wheat and barley with theseisolates.The ProblemTropically adapted sorghums derived from IS-12610 are unusually susceptible to acremoniumwilt. Elite inbreds such as ATx623 and ATx625 andmany hybrids produced with these inbreds areextremely susceptible in Honduras (D. Mechanstock,INTSORMIL Sorghum Breeder, Choluteca;personal communication, 13 Sept 1982). Thevulnerability of some of these sorghums raises theissue of the potential risk of growing these agronomicallysuperior inbreds in locations favoringdisease development. Reaction of sorghum entriesto acremonium wilt in Honduras and Texas aresimilar (Table 1). Differences in reaction and incidenceof disease between these locations may beexplained by the variables of host maturity, degreeof infection, or observer. Losses on an individualplant basis can be total, but affected plants of susceptiblehybrids in one trial produced about half theyield of disease-free controls (Natural et al. 1982).Another aspect of this problem concerns thegeographical distribution of A strictum. In a recentvisit to Honduras, I observed widespread acremoniumwilt in farmers' fields of landrace cultivars. Inmost of these cultivars, the disease appeared todevelop slowly and caused little foliar wilting; howeverin other fields, presumably sown to other cut-Table 1. Incidence of naturally occurring acremoniumwilt among selected sorghum entriesat College Station, Texas, in 1980 andCholuteca, Honduras, in 1982.Sorghum entryCS-3541 (CSV-4)QL-3 (Combine Kafir der.)SC-103-12(IS-410 der.)SC-170-6-17 (IS-12661 der.)SC-326-6 (IS-2816 der.)SC-414-12(IS-2508 der.)SC-748-5 (IS-3552 der.)TAM-428Tx-378Tx-430Tx-623Tx-625Tx-707877-CS-1 (IS-2930 x IS-3922)% of plants with wiltCollegeStation382041118410502061210Choluteca5234017303501510631001725tivars, A. strictum caused severe wilting in up to30% of the plants. Since plant densities were low,crop loss must have been substantial. It is likely thatA. strictum was not introduced; rather it was presentand not recognized. Similar comments can bemade for Sudan and Mexico, where I haveobserved similar symptoms that have yet to bereported. The global distribution and severity ofacremonium wilt awaits further study.Acremonium wilt can be confused with bacterialstreak or symptoms of maize dwarf mosaicbecause the symptoms overlap. This is particularlytrue of cultivars with vascular discoloration andlimited foliar wilting. For example, Riccelli (1980)reported that QL-3 was susceptible to maize dwarfmosaic virus based on symptoms later determinedto have been caused by A. strictum (Silva et al.1983). Most sorghum cultivars appear to be moderatelyresistant, but further evaluation is necessary.Only with the identification of highly resistant parentsand with improved inoculation techniques willit be possible to conduct studies on the inheritanceof resistance.Future Research Needs1. Clearly, further work is needed to elucidate theetiology of acremonium wilt. Sources of inocu-

lum and inoculum survival, as well as the modeof infection, are poorly understood.2. The nature of host resistance to the diseaseneeds to be determined. Recognition of thecauses of infection may provide some insightinto this.3. Studies should be carried out on the relationsbetween wilt and stalk rotting and lodging; anysuch interaction may be significant in areaswhere root infection is important.4. A reliable large-scale field screening techniquemust be developed to determine thenature of known field resistance or susceptibility.Susceptible sorghums may represent theexception. Nevertheless highly resistantsorghums remain undescribed.Diseases, sponsored jointly by Texas A&M University(USA) and ICRISAT. Patancheru, AP. 502 324, India:ICRISAT.SALAMA, I.S. 1979. Investigations of the major stalk, foliar,and grain diseases of sorghum (Sorghum bicolor)including studies on the general nature of resistance.Fourth Annual Report, Field Crops Research Institute,United States Agricultural Research Program, PL 480,Project No. E6-ARS-29, Giza, Egypt.SILVA, E., SAVINO, A., MENA, T.H., PONS, N. [1983.]Acremonium striatum W. Gams en sorgo granifero(Sorghum bicolor (L) Moench) en Venezuela. AgronomiaTropical (in press).ReferencesEL-SHAFEY, HA, ABD-EL-RAHIM, M.F., and REFAAT,M.M. 1979. A new Cephalosporium wilt of grain sorghumin Egypt. Pages 514-532 in Proceedings of the ThirdEgyptian Phytopathological Congress.EL-SHAFEY, HA, and REFAAT, M.M. 1978. Studies onthe stalk rot diseases of grain sorghum in Egypt. AgriculturalResearch Review (Ministry of Agriculture, Cairo)56:71-79.FORBES, G.A., and CRESPO, L.B. 1982. Marchitamientoen sorgo causado por Acremonium strictum Gams. InformationTecnica 89, Estacion Experimental AgropecuariaManfredi, INTA, Argentina.FREDERIKSEN, R.A., NATURAL, M., ROSENOW, D.T.,MORTON, J.B., and ODVODY, G.N. 1980. Acremoniumwilt of sorghum. Sorghum Newsletter 23:134.FREDERIKSEN, R.A., ROSENOW, D.T., and NATURAL, M.1981. Acremonium wilt of sorghum. Pages 77-79 in Proceedingsof the 12th Biennial Grain Sorghum Researchand Utilization Conference, sponsored by the GrainSorghum Producers' Association (GSPA) and SorghumImprovement Conference of North America, Lubbock,Texas. Available from GSPA, Abernathy, Texas, USA.GAMS, W. 1971. Cephalosporium-Artige Schimmelpilze(Hyphomycetes). Stuttgart, Germany: G. Fisher. 242 pp.NATURAL, M.P., FREDERIKSEN, R.A., and ROSENOW,D.T. 1982. Acremonium wilt of sorghum. Plant Disease66:863-865.RICCELLI, M. 1980. Current strategies and progress inbreeding disease-resistant sorghums in Venezuela.Pages 434-453 in Sorghum Diseases, a World Review-Proceedings of the International Workshop on Sorghum51

Nematodes Affecting Sorghum

Plant-Parasitic Nematodes Affecting SorghumL.E. Claflin*SummaryPlant-parasitic nematodes have been shown to cause yield losses in sorghum. Meloidogyne,Tylenchorhynchus, Belonolaimus, Pratylenchus, Xiphinema, and Trichodorus are importantgenera in the evaluation of possible nematode damage in sorghum. Nematology researchutilizing sorghum as the host crop is very limited. The potential interrelationships of fungi,bacteria, and nematodes as they relate to the stalk rot complex in sorghum have not beenresearched in depth.Plant-parasitic nematodes are often convenientlyclassified by their feeding behavior. Ectoparasitesgenerally feed on cells near the surface, or theymay perforate the cell wall with the stylet and insertthe head portion into the cell when feeding. Theyare generally larger and have a longer stylet thanendoparasites. Endoparasites enter the plant, passthrough the maturation process, lay eggs, andcomplete their life process within the plant. Sedentarynematodes enter the root or are attached toplant tissue and remain sessile, whereas migratorynematodes move within the host or between thehost and soil.Nematode damage to field crops is often difficultto ascertain and may closely mimic drought stress,nutrient deficiencies, and other disease and insectproblems. Typical symptoms consist of irregularareas of varying size in which the plants have anunthrifty appearance, closely resembling other rootmaladies. Heavily infested plants are smaller, usuallychlorotic, and have a tendency to wilt due to areduced or unhealthy root system. Below-groundsymptoms of root damage may vary, dependingupon the specific nematode attacking the roots,and may be easily confused with other problems,including herbicide damage, compacted soil (e.g.,plow pans), insect damage, and other diseases. Ingeneral, root cells are destroyed during the feedingprocess, which results in a reduced uptake of waterand nutrients. Most nematodes secrete digestivefluids into the tissue while feeding, and a large partof the injury is caused by a reaction of the tissueand digestive fluids, Endoparasites cause substantialdamage by their movement through the hosttissue.Nematodes Affecting SorghumTable 1 lists those nematode genera that are cosmopolitanand are most likely to be implicated insorghum yield losses. Symptoms on sorghum rootscaused by nematodes would include one or moreof the following:a. Root-knots or galls: Root tissue in close proximityto the nematode's head often assumes abulbous and distorted appearance due to anincrease in cell size (hypertrophy) and cellnumber (hyperplasia). These anatomicalchanges are in response to the injected nematodesalivary secretions. Root swellings arethe principal symptom of the cereal root-knotnematode (Meloidogyne naasi) in sorghum.b. Root lesions: Lesions generally develop whenmigratory endoparasitic nematodes enter andmove in the parenchyma cells of the host root.These cells usually die and cavities develop in*Associate Professor, Department of Plant Pathology, Kansas State University, Manhattan, KS 66506, USA.International Crops Research Institute for the Semi-Arid Tropics. 1984. Sorghum Root and Stalk Rots, a CriticalReview: Proceedings of the Consultative Group Discussion on Research Needs and Strategies for Control ofSorghum Root and Stalk Rot Diseases, 27 Nov- 2 Dec 1983, Bellagio, Italy. Patancheru, A.P. 502 324, India:ICRISAT.53

Table 1. Plant-parasitic nematode genera that are pathogenic on sorghum.Mode of Characteristic Hosts otherNematode parasitism symptoms than sorghumRoot-lesion Endoparasitic Decline in plant vigor, necrotic Grasses, cereals, cabbage,(Pratylenchus spp) root lesions, association with beet, tomato, legumes,microorganisms in causingdisease complexes, low kerneltest weighttobacco; over 400 hostsRoot-knot Endoparasitic Decline in plant vigor, stunting, Grasses, cereals, legumes,(Meloidogyne spp)root galls, proliferation ofbranch roots, reduced stands,delay in floweringcotton, tobacco, tomato, potatoStunt Ectoparasitic Stunting, lack of root develop Grasses, cereals, legumes(Tylenchorhynchus spp)ment, decline of seedling vigor,root tips may be shortand thickenedSting Ectoparasitic Decline in plant vigor, stunting, Cotton, cereals, legumes,(Belonolaimus spp)root systems with very limiteddevelopment, threshold levelin maize is 1 sting nematode/100 cm 3 soil, generally onlydetected in sandy soilsvegetables, tobaccoDagger Ectoparasitic Decline in vigor, poor root Citrus, fruit and shade trees,(Xiphenema spp) development, extensive cereals, grasses, legumes,necrosis of root tissue vegetablesthe tissue. If extensive damage has occurred,the cortex tissue may slough away from theendodermis. Small roots may be girdled byinjuries, which results in root pruning and reducesthe uptake of water and nutrients. Digestiveenzymes are secreted during the feedingprocess, which often results in death of cells.Primary and secondary microorganisms enterthe roots through the wounds caused bynematodes.c. Abnormal or reduced root development: Ectoparasiticnematodes commonly feed on roottissue near the meristematic and cellelongationregions. Either the injection ofenzymes or the stylet entering the cell willcause death of the cell, or that cell will cease toperform its intended function. With extensivefeeding, elongation of root tissue is minimal,while the diameter of the root increases, producingthe symptom of short, thickened roots.In certain cases (e.g., Belonolaimus spp),extensive necrosis develops where the nematodehas fed near the meristematic region anddestroys the ability of the root to grow anddevelop.Sorghum Yield LossesEstimated loss of grain and forage sorghums in theUnited States is 6% (Anonymous 1971). Lossesvary from locality to locality and from areas within aparticular field. Numerous factors are involved,including soil type, rotational sequence with othercrops, tillage practices, and application of insecticidalchemicals. In Kansas, insecticide treatmentsresulted in 43% (1981) and 7% (1982) increases insorghum yields above the untreated control (Claflinet al. 1983). Carbofuran (Furadan) 4F (1.12 kga.i./ha band) and fonofos (Dyfonate, 2.24 kg a.i./haband) were the most effective treatments, increasingyield 56% in 1981 and 15% in 1982. In general,band applications were more effective than infurrowapplications. Tylenchorhynchus martinipopulations increased from 178 (preplant) to2942/100 cm 3 at physiological maturity (Hafez andClaflin 1982). Sorghum growth in soil infested withT. nudus was reduced 10% in fertilized and 56% innonfertilized plots in South Dakota (Smolik 1977),The effect of Quinisulcius acutus (stunt nematode)on foliar and root weight and height ofsorghum plants was enhanced as the nematode54

populations were increased (Table 2). Pratylenchuszeae and 0. acutus were recovered from 61 %of soil samples and 48% of root samples fromsorghum fields in Mississippi (Cuarezma-Teran1983). The economic threshold of 0. acutus was inthe range of 100 to 1000 nematodes/100 cm 3 soil(Table 2).Several root-knot species, including Meloidogyneincognita (Syn. M. incognita acrita) andMeloidogyne acronea, have been reported as parasiteson sorghum. The cotton root-knot nematode(M. incognita) has caused serious losses insorghum when included in a rotational sequencewith cotton (Orr 1967). M. acronea has beenreported only from South Africa (Coetzee 1956,Coetzee and Botha 1965). Typical field symptomsresulting from M, incognita infestations includeirregular areas containing chlorotic and stuntedplants, delayed flowering, and yield reductions upto one-third. Root tissue may exhibit galls, elongatedswellings, and discrete knots or swellingswith root proliferation (Orr and Morey 1978). M.acronea symptoms are subtle, with inconspicuousgalls on roots and limited or no visible effect onplant growth.The cereal root-knot nematode, M. naasi, is aparasite of cereals, grasses, and sugar beet inWales, Belgium, England, Yugoslavia, Iran, and theUnited States. Five physiological races of M. naasiexist; however, only the Kansas isolate (Race 5)was capable of producing egg masses on sorghum(Michell et al. 1973). Prominent symptoms attributedto M. naasi include stunted, chlorotic plants inirregular patterns within sorghum fields (Aytan1968, Aytan and Dickerson 1969). Root galls maybe elongated swellings or discrete knots that arerelatively small in comparison to other root-knotgalls. Infested roots are often curved in the shape ofa hook, horseshoe, or a complete spiral withoutexcessive proliferation of secondary roots, as iscommon with other Meloidogyne spp.P. zeae, Helicotylenchus spp, and Tylenchorhynchuscrassycaudatus were commonlydetected in soil samples from sorghum fields inPuerto Rico (Ayala and Bee-Rodriguez 1978).Aphelenchus, Aphelenchoides, Tylenchus, Pseudhalenchus,Trophurus, Neotylenchus, Longidorus,Meloidogyne, and Rotylenchulus were other generaidentified in lesser numbers from soil and rootsamples of sorghum. P. zeae was implicated incausing death of 2- to 3-week-old sorghum plants.The plants exhibited a purple color, wilted, and diedwithin several days. Roots of these plants assumeda dark red color and the cortex was generallyseparated from the endodermis (Ayala and Bee-Rodriguez 1978).Economic Threshold LevelsResearch involving tolerance levels of sorghum toplant-pathogenic nematodes has received verylimited attention. Various parameters, including thereproductive potential of the nematode species,host plant genotype, and the effect of environment,must be ascertained before establishing thresholdlimits. Other complicating factors in establishinglevels include the interaction of other nematodeswith the target organism, interactions with soilmicroorganisms, and the susceptibility or toleranceof the particular cultivar of the host. Economicthreshold levels of Q. acutus appear to rangebetween 100 and 1000 nematodes/100 cm 3 soil(Table 2). In contrast, only one sting nematode persample (100 cm 3 soil) is an economic thresholdlevel for sorghum in South Carolina (SA Lewis,Table 2. Effect of various inoculum levels of Quinisulclus acutus on sorghum grown under greenhouse conditions.(Source: Cuarezma-Teran 1983.)TreatmentsPlant Top weight (g) Root weight (g)height(cm) Fresh Dry Fresh DryControl 55.87a* 25.43a 3.36a 8.31a 2.51aSupernatant 53.93a 24.41 ab 2.93ab 8.01a 2.25aSterile Supernatant 52.00a 23.25abc 2.98ab 6.03ab 2.25a100 nematodes 55.00a 24.22ab 2.97ab 9.02a 2.42a1000 nematodes 38.37b 17.86bc 2.28b 3.83b 0.83b5000 nematodes 37.27b 17.27c 2.34b 3.82b 1.04b*Means followed by the same letter indicate no significant difference (P

Associate Professor, Clemson University, Clemson,S.C., USA; personal communication, 1983).In preliminary tests, two sorghum accessions(B 35-6 and BTx 378) were found to be less favorablefor nematode reproduction, although not significantlydifferent (Table 3) (L.E.. Claflin and T.C. Todd;unpublished data, 1983). In several instances, thefresh foliar weight of inoculated plants exceededthose of the controls. As expected, greater differenceswere observed in root weights.Disease Complexes InvolvingFungi, Bacteria, and NematodesThe importance of researching various interactionsamong microorganisms was stated very eloquentlyby Fawcett (1931):Investigation with one microorganism keptpure and free from contamination with anyother has been the classical procedure eversince Koch and others perfected the pureculturemethods that facilitate so greatly theseparation of microorganisms. Students inour laboratories have been thoroughly inbredwith the idea that cultures must be pure for asingle organism. This necessary insistenceon pure cultures of single organisms hasperhaps led unconsciously to a feeling that toallow the use of a mixture in plantpathologicalwork is extremely unscientific ifit is not actually a deadly plant pathologicalsin. Nature does not work with pure culturesalone but most frequently with associations.Numerous interactions of nematode, fungal, andbacterial species in disease complexes on varioushosts have been reported (Norton 1978). A comprehensivereview of nematode-fungal diseasecomplexes was published by Powell (1971). Insorghum, interactions involving P. zeae and Curvulariaspp, Fusarium moniliforme, Rhizoctoniasolani, and Macrophomina spp resulted in suppressedroot and top growth (Table 4). Interactionsinvolving Macrophomina phaseolina and Pratylenchushexincisus in sorghum plants with adequatemoisture showed little significant difference in diseaseratings or top weights (Norton 1958). In thedrought-stressed plants, the highest disease ratingas well as the lowest foliar dry weight occurredwhen M. phaseolina and P. hexincisus were mixed.Lodging was observed only when the fungus andnematode were combined.Future Research Priorities1. Nematology research utilizing sorghum as thehost crop has received limited attention. Informationis needed in the following areas:a. surveys to ascertain the genera and speciesof phytoparasitic nematodes presentin samples obtained from diverse areas;b. determination of the effect of nematodes onyield when sorghum is grown in varioussoils, under different cultural practices, andin different climates;c. determination of threshold limits if nematodesare shown to be a major factor inTable 3. Effect of stunt (Tylenchorhynchus martini) nematodes on various grain sorghum accessions.Stunt population* Fresh foliar weight Fresh root weight Plant dry weight(100 cm 3 soil) (g) (g) (g)Pedigree† I‡ C I C I C I CSC 599-NE 1147a§ 0.0 3.07a 2.59a 3.69b 4.79a 2.61 bc 2.95abSC 170-6-17 1060a 0.0 2.63ab 2.13a 4.67ab 5.85a 3.04ab 3.00abB 35-6 880a 0.0 2.53bc 2.58a 3.57b 4.25a 2.02c 2.45abBTx 378 840a 27.0 2.29bc 2.34a 5.71a 5.25a 3.58a 3.24aTx 7078 980a 0.0 2.23bc 2.22a 4.70ab 5.69a 2.76abc 3.31aSC 103-12 1360a 0.0 2.19bc 2.15a 4.77ab 5.98a 2.70abc 3.25abT x 430 1360a 0.0 2.00c 2.36a 5.50a 5.82a 3.18ab 3.12ab*Populations were determined 60 days after inoculation.†Accessions obtained from D.T. Rosenow, Texas A&M Agricultural Experiment Station, Lubbock, Texas, USA.‡Initial inoculum consisted of 500 stunt nematodes per pot; I = inoculated, C = control.§Number8 in a column followed by the same letter are not significantly different (P< 0.05), according to Duncan's Multiple Range Test.58

Table 4. Growth and root necrosis of sorghum plants inoculated with Pratylenchus zeae alone and in combinationswith four soil fungi. (Source: Bee-Rodriguez and Ayala 1977.)TreatmentsFoliar dryRoot(g)Necrosisweight (g) Fresh weight Dry weight index*P. zeae-Curvularia spp 25.1 c† 30.50d 2.6a 0.8dP. zeae-F. moniliforme 27.4abc 32.25cd 3.1a 1.2bcdP. zeae-R. solani 27.5abc 33.85cd 3.2a 2.2abcP. zeae-Macrophomina spp 26.9abc 35.60bcd 3.3a 1.0bcdF. moniliforme 26.4bc 35.65bcd 3.1a 1.8abcR. solani 27.8abc 37.80bcd 3.0a 1.6bcP. zeae 26.4bc 39.20abcd 3.9a 3.2aMacrophomina sp 28.1 abc 42.35abc 3.8a 1.6bcCurvularia sp 28.9ab 45.65ab 3.7a 2.4abControl 29.7a 49.25a 6.0b 0.0d*Scale of 0 (no symptoms) to 5 (extensive necrosis).†Means followed by the same letters do not differ significantly (P < 0.05), according to Duncan's Multiple Range Test.sorghum production. Otherwise controlrecommendations are of limited value.2. The potential importance of nematodes ininteractions with bacterial and fungal incitantsin stalk rot complexes of sorghum has notbeen researched. Information is needed in thefollowing areas:a. the potential synergistic relationshipsbetween nematodes and other incitants;b. the role of nematodes in "breaking" varietalresistance of host plants to fungi (primarilyFusarium spp);c. the potential role of nematodes in providingportals of entry for other microorganisms;d. the role of nematodes in predisposing thehost to invasion and extensive lesion developmentby other microorganisms present inthe rhizosphere. A research project of thistype might be applicable to understandingthe etiology of seedling disease problems.ReferencesANONYMOUS. 1971. Estimated crop losses due to plantparasitic nematodes in the United States. Supplement toJournal of Neonatology, Special Publication No. 1. 7 pp.AYALA, A., and BEE-RODRIGUEZ, D. 1978. Control ofphytoparasitic nematodes attacking sorghum in PuertoRico. Journal of Agriculture of the University of PuertoRico 62:119-132.AYTAN, S. 1968. Pathogenicity, life cycle and host rangeof Meloidogyne naasi Franklin found on sorghum in Kansas.M.Sc. thesis, Kansas State University, USA. 43 pp.AYTAN, S., and DICKERSON, O.J. 1969. Meloidogynenaasi on sorghum in Kansas. Plant Disease Reporter53:737.BEE-RODRIGUEZ, D., and AYALA, A. 1977. Interaction ofPratylenchus zeae with four soil fungi on sorghum. Journalof Agriculture of the University of Puerto Rico 61:501 -506.CLAFLIN, L.E., HAFEZ, S.L., and TODD, T.C. 1983. Effectsof insecticides-nematicides on stunt nematode populationsand grain sorghum yields. Page 145 in Abstracts ofPapers, Fourth International Congress of Plant Pathology,17-24 August, 1983, University of Melbourne, Melbourne,Victoria, Australia. North Melbourne, Victoria, Australia:Rowprint Services.COETZEE, V. 1956. Meloidogyne acronea, a new speciesof root-knot nematode. Nature 177:899-900.COETZEE, V., and BOTHA, H.J. 1965. A redescription ofHypsoperine acronea (Coetzee, 1956) Sledge & Golden,1964 (Nematoda: Heteroderidae), with a note on its biologyand host specificity. Nematologica 11:480-484.CUAREZMA-TERAN, J.A. 1983. Etiology of a sorghumdisease complex in Mississippi, Ph.D. thesis, MississippiState University, Mississippi, USA.FAWCETT, H.S. 1931. The importance of investigationson the effects of known mixtures of microorganisms. Phytopathology21:545-550.57

HAFEZ, S.L., and CLAFLIN, L.E. 1982. Control of plantparasitic nematodes on grain sorghum and yieldresponse. Fungicide and Nematicide Tests (AmericanPhytopathological Society, St.Paul, Minnesota, USA)37:198.MICHELL, R.E., MALEK, R.B., TAYLOR, D.P., andEDWARDS, D.I. 1973. Races of barley root-knot nematode,Meloidogyne naasi: I. Characterization by host preference.Journal of Nematology 5:41 -44.NORTON, D.C. 1958. The association of Pratylenchushexincisus with charcoal rot of sorghum. Phytopathology48:355-358.NORTON, D.C. 1978. Ecology of plant-parasitic nematodes.New York, New York, USA: John Wiley & Sons. 268pp.ORR, C.C. 1967. Observations on cotton root-knot nematodein grain sorghum in West Texas. Plant DiseaseReporter 51:29.ORR, C.C., and MOREY, E.D. 1978. Anatomical responseof grain sorghum roots to Meloidogyne Incognita acrita.Journal of Nematology 10:48-53.SMOLIK, J.D. 1977. Effects of Trichodorus allius andTylenchorhynchus nudus on growth of sorghum. PlantDisease Reporter 61:855-858.58

Spatial and Temporal Succession of Fungal Speciesin Sorghum Stalks as Affected by EnvironmentJ.E. Partridge, J.E. Reed, S.G. Jensen, and G.S. Sidhu*SummarySorghum plants are infected by various fungi, beginning at the seedling stage and continuinguntil maturity. The principal avenue of infection by those fungi that cause stalk rot of matureplants, primarily Fusarium spp and Macrophomina phaseolina (Tassi) Gold., is through theroots. Parasitism is established early and continues until an external stress is placed upon theplant. The hypothesis is offered that heat and/or drought stress effects a perturbation of thenormal biochemical processes of the stalk tissue, resulting in a quasi-defenseless plant Thisstress period allows the internal parasites to begin pathogenesis, which leads to the phenomenonof stalk rot.In order to address the subject of spatial and temporalsuccession of fungal species, the entire lifespanof the sorghum plant must be considered.Accordingly, it is necessary to give at least cursoryconsideration to the various physiological stagesthrough which the plant passes during its developmentalprocess. Inasmuch as pathogenesisoccurs in the stalk, our discussion of physiologicaland biochemical processes of the host will belimited to the stalk. The topics of photosynthateaccumulation and source-sink relationships will beleft to other discussants. This should not be takenas a failure to recognize these interrelationshipsbut rather as an attempt to keep this presentationwithin the constraints of environmental effects asthey affect, or effect, pathogenesis of stalkinhabitingparasites.Additionally, this discussion will be limited tostalk rots involving those pathogens that initiallyexist as parasites early in the life of the plant andbecome pathogens only later as the grain reachesmaturity. We have chosen not to include anthracnose.Its importance has been amply demonstrated(Chowdhury 1936, Bergquist 1973, Dale1963, Wheeler et al. 1972, Wheeler et al. 1974). Ithas been excluded because it is pathogenic uponliving tissue and apparently its mode of pathogenesisis quite different from the stalk-rotting organismsthat are the subject of this discussion(Katsanos and Pappelis 1965, Katsanos and Pappelis1966). For like reasons we have excludedPythium spp.Many of the putative stalk rot pathogens are inreality well-adapted parasites during the greaterpart of the life of the plant and depend on a weakeningof the host in order to become pathogens.Therefore with respect to stalk rots the term pathogenshould be applied with caution.From the outset it must be asserted that sorghumis not maize, and—while both are afflicted by aphenomenon known as stalk rot, are members ofthe grass family, and have a number of commonphysiological and biochemical processes that areinstructive for comparison—it may be an error toconsider that the disease is entirely equivalent inboth crops. Sorghum, though grown as an annual inthe USA and other temperate regions, is primarily anonsenescing perennial (Duncan et al. 1981),*J.E. Partridge - Assistant Professor, J.E. Reed - former graduate student, S,G. Jensen - USDA Plant Pathologist, and G.S.Sidhu - Assistant Professor, Department of Plant Pathology, University of Nebraska, Lincoln, NE 68583-0722, USA.International Crops Research Institute for the Semi-Arid Tropics. 1984. Sorghum Root and Stalk Rots, a CriticalReview: Proceedings of the Consultative Group Discussion on Research Needs and Strategies for Control ofSorghum Root and Stalk Rot Diseases, 27 Nov - 2 Dec 1983, Bellagio, Italy. Patancheru, A.P. 502 324, India:ICRISAT.59

white maize is a senescing annual. Accordingly, thephysiological and biochemical processes of thetwo species are not entirely comparable; thereforethe modes of pathogenesis of the several stalk rotorganisms may or may not be the same in eachhost.S e e d b o r n e O r g a n i s m sTable 1 presents a compilation of various fungalgenera that have been identified in or on seed andare usually reported as part of a head mold complexon sorghum. It is particularly informative toconsider these organisms from the perspective oftheir potential as the initial invaders in a multipleparasite disease. Each of them has also been identifiedas a constituent of the microflora of stalkrottedtissue. The ubiquity of the genera Curvularia,Fusarium (Williams and Rao 1981), and Phomaover such a wide geographic span indicates apotential for universality of the stalk rot phenomenon,rather than a special set of circumstancespeculiar to each locale. While of these three onlythe genus Fusarium has been shown to play amajor role in stalk rot, it must be acknowledged thatTable 1. Geographical distribution of seed-infecting/infesting fungi involved in seedling-, root-, and/or stalkrotsof sorghum. aGenusHelmintho-Location Altemaria Colletotrichum Curvularia Fusarium sporium Nigrospora PhomaBangladesh x x xBrazil x xEast Africa x x x x xEthiopia x xIndia x x x x xItaly x x x xNigeria x x x x x x xPakistan x x xPhilippines x x xPuerto Rico x x x x xSenegal x xThailand x xUSAxVenezuela x xTable 1 references:Location Reference Location ReferenceBangladesh Mian and Ahmed 1980 Italy D'Ercole and Nipoti 1979Brazil Minussi and Kimati 1978 Nigeria Tyagi 1980East Africa Doggett 1980 Pakistan Hamid 1980Ethiopia Hulluka and Gebrekidan 1980 Philippines Dalmacio 1980India Tripathi 1975 Puerto Rico Feliciano et al. 1982Bidari et al. 1978 Senegal Denis and Girard 1980Ravindranath 1980 Thailand Pupipat 1980Siddiqui and Khan 1973 USAVenezuelaBain 1950Castor and Frederiksen 1980Claflin 1981Pady1943Riccelli 1980a. Table 1 is not intended to be a complete compilation of all known reports of fungi that are potential stalk rotters, but only to give anindication of the geographical universality of the genera.60

any organism that invades the juvenile tissue maydebilitate the host sufficiently to allow the successionof other organisms. The lack of identification ofany given genus in any geographic location mayreflect more upon the interest or techniques of thereporting investigator than upon its presence orabsence.Fusarium moniliforme Sheld. establishes itself asan internal seed parasite (Castor and Frederiksen1980, 1981), and even though such fungi mayseem candidates for seed treatment, the omnipresentnature of these organisms in the soil and theirabilities to exist as saprophytes negate the potentialfor this control measure. Therefore the utility ofseed treatment as a control measure for thesefungi may be of more academic interest than economicvalue.Seedling Infectionand Potential InoculumInfection of seedlings and/or the establishment ofseedborne internal parasites as seedling parasitesis nearly coincident with seed germination (Tripathi1975, D'Ercole and Nipoti 1979, Gourley et al. 1977,Bain 1973, Bee-Rodriguez and Ayala 1977). Withrespect to charcoal rot, the necessity for seedlinginfection/infestation by Macrophomina phaseolinawas documented by Odvody and Dunkle (1979),and is assured by the presence of the sclerotia insoil and their ability to survive (Chidambaram andMathur 1975; Jadhav 1978; Shokes et al. 1977;Bhattacharya and Samaddar 1976; Livingston1945a, 1945b) more than one cropping seasondevoid of host material (Cook et al. 1973, Watanabeet al. 1970). Livingston (1945a, 1945b) reportedthat seedling blight occurred as a result of infectionof the primary roots by M. phaseolina. In view of thework of Smith (1969a, 1969b), it is probable thatroot exudates from the sorghum seedlings triggeredsclerotial germination. In greenhouse experiments,soil temperatures above 30°C resulted in74% infection and up to 30% blighted seedlings(Uppal et al. 1936, Livingston 1945a, 1945b). Theimportance of soil moisture in conjunction withtemperature has been addressed by variousworkers (Shokes et al. 1977, Odvody and Dunkle1979, Edmunds et al. 1964). If infection occurredprior to the emergence of secondary roots, theplants succumbed. Less severely diseased seedlingswere able to establish secondary roots, andunder favorable conditions of sufficient soil moisture,were able to grow to mature plants. Under fieldconditions, the extent of infection, though not catalogued(Livingston 1945a), was believed to be high.The result of this high level of infection was that M.phaseolina was probably systemic in a large percentageof the surviving plants, even though nosymptoms were obvious until after a period ofenvironmental stress.Though several pathogenic strains of M. phaseolinahave been reported (Khan et al. 1976), thesignificance of various strains and their differentmodes of pathogenesis have yet to be investigatedor experimentally considered in the development ofresistant sorghums.The work of Reed (1982) and Reed et al. (1982,1983) indicates that, even in fields where M. phaseolinadoes not play an obvious role in stalk rot,few (if any) seedlings are entirely free of otherinternal parasites. A consolidation of Reed's analysisof isolation data from various stages of plantgrowth is presented in Tables 2, 3 and 4.The data in Tables 2 through 4 are the result of 3years of field experiments and as such have theadvantage of allowing one to assess the import ofany given species through the season and observeTable 2. Percentage of isolation of fungal speciesfrom sorghum seedlings. aFungal species 2 wks 4 wks 6 wksFrom stalksF. moniliforme 0 0 5F. graminearum 7 6 5F. "roseum" 0 0 0F. tricinctum 1 1 1F. equiseti 8 8 8F. oxysporum 4 4 4Alternaria spp 10 10 10Epicoccum spp 0 0 0From rootsF. moniliforme 5 5 10F. graminearum 7 10 10F. "roseum" 5 3 5F. equiseti 15 10 15F. oxysporum 20 20 20Alternaria spp 5 20 20Epicoccum spp 0 0 0a. Composite of isolation data taken from Reed (1982). Isolationswere taken from apparently healthy tissue and weremade onto potato dextrose agar. "Stalks" refers to isolationsmade from the intemodal tissue between the second and thirdnodes above the soil level. "Roots" refers to crown tissue andmajor roots.61

Table 3. Percentage of isolation of fungal speciesfrom sorghum plants between floweringand soft dough stages. aFungal species 8wks 10 wks 12 wksFrom stalksF. moniliforme 12 40 50F. graminearum 5 6 10F. "roseum" 5 8 10F. tricinctum 1 5 9F. equiseti 8 15 10F oxysporum 4 6 8Alternaria spp 15 25 20Epicoccum spp 0 0 12From rootsF. moniliforme 10 15 20F. graminearum 12 12 20F. "roseum" 5 8 15F. equiseti 15 25 20F. oxysporum 20 15 10Alternaria spp 25 40 60Trichoderma spp 40 25 15Epicoccum spp 0 5 50a. Composite of isolation data taken from Reed (1982). Isolationswere taken from apparently healthy tissue and weremade onto potato dextrose agar. "Stalks" refers to isolationsmade from the internodal tissue between the second and thirdnodes above the soil level. "Roots" refers to crown tissue andmajor roots.Table 4. Percentage of isolation of fungal speciesfrom sorghum plant between the soft doughand "mature" stages. aFungal species 14 wks 16 wks 18 WksFrom stalksF. moniliforme 50 70 40F. graminearum 12 12 30F. "roseum" 12 12 25F. tricinctum 15 12 15F. equiseti 12 15 15F. oxysporum 10 8 6Alternaria spp 30 25 15Epicoccum spp 20 25 20From rootsF. moniliforme 20 30 40F. graminearum 25 20 25F. "roseum" 15 15 15F. equiseti 15 20 15F. oxysporum 15 5 5Alternaria spp 50 50 50Trichoderma spp 25 25 25Epicoccum spp 30 30 25a. Composite of isolation data taken from Reed (1982). Isolationswere taken from apparently healthy tissue and weremade onto potato dextrose agar. "Stalks" refers to isolationsmade from the internodal tissue between the second and thirdnodes above the soil level. "Roots" refers to crown tissue andmajor roots.repeated patterns from year to year. In view of thealleged involvement of F. moniliforme as a majorcontributor in stalk rot (Tullis 1951), it is instructiveto note that it is not a primary colonizer of seedlingsthrough root infection. Under the conditions of thisstudy the species F. graminearum, F. equiseti(Cda.) Sacc, and Altemaria spp are probably moreimportant in the early colonization of seedlings thanare any other species. For comparison to otherwork, it should be noted that the study by Reed et al.was conducted in a conservation tillage systeminvolving a wheat-fallow rotation and no cultivationduring the crop season. One might expect anincreased inoculum potential for F. graminearum,due in part to the wheat in the rotation. The lack oftillage during the crop season is important for discussionbecause the mode of infection by the organismsisolated must be through means other thancultivation root wounding. The results from this typeof tillage system relate well to cultural methods thatare not dependent on mechanized agriculture andto efforts aimed at establishing conservation tillagepractices.During the seedling stages of growth, nearly all ofthe increase in dry weight is in leaf and root tissue,with a relatively small increase in the weight of thecrown and stalk, and fungi in the stalk are in anenvironment completely different from that at theplant's maturity when stalk rot is manifested. Beginningat differentiation of the growing point, the firstof two major shifts in growth begins. Leaf expansionis completed, and there is a great increase in stalkvolume and dry weight. Stalk cells expand andelongate, and cell density decreases very rapidly.The second major change occurs at anthesis whenemphasis shifts from the stalk to the head.With the onset of flowering, a very dramatic shiftin the metabolic activities takes place within thenodes of the plant. Within 5 days of flowering theactivity of phenylalanine ammonia lyase (PAL)plummets to a neglegible level, and by this time theanabolic glycosidases have been severelyreduced in activity (J.E. Partridge, unpublisheddata, 1982). The activities of the stalk change fromrapid growth and expansion to maintenance andphotosynthate accumulation, and finally to translo-62

cation for grain fill. These metabolic activities andshifts in composition directed towards accumulationof materials into grain render the plant evenmore vulnerable to pathogenic activities from itsinternal parasites.Postflowering toSoft Dough StagesTable 3 presents data showing that during this timethe stalk becomes even more heavily parasitizedby an increasing number of fungal species. Themost obvious invader is F. moniliforme, which isisolated with increasing frequency well into the12th week. However, other species are also parasitizingthe stalk, though apparently at a lesser frequencythan F. moniliforme. These include F.graminearum, F. roseum, F. equiseti, and Alternariaspp. The root system (which has largely ceasedgrowth and expansion by this time) continues to becolonized by various species. The increase incolonization of roots by Alternaria spp and Trichodermaspp, even when care has been taken toselect apparently healthy tissue, may be an indicationof increasing saprophytic activity on moremature or senescing tissue.Evidence indicates that the general pattern ofcolonization of sorghum stalks and roots by fungi ismuch the same as that reported for maize (Kommedahlet al. 1979, Young and Kucharek 1977,Warren and Kommedahl 1973). The massivecolonization of stalk tissue appears to occur concomitantlywith the onset of flowering, but rootsseem to be inhabited by fungi regardless of thegrowth stage of the plant. Fungi are more readilyisolated from both stalks and roots as the cropmatures.The fungal species colonizing sorghum insouthwestern Nebraska are similar to thosereported on maize, especially in the central UnitedStates. According to Christensen and Wilcoxson(1966), F. moniliforme and F. graminearum arecommonly associated with ear and stalk rot ofmaize, and Nigrospora spp are less common stalkrot pathogens of maize. Trichoderma spp andAltemaria spp are frequent secondary invaders ofrotted maize stalks. Of the Fusarium species thatwere isolated from sorghum in this study, all arereported to be associated with maize, usually asstem or root parasites.M. phaseolina was noticeably absent fromsorghum stalks and roots throughout the course ofthe study by Reed et al. (1983). Since charcoalstalk rot of sorghum is fairly common in westernNebraska, it is surprising that M. phaseolina wasnot found as a common inhabitant of sorghumstalks and roots. Since only symptomless plantswere sampled, the probability of isolating M. phaseolinamay have been low due to the absence ofenvironmental conditions favorable for its growth.As mentioned earlier, charcoal rot is favored byhigh soil temperature and low soil moisture. Of thethree seasons in our study, two were unusually cooland moist. The 1980 season most closely approximated"normal" weather conditions for westernNebraska, and even that season was not extremelyhot or dry. Additionally, conservation tillage, whichwas practiced on the test plots, tends to conservesoil moisture and reduce fluctuations in soiltemperature. This cultural practice may have beeneffective in reducing temperature and moisturestress in the roots and thereby inhibiting infectionand ramification by this parasite (Doupnik and Boosalis1980; Doupnik et al. 1975a, 1975b; Edmundset al. 1975)."Mature" PlantsThe difference between maize (the annual) andsorghum (the perennial) should be noted again atthis point. The dry weight percent composition ofthe maize stalk increases as the plant matures, butthe stalk of the sorghum tends to retain a relativelyconsistent dry weight until it is killed by frost. Atleast that is the trend in Nebraska, where the plantingis done in a cool moist spring, and the plantgrows and flowers during a hot dry summer andmatures during a progressively cooler fall. Figure 1shows data (S.G. Jensen, unpublished data, 1983)summarizing several dates of harvest and severalgenotypes over 2 years. Plants did not dry downfrom the base to the head or vice versa; in fact theyshowed little tendency to dry down at all. The crownand the peduncle had the highest level of dry matter,while the middle stalk tissue was the mostsucculent. These trends show that even within thesame stalk there is a gradient of microenvironmentalconditions influencing the growth and pathogenicityof the various fungi.It should also be noted that in our growing conditionsthere are two general types of tissue necrosisfrequently observed. One of these leads to a collapseof the tissue in the base of the plant, prematurenecrosis of the whole plant, and the lodging of63

100908070605040302010Crown14 16 18 20 22Percent dry weighto f s t a l k t i s s u eFigure 1. Plant height versus percent dryweight Twenty plants were harvested on eachof five dates from soft dough stage to grainmaturity. The average percentage of dry weightof the tissue versus the height of the tissue onthe plant is presented.the plant at or near the ground. The second type ofnecrosis occurs in the peduncle and leads to apremature ripening of the head, with or withoutbreaking of the peduncle. Tissues with either ofthese conditions have a similar dry weight composition,but it is not known if there is a relationshipbetween that composition and/or the metabolicactivities associated with it and the occurrence ofrot.Although it was not tested statistically, a relationshipwas observed between weather conditionsand the number of fungal species found in stalktissue. The seasons were progressively cooler andwetter from 1980 to 1982, and progressively fewerspecies were recovered from stalks over the threeseasons. Planting was delayed in 1981 and 1982(Figs. 2a and b), resulting in a shorter growingseason and, because of a cool fall, slower cropmaturation rate. It was difficult to determinewhether the decreases in fungal species were dueto climatic conditions, slow maturation rate, lack ofstress on the plants, or a combination of all of thesefactors. The most important observation is that thesequence of infection of stalk tissue by variousspecies was similar during all 3 years, even thoughthe relative abundance of each species differedfrom year to year. In addition, the sequence couldbe associated with stages of plant maturity. Thissuggests that the sequence of infection is a relativelystable and predictable process, associatedwith physiological and metabolic changes withinthe stalk as it matures.As the head approached maturity, F. moniliformewas the dominant species isolated from stalktissue, but it is uncertain whether it predominatedby being the most active competitor or if it succeededsimply by default. During 1980 and 1981 aninverse relationship existed between the isolationpercentage of F. moniliforme from stalks and that ofF. graminearum and the "roseum" group when theywere present: when the incidence of F. moniliformedeclined, the incidence of these other fungiincreased, and the converse was also observed.Populations of F. equiseti, F. oxysporum Schlect.emend Snyd. et Hans., and F. solani (Mart.) Appel etWr. emend Snyd. et Hans appeared to follow asimilar but less striking pattern in inverse relation toF. moniliforme.In 1982 F. graminearum and the "roseum" groupwere rarely isolated, while F. moniliforme was consistentlyisolated. In the first 2 years, it appearedthat populations of F. moniliforme were adverselyaffected by the composition of stalk tissue as theheads approached maturity, and by the first killingfrost. In 1982, though, neither of these trends wasobserved, possibly because the stalks were stillsomewhat immature at the first frost date, offering agreater amount of moisture and greater protectionfrom frost damage.On one hand it might be argued, first, that F.moniliforme influenced the incidence of the otherFusarium species, as well as having the advantageof being the first to colonize the tissue. Secondly,the decline of F. moniliforme could be directly associatedwith changes in environmental conditions. Itis possible that when environmental conditions,such as lower temperatures and greater moisturelevel, favor the growth of F. moniliforme, other speciesare less able competitors. These other speciesmay be better survivors and may be able tocolonize stalks when the population of F. monili-64

300250Stalks 300198019811982250Roots19811982SDA200200BHD150MHD150FBASD10050FBASD100 FHDASD50BFB A SDJ u l y Aug Sept Oct J u l y Aug Sept OctF = flag leaf stageB = boot stageA = anthesisSD = soft dough stagerepresents the approximate time of the frost kill.HD = hard dough stageM = grain maturityFigure 2a and b. Isolation frequency of fungal species in stalks and roots of sorghum. Each pointrepresents the number of species isolated expressed as a percentage of the total number of samplescollected on that date. Approximate dates of occurrence of plant developmental stages are indicated.(Source: Reed 1982.)forme is reduced. However, this same line of reasoningmay also be offered to support the converseargument that F. moniliforme does not influence thepopulations of other Fusarium species, but insteadis influenced by them. It may be argued that whenenvironmental stresses, such as higher temperaturesand lower moisture levels, are placed uponthe plant, the other Fusarium species are more ablecompetitors, and the population of F. moniliforme isreduced because of their increased activities. Thisquestion could not be resolved in an observationallybased study such as Reed's because shenoted only the presence or absence of each species.The use of an in vivo assay (Marshall andPartridge 1981, Partridge 1981, Partridge and Marshall1981) that assesses the abundance andactivity of individual species would be desirable toadequately address the significance of eachspecies.Sorghum roots were colonized by species ofFusarium, Alternaria, and Epicoccum, all of whichare common root inhabitants. Of the Fusarium species,F. equiseti, F. oxysporum, and F. solani colonizedroots earlier than did F. moniliforme, F.graminearum, and the "roseum" group. This maybe indicative of higher initial populations of thesespecies due to their ability to overwinter in soil aschlamydospores. The sequence of infectionobserved in roots in 1981 was closely paralleled in1982, which may be due to the similarity of environmentalconditions over the two seasons, or it mayhave occurred regardless of environmental condi-65

tions. By observing root colonization over thecourse of several seasons, it should be possible todetermine whether the sequence of infectionoccurs independently of weather conditions and isdependent on the stage of plant maturity or whethera significant interaction occurs between the two.The early colonization of roots may indicate thatroot infection leads to stalk infection, an infectionpathway that has often been suggested in the literature(Kommedahl et al. 1979, Young andKucharek 1977). In our study, an increase in rootpopulation of some species appeared to precedean increase in stalk populations. However, in 1981it was not observed whether roots and stalks of thesame plant were colonized by the same species,and in 1982 too few species colonized stalks toafford a comparison. Therefore, it could not bedetermined if a correlation actually existed. Rootcolonization is likely to be one of several ways bywhich stalk colonization occurs.The statistical analysis of stalk colonization by F.moniliforme and F. roseum presented by Reed(1982) clearly shows that the incidence of thesefungi in stalks increased as the seasons progressed.However, the absence of statistically significantvarietal differences in fungal colonizationwas open to interpretation as to whether the analysisaccurately reflected the biological trends thatmay have been occurring. In Reed's study, thesample sizes were small; therefore intravarietalvariation may have masked some intervarietal differences.The fact that some significant varietaldifferences were observed indicated that significantdifferences among varieties may occur inmore instances than were detected in her study.These differences may become apparent if anexperimental design is employed that increasessample size.The association of stress conditions, senescence,and stalk rot of maize and sorghum is welldocumented (Edmunds 1964, Edmunds et al. 1964,Odvody and Dunkle 1975, Odvody and Dunkle1979, Hsi 1961, Patil et al. 1979, Trimboli and Burgess1983, Wadsworth and Sieglinger 1950), butthe interrelationship between host and parasite(s)in the development of the disease is not understood.Research data (Reed 1982, Reed et al. 1983,Bain 1973) demonstrates that fungi are present instalk and root tissue throughout most of the life ofthe plant. Therefore, if microbial interactions dooccur within plant tissue, they may be occurringvery early in the life of the plant. Similarly, interactionsbetween the host and these microorganismsmay begin early and continue throughout the host'sgrowth and development. These data are notnecessarily in conflict with those of Trimboli andBurgess (1983), even though one can reach thesame or different conclusions from Trimboli's data.Trimboli's data were taken primarily from plantsinfected in the greenhouse by a single organism,while Reed's data are of field origin. The presenceof fungi in stalks and roots of sorghum in theabsence of any symptoms of stalk rot indicates thatfungal colonization of plant tissue does not, in andof itself, lead to development of the disease. Thenature of the interactions occurring within planttissue cannot be determined from this study; however,one may speculate that a balance existsbetween fungal activity within plant tissue and theability of the host to withstand such activity. Thisbalance may be shifted by factors adversely affectingthe host or by conditions that favor increasedfungal activity. The microorganisms may becomedestructive to stalk tissue, leading to the developmentof stalk rot.The Stress HypothesisIn general, stalk rots are dependent upon stressphenomena for the onset of pathogenesis. Dodd's(1977; 1980a, b,c) hypothesis of photosyntheticstress may explain only a single type of stressplaced upon a plant: stress related to reproduction.If applicable, it would seem that photosyntheticstress would probably play a larger role in senescingthan in nonsenescing plants. Plants undergo anumber of stresses: insect feeding (Frederiksenand Daniels 1970), reproduction (Edmunds andVoigt 1966), and environmental—e.g., heat anddrought. These have been examined under controlledconditions in maize and/or sorghum. Sincethe photosynthetic stress, owing to the availabilityof solar radiation, is less variable than eithertemperature or moisture, this discussion cannot becomplete without consideration of these twostresses on the basic biochemistry of the sorghumplant.Plant cells respond to stress with an alteredmetabolism (Altschuler and Mascarenhas 1982,Bronson and Scheffer 1977, Flores and Galston1982, Key et al. 1981, Schoeneweiss 1975). One ofthe responses to heat or drought stress is the synthesisof a new class of proteins (stress proteins).The observation of these changes is not new(Hsiao 1970); however, our understanding of their66

ole in the cell is (Baszczynski and Walden 1982).When stress occurs, gramineous cells respond byproducing a new messenger RNA (Baszczynski etal. 1983). Once produced, this stress mRNA is thepredominant messenger that can be translated bythe ribosomes. At present it is unclear whether thisis the only type of mRNA that can be translatedduring this period. Neither the mechanism by whichthe stress mRNA is able to control protein synthesisnor the function of the new proteins is completelyunderstood. Suffice it for this discussion to say thatthe proteins that are synthesized are probably forthe purpose of repairing any damage that may haveoccurred to the cell during the stress period. Unlessthe severity of the stress is sufficient to cause celldeath, the length of the repair process is proportionalto the amount of stress (Baszczynski et al.1983).With regard to stalk rot, since only repair proteinsare being produced after an environmental stress,the plant is in a very vulnerable situation withrespect to its own defense. For the sake of example,if a heat stress of 35°C is placed on a maizeplant (or sorghum, for this example), it will begin toproduce heat stress proteins within 15 min. It willcontinue to produce those proteins for as long asthe stress is applied. Realistically, in the field, thismight be for 6 h or longer. During this stress periodthe plant will be vulnerable to pathogenic activity.Once the temperature is reduced to 27°C (which inthe field may take a number of hours) the heatstress proteins will continue to be synthesized forup to 8 additional hours (Baszczynski and Walden1982). Therefore the plant is vulnerable to pathogensfor a minimum of 14 consecutive hours.If the environmental heat stress is compoundedwith a concomitant drought stress, then the effectupon the plant may be extremely severe. Additionally,if the environment is unfavorable during successivedays, as is often the case, then in effectthose organisms that have established themselvesas parasites will have both the opportunity and thecompetitive advantage to begin pathogenesis.Unfortunately, the environmental conditions describedand the resulting pathogenesis are commonand annual occurrences in much of the maize- andsorghum-growing areas. Therefore the hypothesisis offered that stress-induced (primarily temperatureand moisture) perturbations in the biochemicalprocesses of the plant weaken or curtail its ability toinhibit pathogenesis by its internal parasites forsufficient time that the internal parasites gain theparasitic advantage and stalk rot begins.Recommendationsfor Future Research1. It is necessary to study organisms involved asinternal parasites of sorghum during the entirelife of the plant in expanded geographicalareas. One of the difficulties of stalk rotresearch is the lack of data collected fromsingle plots over a number of years and publishedin refereed journals. It is exceedinglydifficult to attempt to construct a picture of therole of parasites in stalk rot from fragmentarydata. At present, the best one can do is toattempt to draw conclusions based upon one'sown data, with all of the accompanying geographicallimitations. Obviously, in order toarrive at a universal conclusion about the roleof the various parasites, we must have replicateddata from a wide-ranging number ofgeographical sites. We propose thatresearchers:a. publish information based only upon replicated(not single year) data;b. identify the genotype of the sorghum plantsunder investigation;c. collect and publish data that pertain to theenvironmental conditions under which theircrop is grown;d. conduct research using proper mycologicaltools; ande. encourage, primarily through colleagues orinternational students, the isolation anddescription of the internal parasite flora ofsorghum plants in countries wheresorghum is grown.2. The tools of plant molecular biology are availableand must be applied to the study of stalkrots. In order to understand and ultimatelysolve the stalk rot mystery, we must gain anunderstanding of the various interactions ofhost and parasite(s) as affected by the environment.Considerable data have accumulatedto substantiate the fact that an interactiondoes occur. A challenge for the future is todefine what the plant recognizes as stress andto understand both the mechanism for and the67

magnitude of the plant's response to the variousstresses presented to it. As an example, ifheat stress is a factor, one should be able todetermine;a. the temperature and duration necessary toinduce altered biochemical activity;b. the nature of the biochemical changes thatoccur;c. the variations that occur between hybrids;d. the exacerbation of heat stress by droughtstress, or vice versa; ande. a means to apply this knowledge to theselection of hybrids.3. Research activity on the basic biochemicalprocesses of the sorghum stalk should beincreased to provide a basis for understandingthe parasitism and pathogenesis of the putativestalk-rotting organisms. Basic questionsthat should be addressed are:a. why are stalks apparently relatively free ofparasitism until postanthesis;b. whether there are antifungal compoundsnormally produced by sorghum plants thatinhibit parasites from becoming pathogens;andc. whether the normal cyanogenic compoundshave any role in the stalk rotsyndrome.4. Increased research emphasis should beplaced on determining the long-range effectsof conservation tillage or other culturalmethods on the host-parasite interactions thatlead to stalk rots.AcknowledgmentsThis research was funded in part by grants from:Stauffer Chemical Company (J.E. Partridge); TheRockefeller Foundation (J.E. Partridge); andINTSORMIL, AID/DSAN/XII/G-0149 (J.E. Partridgeand S.G. Jensen).ReferencesALTSCHULER, M., and MASCARENHAS, J.P. 1982. Heatshock proteins and effects of heat shock in plants. PlantMolecular Biology 1:103-116.BAIN, D.C. 1950. Fungi recovered from seed of Sorghumvulgare. Phytopathology 40:521 -522.BAIN, D.C. 1973. Association of Fusarium moniliformewith infection of sorghum seedlings by Sclerosporasorghi. Phytopathology 63:197-198.BASZCZYNSKI, C.L., and WALDEN, D.B. 1982. Regulationof gene expression in corn (Zea mays L) by heatshock. Canadian Journal of Biochemistry 60:569-579.BASZCZYNSKI, C.L., WALDEN, D.B., and ATKINSON,B.G. 1983. Analysis of the in vitro translation productsfrom RNAs of heat-shocked seedlings. Maize GeneticsCooperation Newsletter (ed. E.H. Coe, University of Missouri,Columbia, Missouri, USA) 57:161-163.BEE-RODRIGUEZ, D., and AYALA, A. 1977. Interaction ofPratylenchus zeae with four soil fungi on sorghum. Journalof Agriculture of the University of Puerto Rico 61:501 -506.BERGQUIST, R.R. 1973. Colletotrichum graminicola onSorghum bicolor in Hawaii. Plant Disease Reporter57:272-275.BHATTACHARYA, M., and SAMADDAR, K.R. 1976.Epidemiological studies on jute diseases. Survival ofMacrophomina phaseoli (Maubl.) Ashby in soil. Plant Soil44:27-36.BIDARI, V.B., SATYANARAYAN H.V., HEGDE, R.K., andPONNAPPA, K.M. 1978. Effect of fungicides against theseed rot and seedling blight of hybrid sorghum CSH-5.Mysore Journal of Agricultural Sciences 12:587-593.BRONSON, C.R., and SCHEFFER, R.P. 1977. Heatinducedand aging- induced tolerance of sorghum andoat tissues to host selective toxins. Phytopathology67:1232-1238.CASTOR, L.L., and FREDERIKSEN, R.A. 1980. Fusariumand Curvularia grain molds in Texas. Pages 93-102 inSorghum Diseases, a World Review: Proceedings of theInternational Workshop on Sorghum Diseases, sponsoredby Texas A&M University (USA) and ICRISAT.Patancheru, A.P. 502 324, India: ICRISAT.CASTOR, L.L., and FREDERIKSEN, R.A. 1981. Histopathologyof Fusarium moniliforme infection of sorghumkernels, Phytopathology 71:208.CHIDAMBARAM, P., and MATHUR, S.B. 1975. Productionof pycnidia by Macrophomina phaseolina. Transactionsof the British Mycological Society 64:165-168.68

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SHOKES, F.M., LYDA, S.D., and JORDAN, W.R. 1977.Effect of water potential on the growth and survival ofMacrophomina phaseolina, Phytopathology 67:239-241.SIDDIQUI, M.R., and KHAN, I.D. 1973. Fungi and factorsassociated with the development of sorghum ear-molds.Transactions of the Mycological Society (Japan) 14:289-293.SMITH, W.H. 1969a. Comparison of mycelial and sclerotialinoculum of Macrophomina phaseoli in the mortality ofpine seedlings under varying soil conditions. Phytopathology59:379-382.SMITH, W.H. 1969b. Germination of Macrophomina phaseolisclerotia as affected by Pinus lambertiana root exudate.Canadian Journal of Microbiology 15:1387-1391.TRIMBOLI, D.S., and BURGESS, L.W. 1983. Reproductionof Fusarium moniliforme basal stalk rot and root rot ofgrain sorghum in the greenhouse. Plant Disease 67:891 -894.TRIPATHI, R.K. 1975. Head fungi of sorghum phytotoxinsand their effects on seed germination. Indian Phytopathology24:499-501.TULLIS, E.C. 1951. Fusarium moniliforme, the cause of astalk rot of sorghum in Texas. Phytopathology 41:529-535.TYAGI, P.D. 1980. Sorghum diseases in Nigeria. Pages45-52 in Sorghum Diseases, a World Review: Proceedingsof the International Workshop on Sorghum Diseases,sponsored jointly by Texas A&M University (USA) andICRISAT. Patancheru, A.P. 502 324, India: ICRISAT.UPPAL, B.N., KOLHATKAR, K.G., and PATEL, M.K. 1936.Blight and hollow stem of sorghum. Indian Journal ofAgricultural Science 6:1323-1334.WADSWORTH, D.F., and SIEGLINGER, J.B. 1950. Charcoalrot of sorghum. Oklahoma Agricultural ExperimentStation Bulletin No. B-355. Stillwater, Oklahoma, USA:Oklahoma A&M College and U.S. Department of Agriculture.7 pp.WARREN, H.L, and KOMMEDAHL, T. 1973. Prevalenceand pathogenicity to corn of Fusarium species fromcrown roots, rhizosphere, residues, and soil. Phytopathology63:1288-1290.WATANABE, T., SMITH, R.S., Jr., and SNYDER, W.C.1970. Populations of Macrophomina phaseoli in soil asaffected by fumigation and cropping. Phytopathology60:1717-1719.WILLIAMS, R.J., and RAO, K.N. 1981. A review of sorghumgrain molds. Tropical Pest Management 27:200-211.YOUNG, T.R., and KUCHAREK, T.A. 1977. Succession offungal communities in roots and stalk of hybrid field corngrown in Florida. Plant Disease Reporter 61:76-80.QuestionsWilliams:You indicated a belief that Fusarium graminearumis more important in stalk rot than F. moniliforme. Isthis just for your location or do you think it is generallyapplicable?Partridge:The data presented speak specifically to our plotsin Western Nebraska; however, Kommedahl andWindels [1979] have made the same conclusionfor maize in Minnesota. Nonetheless we would becautious toward making a statement ''in general,"though it may be true.Claflin:Was each determination a result of hyphal-tip cultures?Who identified the cultures?Partridge:Yes, we used hyphal tip cultures. Janet Reed (master'sdegree candidate) and I identified them, andthe identifications were confirmed by Dr. Paul Nelson,Fusarium Research Center, PennsylvaniaState University.Doupnik:Does it matter which species of Fusarium is theactual causal agent of fusarium stalk rot in terms ofmechanism of pathogenicity and control measuresor developmental genetic resistance?Partridge:Yes, our data strongly indicate that one can selectfor separate resistance to each species, whateverthe mechanisms may be.WHEELER, H., POLITIS, D.J., and PONELEIT, C.G, 1974.Pathogenicity, host range, and distribution of Colletotrichumgramlnicola on corn. Phytopathology 64:293-296.WHEELER, H., POLITIS, D.J., and WILLIAMS, A.S. 1972.Pathogenicity, host range, and distribution of Colletotrichumgraminicola on maize. Phytopathology 62:808(abstract).71

Sorghum Root and Stalk Rots:Basic Disease ProblemsSummary and SynthesisL.K. Mughogho*The eight background papers on basic diseaseproblems provide an overall view of the biology ofthe causal agents and the epidemiology of root andstalk rot diseases. Since the effects of plant physiologicaland environmental factors and diseasecontrol are presented in later sessions, my commentswill be confined to crop loss and someaspects of the biology of the causal organisms.Crop Loss Caused byRoot and Stalk RotsAll the authors of the background papers on specificdiseases have reported that root and stalk rotscause crop losses. However, the few data availableare from experiments conducted at research stationsor in glasshouses. There is a dearth of quantitativecrop loss data from farmers' fields. Unlesssorghum scientists are able to show that root andstalk rots cause unacceptable crop losses infarmers' fields, there is little justification for funds tobe spent on research for their control. I wouldrecommend that systematic crop loss surveys infarmers' fields be condugted in areas where rootand stalk rots are thought to be economicallyimportant.Causal Organismsand their DistributionOf a number of organisms often isolated from diseasedroots and stalks, the well-known causalagents are the fungi Macrophomina phaseolina,Fusarium moniliforme, Periconia circinata, Pythiumspp, and Colletotrichum graminicola.M.phaseolina and F. moniliforme appear to bewidely distributed in sorghum-growing areas. P.circinata, formerly thought to be restricted to theUSA, has recently been reported from Australia,where it appears to cause little damage to sorghum(Mayers 1976). Perhaps P. circinata is more widespreadin sorghum-growing areas than has hithertobeen reported, and surveys like those conductedby Mayers in Australia would help to determine itsdistribution.The identity of the Pythium spp, particularly thoseimplicated in root rots, is still incomplete, as is theirdistribution and importance on a regional or globalbasis.Recently, Acremonium strictum, a vascular pathogenthat causes leaf and stalk death, has beenrecognized as an important disease in the Americas.The occurrence of this pathogen in other partsof the world needs to be watched since the diseasecan be very destructive.Other fungus-incited diseases not included inthe presentations but reported by Tarr (1962)include pink root rot (Pyrenochaeta terrestris),southern sclerotial rot (Corticium rolfsii), and rhizoctoniastalk rot (C. solani). Bacteria, particularlyErwinia spp, have also been implicated as causalagents of stalk rots in the Philippines (Karganillaand Exconde 1972), in India (Anahosur 1979),Nigeria (King 1973), and the USA (Zummo 1969).Very little is known about the etiology of these diseases.This is an obvious area for future research.*Principal Plant Pathologist, ICRISAT.International Crops Research Institute for the Semi-Arid Tropics. 1984. Sorghum Root and Stalk Rots, a CriticalReview: Proceedings of the Consultative Group Discussion on Research Needs and Strategies for Control ofSorghum Root and Stalk Rot Diseases, 27 Nov - 2 Dec 1983, Bellagio, Italy. Patancheru, A.P. 502 324, India;ICRISAT.73

Diseases of Complex EtiologyWith the exception of anthracnose, acremoniumwilt, and pokka boeng where initial infection isthrough the stem or panicle, all the other diseasesconsidered in the background papers appear to beof complex etiology involving more than one pathogenor pathogen species. This has been clearlybrought out in the papers by Zummo, Mughoghoand Pande, Partridge et al., and Claflin. The frequentassociation of the causal agents in isolationsfrom diseased roots and stalks needs investigationto determine the nature of association, i.e., whetherthe organisms can cause disease singly, in succession,or together, and if synergism occurs. Thework of Partridge and coworkers at the University ofNebraska on the temporal and spatial successionof fungi on roots and stalks should be conducted atother sorghum-growing locations worldwide todetermine the nature of the association, and alsothe pathogen species involved at differentlocations.The role of nematodes in the root and stalk diseasecomplex has hardly been researched, and theareas of future research suggested by Claflin needattention.Other Aspects of the Biologyof Causal OrganismsVery little is known about pathogen dissemination,survival, and source and form of initial inoculum formost of the root and stalk rot diseases. The possibleexistence of physiological races, as has beenshown for anthracnose, also needs elucidation.This is important in utilization of resistance in diseasecontrol.ReferencesANAHOSUR, K.H. 1979. Bacterial stalk rot of sorghum inregional research station, Dharwad. Sorghum Newsletter22:121.KARGANILLA, A.D., and EXCONDE, O.R. 1972. Bacterialstalk rot of corn and sorghum. Philippine Phytopathologist8:4 (abstract).KING, S.B. 1973. Plant pathology annual report(sorghum): Major Cereals in Africa Project. Samaru, Nigeria:Institute of Agricultural Research.MAYERS, P.E. 1976. The first recording of milo diseaseand Periconia circinata on sorghums in Australia. AustralianPlant Pathology Society Newsletter 5:59-60.TARR, S.A.J. 1962. Diseases of sorghum, sudan grassand broom corn. Kew, Surrey, U.K.; CommonwealthMycological Institute. 380 pp.ZUMMO, N. 1969. Bacterial soft rot, a new disease ofsweet sorghum. Phytopathology 59:119 (abstract).DiscussionEtiology/SuccessionDoupnik:Dr. Zummo, is root rot a prerequisite to stalk rot?Zummo:When fusarium stalk rot is found, root damage isfound with itDoupnik:If fusarium stalk rot comes first, are the roots predisposedto infection?Zummo:You can have fusarium root rot without stalk rot Butyou don't see stalk rot without root rot.Frederiksen:Fusarium stalk rot can come from rachis andpeduncle infection and move down the stalk underwet weather conditions.Mughogho:Macrophomina stalk rot is preceded by root rot.74

Partridge:We need to distinguish between root rot and rootparasitism.Pappelis:Our attention has centered on one pathogen. Weshould broaden the discussion to include the rootrot and stalk rot complex. It is a multiple entrysystem involving many pathogens. Some may beprimary and some may be secondary invaders.Sinclair:We have found that Colletotrichum and Macrophominacause symptomless, latent infection insoybean. In such plants we can induce symptomsand signs of the pathogen in the laboratory usingdesiccant herbicides. I suggest that sorghumpathologists should look at multiloci infections thatmay take place early in the growing season. Theexpression of symptoms may not occur until stimulatedby some factor.Pappelis:Another thing to consider is systemic infection byvarious pathogens.Sinclair:We need to distinguish between true systemicinfection in the vascular system and multilociinfection.Schneider:In the case of Fusarium moniliforme in maize and F.oxysporum in celery, there are multiple sites ofentry in the root system, but only a small proportionof these localized infections then becomesystemic.Williams:What is the role of seedborne inoculum?Partridge:In my experience Fusarium moniliforme and F. graminearummove with the seed; as much as 20% ormore of the seed will be infected.Claflin:I have observed that tunneling by the Southwesternor European corn [maize] borer results in infectionwithin the damaged internode, i.e., it does notspread beyond the upper or lower node.Pappelis:In maize the pith parenchyma is dead, and the livingcells of the nodes form a barrier to the spread of thefungus. In the case of sorghum, often this barrierdoes not exist.Zummo:In the case of sugarcane and Colletotrichum falcatumthere are varieties that allow free flow of conidiaand mycelium through the node, and these areconsidered to be susceptible/Those varieties thatprevent the fungus from moving through the nodeare considered to be resistant.Pappelis:If cell death occurs, the fungus will spread followingthe pattern of cell death.Clark:The infection occurs under certain conditions. Weneed to know more about the conditions and propertiesof the cells when infection occurs.Odvody:In our studies we have never seen the macrophominastalk rot phase without the root rot phase.Sinclair:As far as I know, sorghum pathologists have notpresented evidence of the spread of infection fromthe roots through the crown into the stalk.Partridge:I have a student (Janet Reed) whose master'sdegree thesis contains data on this subject ofsequential isolations.Frederiksen:Edmunds in 1964 and Odvody in about 1978 haveclearly shown that root infection precedes stalkinfection.Partridge:In our studies using multiple pathogens on maizefollowing toothpick inoculation, we always foundsequential movement of the pathogens up andsometimes down, but never skipping nodes,McBee:Has anyone related successions to growth stage insorghum?75

Pappelis:Cell death in the cortical region of the roots canoccur within a few days after the seeds are plantedor will not occur at all until the plant is stressed. Thesuccession of fungi isolated from roots maydepend upon the physiological status of the roots,and this is not measured by isolation techniques.McBee:In sorghum there's a drastic change in carbohydratemetabolism and photosynthate partitioningas heading occurs and a deterioration of the rootcaused by development of the kernel sink. Whateffect does this have on timing of root infection?Pappelis:Translocation patterns have not been presented inany of the papers on sorghum. Hearing noresponse, gentlemen, should we go back to thesubject of succession?Partridge:As a general rule, root and stalk pathogens arerestricted to the root and crown area on maize untilanthesis, after which there is ramification. I feel thatsorghum faces the same general pattern, but thedata are not as conclusive.Eastin:There is a heavy flow of metabolites to the rootsprior to anthesis and up to 7 to 10 days thereafter.At the soft-dough stage there is no such flow to theroots in some types of sorghum.Pappelis:After anthesis, cells in the stalk die, sucroseincreases, and reducing sugars decrease. Theother problem with anthesis is that there is no linkagebetween cell death in the roots and stalk. Thereis a barrier that prevents the spread of root pathogensinto the stalk. After anthesis this barrier nolonger exists; i.e., the cells in the root-stalk junctiondie.Williams:Is it possible that drought stress results fromimpaired water uptake by infected roots?Rosenow:If you injure the plant with either a sterile or aFusarium infested toothpick, stalk rot will develop atthat site. If the pathogen was there before that time,as indicated by the work of Partridge, why did it notcause stalk rot?Partridge:If Fusarium equiseti and F. graminearum are theprimary pathogens of sorghum roots in the field,then there is a decreased spread of F. moniliforme.Thus stalk rot caused by F. moniliforme may bedecreased by the presence of other species ofFusarium.Inoculation/Screeningfor ResistancePappelis:Fusarium moniliforme can be isolated from stalks,but it appears to be localized in vascular tissuesand remains there as though its growth is inhibited.When we use inoculation methods, we place thepathogen in the pith parenchyma, and if the cellsare dead, it spreads throughout the tissue. Theremust be a physiological explanation for thisinhibition.Mughogho:If what you are saying is correct, screening forresistance to charcoal rot using the toothpickmethod is not the appropriate method. This supportsthe point of view we presented in our paper.Pappelis:In the case of Macrophomina, the fungus willspread through areas of parenchyma cells, and inthis way it is not like Fusarium.Sinclair:In our studies on soybean we have found that severalfungi can colonize the seed or the plant at thesame time. These fungi have different "ecologicalniches" and can develop independently of oneanother, but when we inoculate we upset thisrelationship.Pappelis:The concept is either the fungus grows in deadcells until it comes in contact with living cells,where it stops for physiological reasons; or thepathogen induces senescence and death of theliving cell. An example of the first condition is thebehavior of Diplodia maydis, and the second is thatof Colletotrichum graminicola.76

Frederiksen:It has been suggested that the toothpick methodisn't appropriate for screening sorghum lines forresistance to charcoal rot. However, I haven'tfound a method superior to it. Perhaps we shoulddiscuss other methods, such as Rosenow'smethod.Mughogho:We find it difficult touse the toothpick technique.Our results vary from season to season, and thedevelopment of disease depends on the predispositionof the plant to infection. In order to produceconsistent results, the plants should be predisposedto infection.Pappelis:It's important when using the toothpick method toplace the inoculum in the internode rather than thenode.Frederiksen:The results using the toothpick method for screeningfor resistance to Fusarium are highly correlatedwith fungal infections in the field. This inoculationprocedure provides a uniform method for testinggenotypes.Pappelis:In maize the time of inoculation was found to beimportant to obtain the best results in screening fordisease resistance. The same studies need to bedone in sorghum. The purpose of inoculating is tobe sure that there is no disease escape.Partridge:We find that we can't obtain typical fusarium stalkrot symptoms in the greenhouse by using one speciesalone; we must use at least two and sometimesthree species of Fusarium.Claflin:How do you test for stalk rot decay following toothpickinoculation? Do you squeeze the stalk?Pappelis:There is a difference between stalk rot and lodgingresistance. If you study stalk rot, you must cut thestalk in order to make stalk rot evaluations.Williams:One point in favor of the toothpick method as describedby Frederiksen is that it eliminates variableinoculum load. Dr. Mughogho, since you didn't usethe toothpick method in the field screening experimentsdescribed in your paper, what was your fieldblock design?Mughogho:Our plot size was 18 meters square in a checkerboardpattern.Williams:Since your lines don't flower at the same time, howdo you impose the water stress at the same physiologicalstage?Mughogho:We have classified our lines according to floweringstage and grow them as separate plots.Frederiksen:Another way to reduce the variability in inoculationstudies conducted in the field is to use a highlyvirulent isolate.Rosenow:Dr. Pappelis, have you done pith condition ratingson juicy and pithy sorghum lines and related that tostalk rot?Pappelis:Yes, using plasmolysis and deplasmolysis you canidentify living and dead cells in these lines. I'mspeaking about anthracnose evaluation with pathogensspreading through dead cells. Succulentlines are composed of living cells and pithy linesconsist of dead cells.Mughogho:We should ask what is the best screening techniquefor each one of these pathogens, and we alsoneed to know more about the interactions betweenthese pathogens. We would like some suggestionsand advice from this meeting about how to handlethese problems.Schneider:Do you standardize the methods for quantifying thewater stress factor in evaluating the breedinglines?Mughogho:We have used two methods: (1) the line sourceirrigation technique, and (2) withdrawal of irrigationin dry areas at the appropriate time.77

Schneider:It seems to me that measurements of plant waterstatus rather than soil water status should be made.Seetharama:We do measure leaf temperature and this correspondswell as an indicator of stress levels. However,a single measurement of plant water statusdoes not give a good indication of stalk rotsusceptibility.Frederiksen:We should look at fungus variability as well asinoculation technique. Clearly these fungi consistof many physiological races. We find variability inour anthracnose isolates. Dr. Partridge, I would liketo know more about your Fusarium isolation.Partridge:We must identify all of the organisms in the stalkand determine which are the pathogens. Our findingssuggest that Fusarium moniliforme does notcause stalk rot alone and may not be the primarypathogen involved.Pappelis:We should bring up other topics. I want to refer to J.Kuc's work [Pages 157-178 in Active defensemechanisms in plants (ed. R.K.S. Wood), 1982. PlenumPress, New York and London] where he challengedplants with incompatible pathogens andinduced resistance to compatible ones. Doesanyone have further information on this subject asit relates to root diseases of sorghum or othercrops?Schneider:I have had some experience in this area. In workwith Fusarium oxysporum on celery and F. moniliformeon maize, we find that localized root infectionby incompatible pathogens protects the root frominfection by compatible pathogens and that there isa finite number of infection sites per unit root length.Partridge:Is that protection of sites or inhibition of one organismby another?Partridge:As the root grows, is the new tissue protected bythe previous infections?Schneider:No, the new root tip is susceptible and must becontinually protected.Pappelis:Pathologists seem to ignore the obvious whenworking on stalk rots. There are no shortcuts. Youmust inoculate and evaluate disease response toavoid disease escape until the cause and effect"story" is so well understood that a predictive statementcan be formulated to apply to all conditions atall locations: the universal, the hypothesis, the law.To that end, I believe we need to establish thefollowing:1. a disease nursery with the best inoculationmethods and rating systems to evaluate varietiesand hybrids;2. drought stress plots in which the best inoculationmethods and rating systems are used toevaluate stress effects on varietal and hybridresponses to the pathogen;3. fumigated control plots and reinfested testplots where we can introduce soil inoculumsingly or in mixtures.4. nematode soil "bins" where fumigated soilscan be infested with nematodes and fungalpathogens to test their interactions on root rotproduction.5. the adoption of pith condition rating systemsfor stalks and roots and use of these in theabove.Stalk rot and standability must be studied individuallyand together in the above conditions. Theprocedures involve much labor. Nevertheless, it isessential. We must use the best methods we haveand improve them until we develop the universalstatements relevant to resistance and susceptibilityto each of the major pathogens we are nowdiscussing.Schneider:Apparently it's competition by elimination ofsubstrates.78

Physiological andEnvironmental Factorsin Root and Stalk Rot Diseases

The Role of Edaphic Factorsin Disease DevelopmentW.R. Jordan, R.B. Clark, and N. Seetharama*SummaryThis paper presents a brief overview of the roles of abiotic stresses in the modification ofprocesses contributing to the growth and grain yield of sorghum in both the absence andpresence of biotic (disease) stresses. Water, temperature, and nutrient stresses promote yieldlosses through their effects on interception of solar radiation and production of photosynthate.Formation and maintenance of active green leaf area is essential for continued production ofphotosynthate to maintain carbon and energy flow to both developing grain and plant tissues.Abiotic stresses predispose host tissues to pathogen invasion and promote proliferation andspread of disease in plant tissues, but the mechanism(s) are unknown. The association ofcharcoal rot with stress during grain filling lends support to the view that carbohydratemobilization from stalk and root tissues may be intimately associated with host resistance.Further research is needed to define the nature of changes induced by stress that predisposehost roots to infection. Since infection and proliferation of the pathogen in host tissues seem tobe controlled independently, the changes allowing spread should be studied further. Finally,interactions of abiotic stresses should be studied in a manner that will allow formulation ofhost-pathogen models necessary to explore possible common bases for disease developmentand resistance.Edaphic factors such as water, temperature, andnutrition are universally recognized as important inthe development and spread of disease in cropplants. Just as atmospheric turbulence, humidity,and other general features of the aerial climate areimportant to the epidemiology of disease causedby airborne pathogens, issues such as soil watercontent and potential, soil temperature, and mineralion availability are central to our understandingof diseases caused by soilborne pathogens.Relatively few research reports deal specificallywith effects of the environment on root and stalkdiseases. In fact, the ICRISAT program appears tobe the only major research effort currently dealingwith these problems in sorghum. It is our intentionnot only to review known environmental effects onthe development and severity of root and stalk rotsin sorghum, but also to provide insights into theeffects of specific edaphic factors on the host andpathogen, and their interaction. Because sorghumis a major crop of the semi-arid zones, especially indeveloping countries, we will concentrate on problemsassociated with deficiencies in supplies of soilwater and mineral nutrients.*Director, Texas Water Resources Institute, Texas A&M University, College Station, TX 77843, USA; Research Chemist,USDA-ARS, Kiesselbach Crops Research Laboratory, University of Nebraska, Lincoln, NE 68583, USA; and PlantPhysiologist, ICRISAT, Patancheru, AP. 502 324, India.International Crops Research Institute for the Semi-Arid Tropics. 1984. Sorghum Root and Stalk Rots, a CriticalReview: Proceedings of the Consultative Group Discussion on Research Needs and Strategies for Control ofSorghum Root and Stalk Rot Diseases, 27 Nov - 2 Dec 1983, Bellagio, Italy. Patancheru, A P . 502 324, India:ICRISAT.81

Water in the Soil-Plant-Atmosphere ContinuumWater exists as a continuum from the soil, throughthe plant, and into the atmosphere. The phasechange from liquid water to water vapor within theleaf does not alter this fact. Water moves in such acontinuum from regions of high free energy (highwater potential) to regions of low free energy (lowwater potential). Thus, water transpired by a cropflows from moist soil with a relatively high waterpotential through the plants and into the atmospherealong a water-potential gradient. Typically,soil water potentials (ψ s ) will range between -0.01and -15 bars, while leaf water potentials ( Ψ L ) ofmesophytic plants will range between -1 and -30bars, and atmospheric water potentials will rangebetween -100 and -1000 bars. Just as typically, ψ smay vary from -100 bars or less at the soil surfaceto -0.01 bars deeper in the soil profile, while theatmospheric water potential may decrease by1000 bars or more between dawn and midday. Atany instant, ψ L represents an integration of atmosphericdemand and the capacity of the soil tosupply water as modulated by the plants' ability toregulate water loss. In this section, we examine soiland plant characteristics that determine rates ofwater flow through the continuum.Water Flow in SoilsOver long periods of time, root systems grow to theextremes permitted by physical and chemical constraints,allowing the crop access to water storeddeep in the soil profile. However, over short timeintervals, it is Water movement through soil ratherthan root growth that allows uptake of sufficientquantities of water to prevent harmful desiccation.Water flow from the bulk soil to the rhizosphereoccurs in response to ψ s gradients arising fromwater uptake by roots.The hydraulic conductivity (H) of a soil is a measureof its capacity to transmit water. A very strongfunction of ψ s , H may change from 10 cm day -1 fora wet soil to as little as 10 -8 cm day -1 at the lowerlimit of water availability. Reicosky and Ritchie(1976) found that the rate of water flow through soildid not limit water availability to growing crops ofmaize and sorghum until water extraction caused Hto fall below about 10 -6 to 10 -7 cm day -1 . When Hfell below this value, the roots were no longer ableto absorb water at rates sufficient to satisfy theevaporative demand and water stress (low Ψ L )resulted. Since the experiments were conducted atdifferent locations and on different soils, their estimatefor H may be a general result for well-rootedcrops. Unfortunately, the relationship between Hand soil water content (θv) is unique for each soil(and region of the soil profile); therefore the lowerlimit of H cannot be translated simply into θv, aquantity more frequently available. For sandy andclay soils, H reached 10 -6 to 10 -7 cm day -1 at ψ s of-1 and -8 bars, respectively.Water Flow in PlantsAs in the case of soil, water flow in plants occurs inresponse to a water potential gradient betweensites of water absorption in roots and sites of evaporationin leaves. Flow through plant tissues is mostconveniently discussed in terms of the familiarelectrical analog: water flow is analogous to theflow of electricity as described by Ohm's Law.Thus, the flow (flux) is directly related to the drivingforce ( ψ gradient in plants) and inversely related tothe resistance to flow. Major resistances appear toreside in the radial path of flow between the rootsurface and the root xylem, and at the stomates.For sorghum, the axial transport of water throughhealthy roots encounters little resistance (Meyerand Ritchie 1980). Therefore, when soil water isfreely available to the crop, high rates of transpirationare maintained with a minimal depression ofψ L . Values of ψ L for healthy, well-wateredsorghum usually range between -8 and -14 barsduring peak transpiration periods, increasing tonear zero bars before dawn. In some situations, thepredawn value of ψ L or the ψ L of leaves covered toprevent water loss may be taken as an estimate ofthe ψs surrounding the roots.Pathogens causing root and/or stalk diseasemay alter the resistance to water flow throughtissues in one of at least four ways:1. If infection occurs through the root cortex andlesions develop in cortical tissues, the intimateroot-soil contact may be destroyed. The neteffect is to reduce the total root length in contactwith soil, thus increasing the resistance inthe radial pathway.2. If the pathogen produces toxins, the permeabilityof root tissues to water may be altered, or,if the toxins enter the transpiration stream,82

stomates may be affected. This aspect ofhost-pathogen interaction is not well studied,but either increases or decreases in membranepermeability appear possible.3. Vessel plugging may occur either with tissuesof the pathogen (e.g., fungal mycelia) or byinduction of tyloses. This mechanism mayresult in a dramatic increase in axial resistanceof the affected root, but if only a few rootsare affected the consequences may be minimal,depending upon the soil water supply.4. Finally, root deterioration reduces the transportcapacity, but from a water supply standpoint,sorghum appears to "overproduce"roots, since loss of up to 50% of the root axisappears to have little impact on ψ L so long aswater is freely available to the remaining roots.This latter generalization may not hold true fornutrition, and almost certainly would not betrue for crops grown in water-limitedenvironments.Water Flow in theIntegrated Soil-Plant SystemSeveral references were made in preceding sectionsto the dynamic nature of water potentials, bothspatially and temporally, but visualization of theinterdependence of soil, atmosphere, and plant isdifficult. The question remains as to how soil andplant properties act in concert to regulate the flowof water through the system so the plant canremain relatively stress free. One means of examiningthis problem is through use of simulationmodels based on descriptions of flow in soil andplants as presented by Jordan and Miller (1980). Anexample of a sorghum crop growing in a drying claysoil is illustrated in Figure 1. If we assume that ψ Lremains constant at -15 bars (minimal plant stress)and the average root-length density is 1.0 cm root(cm 3 soil) -1 , then a flow rate equivalent to 0.8 mmh -1 can be met only if the average ψ s is aboveabout -1.5 bars. This flow rate is in the range ofthose experienced in semi-arid field environments.If, on the other hand, flow rates are as low as 0.2mm h -1 (cloudy, humid situation), then these ratescould be met from a drier soil at a ψ s of about -4.5bars. Although this treatment and example are simplistic,they serve to illustrate the complex interactionof system components under realisticenvironmental conditions. An understanding of5020105.02.01.00.5q = Variable, mm/haΔ Z= 1.25 m from 0.5 to 1.75 mψ L = -15 bars0.1-0.1 -0.2 -0.5 -1.0 -2.0 -5.0 -10 -15Soil water p o t e n t i a lFigure 1. Predicted relations among rootlength density, soil water potential, and transpirationrate (q) for sorghum plants at a constantleaf water potential of -15 bars. Water uptake isassumed to come from a 1.25-m soil layer (Δ z)between 0.5 m and 1.75 m deep. (Source: Jordanand Miller 1980.)these interactions is central to understanding plantperformance in both healthy and diseasedconditions.Soil Water Deficitand Crop Productivityq = 0.80.4(bars)0.20.1Sorghum is grown in large areas of the semi-aridtropics because of its ability to produce grain underwater-limited conditions. Factors contributing tosorghum's drought resistance have been detailedelsewhere (Jordan and Monk 1980, Jordan et al.1983, Seetharama et al. 1982, Simpson 1981), butthe fact remains that serious yield losses resultfrom moderate to severe soil water deficits (Blum1970, Garrity et al. 1982). Eastin et al. describe thesensitivities of sorghum to environmental stressesin these proceedings, and hence only a brief discussionof the effects of soil water deficits on development,activity, and duration of various83

carbohydrate sources and sinks is presented toexamine how root and stalk diseases effect yieldreductions. For a more complete treatment of waterrelations of sorghum, readers are referred to recentreviews by Jordan (1983), Turner and Burch(1983), and Krieg (1983).So long as cultural and environmental constraintsare minimal, total dry matter productionappears to be linearly related to the total solarradiation intercepted by a crop during the growingseason (Monteith 1977). Light interceptiondepends primarily on the seasonal distribution ofthe leaf area index (LAI); therefore factors thatmodify rates of leaf area development and maintenancemay also modify the potential for grain yield.On a whole-plant basis, the leaf area present atany time is a complex function of leaf numbers, leafsizes, and leaf longevity. Leaf number is fixed withinrelatively narrow limits by the maturity of the cultivar,and the ultimate number of leaves formed perplant appears to be relatively unaffected by soilwater deficits (Kannangara et al. 1983; W.R. Jordanand G.F. Arkin, Blackland Research Center, Temple,Texas, USA, unpublished data, 1982), althoughrates of leaf appearance are reduced. Since leafappearance is strongly dependent on cellularexpansion, and expansion is inhibited by waterdeficits (Boyer 1970; Hsiao et al. 1976a, 1976b), thereduction in leaf appearance rates is believed toresult primarily from an inhibition of expansion. Thenet result from soil water deficits that develop progressivelyduring vegetative growth is an overallreduction in leaf area per plant, as illustrated inFigure 2 (Jordan 1983), due primarily to reductionsin final leaf sizes. During severe drought, formationof new leaf area may stop completely, giving theappearance that the crop is in a state of suspendedanimation (growth) while awaiting rainfall.Reports dealing with the longevity of leaves duringperiods of drought are both sketchy and contradictory.Much of the confusion arises from failuresto consider crop phenology and the rate and severityof water stress when evaluating effects ofdrought on leaf longevity. Recent results suggestthat the longevity of individual leaves is notseriously altered by water deficits that developgradually over long periods during vegetativegrowth stages, but rapid development of waterdeficits may accelerate senescence of lowerleaves (Wilson and Allison 1978, Stout et al. 1978,Jordan 1983). However, if water deficits developafter anthesis, leaf senescence may be accelerateddue to translocation of carbohydrates and2520151050Stored soilwater onlyIrrigated weeklyuntil 55 DAP100 200 300 400 500 600Mean leaf size (cm 2 )Figure 2. Vertical distribution of leaf area for100 M sorghum plants grown on stored soilwater or irrigated weekly until 55 days afterplanting (DAP). (Source: J.T. Ritchie, R.G.C.Smith, J.E. Begg, and W.E. Lonkerd, BlacklandResearch Center, Temple, Texas, USA; unpublisheddata, 1978.)nitrogenous compounds to developing grain. Thisaspect of dry matter redistribution will be enlargedupon in following sections.The seasonal pattern of dry-matter accumulationin sorghum is illustrated in Figure 3 (Krieg1983). The period between panicle initiation andflowering, usually referred to as growth stage 2(GS2), is a time of rapid increases in leaf area anddry matter and is the period when the potentialgrain number is determined. It is during GS2 thatthe crop expresses maximum sensitivity to environmentalstresses, including water, heat, and light(Eastin et al., these proceedings). The causesunderlying yield reductions from water deficit duringGS2 are not fully understood, but Fischer'sanalytical framework of wheat growth and yieldunder water-limited conditions suggests that afunctional balance exists between viable leaf area(source) and potential grain numbers (sink), providedthat water deficits develop slowly (Fischer1979). If this analysis also holds true for sorghum,some sort of feedback regulation between source(leaves) and sink (panicle) is implied. Whether this"communication" between source and sink arisesfrom disruptions in the flow of organic energy andcarbon sources from leaves to panicle, or from84

8510080604020Emer.Total dry wt.Leaf areaGrain wt.Total wt.PanicleinitiationFlowerGrowth stagePhys.mat.Figure 3. Fractional total dry weight, green leafarea, and harvest index of sorghum grown forgrain as a function of growth stage. (Source:Krieg 1983.)changes in the hormone balance of the panicle, isunknown (Krieg 1983). Regardless of the basiccauses, the net effect of water deficit is expressedsoon after anthesis as fewer grains per panicle, asevidenced by small panicles in general or by sterilebranches within panicles (head blasting). Inextreme cases the entire panicle may be sterile,either because the florets failed to develop orbecause they aborted.Actual yields under favorable conditions arelimited by source activity: that is, by the photosyntheticcapacity of the leaves, stem, and panicle(Krieg 1983). Overall source activity is limited bysoil water deficit through its inhibitory effect on totalplant dry weight at anthesis, green leaf arearemaining after anthesis, and production and translocationof photosynthate during the grain-fillingperiod (GS3). As illustrated in Figure 3, grain fillingoccurs during a period when green leaf area isdecreasing. It is not clear how much dry matter istranslocated from senescing sorghum leaves, butin cases of crops well supplied with water, the lossof lower leaves probably has little impact on grainyield. However, if LAI is already low and the loss ofleaf area after anthesis is accelerated by drought,serious source limitations may result from aninability to intercept sufficient radiation. In addition,the production of photosynthate may be reducedby stomatal closure during periods of peak evaporativedemand when ψ L is low, further reducing theflow of materials required to maintain grain growth.While some preanthesis assimilate is translocatedfrom stem and leaves to grain under normarconditions,proportionately more may be translocated asphotosynthate production rates fall due to droughtduring GS3. Results with most commercialsorghum hybrids suggest that the harvest index(HI) is maintained at relatively constant values asyields are reduced up to 50% by soil water deficits(Garrity et al. 1982), but that HI falls at extremelylow grain yields (Blum 1970).The total amount of dry matter stored in stem andleaves that is capable of translocation to developinggrain is not known, but recent results withsenescent and nonsenescent cultivars suggestthat genotypic variability for this trait does exist forsorghum. Depletion of stem (and root?) reservesduring GS3 may predispose senescent cultivars toinfection by soilborne pathogens, especiallyMacrophomina phaseolina, the causal organism ofcharcoal rot, but a direct causal relationship hasnot been established. However, it is clear thatdevelopment of root or stalk diseases that interferewith absorption or transport of water will createinternal water deficits, with consequences similarto those described above for soil water deficits.Disease Developmentand Soil Water SupplyRoot and stalk rot diseases of sorghum oftendevelop most dramatically during GS3, when wateris in short supply and soil temperatures are high.Charcoal rot, a serious disease of sorghum andmaize, is expressed in this circumstance, butresearch reports on the causal pathogen and itsinteraction with the soil environment and host areindeed few. Even considering this paucity of information,the charcoal rot problem appears to be thebest studied example of a stalk or root diseasecausing serious crop losses in, sorghum (Mughoghoand Pande, these proceedings). The discussionin the following sections will concentrate onthose reports dealing with the effects of soil waterdeficits on M. phaseolina and the development ofcharcoal rot.Effects of ψ s on M. phaseolinaEffects of low water potential on the germination ofsclerotia and growth of mycelia have apparentlybeen studied in detail only in the laboratory, using

artificial media (Dhingra and Sinclair 1978). Sclerotialgermination in culture occurs over a wide rangeof water potentials and temperatures, includingthose expected in the field during drought (Odvodyand Dunkle 1979, Shokes et al. 1977). The sclerotiaappear well adapted for survival for long periods indry soil, but exposure to wet soil (-0.01 bar) at 30°Cfor 2 weeks decreased survival in one test (Shokeset al.1977).Since sclerotia germinate readily in culture overa wide range of conditions, the question of controlof germination under favorable soil conditions naturallyarises. Some form of nutrient-dependent fungistasisis most often alluded to as a germinationcontrol (Ayanru and Green 1974). Odvody andDunkle (1979) observed higher germination onpotato dextrose agar at low osmotic potentials (

87stress, insufficient to cause visible symptoms,resulted in pith discoloration or stalk rot in 60.3% ofthe plants during the pretassel stage of development,25.3% during postpollination, and 7.7% duringgrain filling. Even though the stress was mild( ΨL about 2 bars lower than well-watered controls),root senescence was accelerated in uninfestedtreatments and enhanced infection and root colonizationoccurred in infested treatments, causing theresistance to water flow to increase about twofold.The causal organism was believed to be Fusariummoniliforme.Similar results were obtained with sorghumgrowing in pots infested with sclerotia of M. phaseolina(Odvody and Dunkle 1979). When waterstressedduring the soft dough stage, 83% of thefertile CK60 plants developed charcoal rot symptoms,while male-sterile plants were symptomless.Since both fertile and male-sterile plants had highrates of root infection, male-sterile plants apparentlypossessed some mechanism to retard spreadof the infection. Also, since nonstressed plantsgrowing in infested soil remained relatively infectionfree, stress appeared to promote initial infectionof host roots.Studies at ICRISAT provide evidence that charcoalrot development is related to the severity aswell as the timing of soil water deficits. Using aline-source sprinkler system to establish a gradientin soil water deficit, Seetharama et al. (unpublisheddata, 1983) examined the relationship between theamount of water applied during GS3 (distance fromthe line source) and the fraction of plants developingsoft stalks following toothpick inoculation (Fig.4). A linear response between distance from theline source and disease development is clearlyillustrated for both years, supporting the view thatdisease severity and drought severity are coupledduring the period when the sink demand fromdeveloping grain' is large. Grain yield decreasedlinearly with distance from the line source in bothyears. Additional observations provided evidencethat the rate at which disease spread from the pointof inoculation increased with time after flowering,as well as with stress severity, supporting earlierfindings by Edmunds (1964) and Livingston (1945).While the concept of edaphic factors in "preconditioning''or "predisposition" of host plants to diseaseis certainly not new (Schoeneweiss 1978;Yarwood 1976; Dodd 1980a, 1980b), underlyingmechanisms remain largely unknown. Recently,Dodd (1980a, 1980b) proposed an explanation ofpredisposition based on the carbohydrate status of70605040302010019770 2 4 6 8 10 12 14Distance from l i n e source (m)Figure 4. Relation between charcoal rot development(plants with soft stalk) and soil watersupply after anthesis (distance from linesource) for CSH-6 sorghum grown at Hyderabad,India, in 1977 and 1978. (Source: Seetharamaet a/., ICRISAT; unpublished data, 1983.)root tissues and the influence of soil water deficitson deposits and withdrawals from the sink. In thisconcept, carbohydrate depletion in root tissuesweakens the cellular defense mechanisms, allowingthe invasion and spread of disease. The effectsof soil water deficit on production and redistributionof photosynthate were discussed in earlier sections,and Dodd's concept is supported by work ofEdmunds and Voigt (1966), Edmunds et al. (1964,1965) and Odvody and Dunkle (1979). However,although no alternative explanations of this predispositionphenomenon enjoy wide acceptance, itseems unlikely that any concept based on simplechanges in carbohydrate status of roots or stalkswill hold up to critical examination. McBee discussesthe question of stem reserves in greaterdetail in these proceedings.Disease Developmentand Temperature1978Throughout the sorghum-growing regions, hightemperatures normally accompany droughts, but

seldom have the effects of high temperature per sebeen separated from those due to water deficits. AC 4 species, sorghum is adapted to hot, highradiationregimes, but these same conditions areoften cited as facilitating disease incidence anddevelopment. In the following sections we explorethe effects of high temperatures on the host andpathogen and speculate on the role of this stress onhost-pathogen interaction.Sorghum Responseto High TemperatureThe effects of both super- and supraoptimaltemperatures on sorghum have been recentlyreviewed (Peacock 1982), with the conclusion thatconsequences of high temperatures are mostserious when they coincide with the critical growthstages of the crop. Thus, germination and emergenceare viewed as critical to obtaining an adequateplant population, development andmaintenance of leaf area as critical to photosynthateproduction, and panicle development andgrowth as critical to yield potential. Since root andstalk rots are normally associated with late-seasonstresses, we will consider only those effectsobserved during GS2 and GS3.The importance of leaf-area development andmaintenance has already been discussed withrespect to water. Numerous reports document thefact that the general effects of moderate increasesin temperature are reflected in faster growth ratesin general, as evidenced by earlier maturity. Thisfact is incorporated in several plant growth modelsin which process rates are governed by heat-unitaccumulation rates. The question of optimumtemperature or leaf-area development remainsunresolved because much of the growth data collectedin controlled environments is not directlyapplicable to crops grown in a field environment.Data from ICRISAT (Peacock 1982) suggest thatleaf extension rates are greatest at an air temperatureof about 34°C and that final leaf number andleaf area increase as temperatures increase from25/20°C (day T/night T) to 35/25°C. AlthoughQuinby et al. (1973) reported genetic variation inleaf growth in relation to air temperature, little useseems to have been made of this information andlittfe effort appears to be directed toward identificationof genotypes capable of growth maintenanceat high temperatures. Escalada and Plucknett(1975) reported enhanced tillering as temperatureswere increased from 23.9/15.5°C to 32.2/23.9°C,so long as daylengths also increased, suggesting alink between tiller development and total photosynthatesupply.The effects of temperature on yield and yieldcomponents have been studied at several locations,with the conclusion that grain numbers perpanicle are not reduced by growth at temperaturesas high as 35/25°C. However, yield is markedlyreduced by these high temperatures due to areduction in weight per grain. Excessively hightemperatures during panicle development oftenresult in head blasting or localized abortion withinthe panicle, but these effects have not been welldocumented, nor have the effects of temperaturebeen separated from those due to dehydration.Leaf firing occurs in the field in response to hot,dry conditions, and variability in both the extent andpattern of firing appears to be under genetic control.Peacock (1979) reported firing in hybrid RS-610 when leaf temperatures exceeded 43°C, but atleast some germplasm will tolerate leaf temperaturesas high as 55°C (Peacock 1982). Leaf firing isone component used in the Texas AgriculturalExperiment Station breeding program as a selectioncriterion for drought tolerance (Rosenow et al.1983).The causes underlying heat-induced firing arenot known, but other evidence also suggests thatgenetic variability exists for heat tolerance. In onetest, grain yields of M35-1 conversion hybridsgrowing under conditions of heat stress inNebraska were correlated with an estimate of heattolerance based on electrolyte leakage from damagedleaf cells (Sullivan and Ross 1979). Otherreports document the existence of substantialgenotypic variability for heat tolerance based onthis method (Sullivan 1972, Jordan and Sullivan1982). Genetic variability in the ability to maintainhigh photosynthetic rates at temperatures between40° and 43°C also exists (Norcio 1976), but presentevidence suggests that photosynthetic rates wouldbe greatly reduced in the range of 44° to 48°C, wellbelow the temperature causing firing in someIndian cultivars.Temperature andHost-Pathogen InteractionEven though hot, dry conditions enhance charcoalrot on susceptible sorghum cultivars, there is littleevidence that heat stress per se plays a role in88

disease incidence or development At least onecausal organism seems well adapted to the hightemperatures that exist near the surface of drysoils. Mycelia of M. phaseolina are capable ofgrowth to at least 40°C in culture (Odvody andDunkle 1979), as are many other soilbome fungi.Although unexplained, the growth optimum of thefungus shifts to lower water potentials at highertemperatures, suggesting a unique form of adaptationto the high T-low ψ s conditions expected nearthe surface as the soil dries.Bell (1982) recently proposed a model showinghow temperature may differentially affect the rateof pathogen colonization and active host resistanceto differences in relative resistance. HisModel A, illustrated in Figure 5, is cited as an exampleapplicable to charcoal rot caused by M. phaseolina.In this case, host resistance reaches itsmaximum at temperatures near or slightly belowthose optimum for growth, but lower than temperaturesfor maximum rates of pathogen colonization.Since relative resistance is the ratio of the tworates, increases in temperature result in a declinein relative resistance. While these general predictionsappear superficially plausible, there is nodirect experimental evidence to support thishypothesis.Disease Developmentand Mineral NutritionSpecific Element Effects on DiseaseEach mineral element essential to plant growth hasbeen implicated in disease incidence or severity,as have many not considered essential. The bodyof literature dealing with interactions between mineralelements and plant disease in general is extensive(e.g., reviews by Graham 1983, and Huber1978,1980), but few reports deal specifically withsorghum. Reported effects of specific elements onsome of the organisms associated with root andstalk rots are summarized in Table 1 .Macronutrients (N, P, K, Ca, Mg, and S) generallyhave no effects on disease resistance at supraoptimallevels, but usually have their effects only atlow or deficient levels. On the other hand, themicronutrients (Cu, B, Mn, Fe, and Zn) have pro-1.01.0HRPC0.00.010 20 30 40 10 20 30 40 50Temperature (°C)Figure 5. Illustrations of how temperature affects the relative resistance of a host based on its effectson the speed of pathogen colonization and speed of active host resistance. The resultant pattern ofdecrease in relative resistance at increasing temperatures fits observations of charcoal rot ofsorghum caused by Macrophomina phaseolina (Adapted from Bell 1982.)89

Table 1. Summary of reported interactions of mineral elements and disease for some root/stalk rot pathogens.(Source: Huber 1980.)Mineral elementPathogen NH4 N03 P L Ca Mg S Na Mn Fe Zn B CuDiplodia zeae D a I I DFusarium colmorum D D D DFusarium moniliforme I D DFusarium nivale D DFusarium roseum I D DGibberella zeae D ± ± DOphiobolus graminis D ± D D I DPhythium arrhenomanes D ± DRhizoctonia solani I D D I D D D D Da. Incidence of disease decreased (D). increased (I), or dependent on hosts or environmental conditions (+).nounced effects on disease resistance at supraoptimallevels as well as at low or deficient levels.These responses are probably because themacronutrients are involved in compositional,structural, conformational, and osmotic functionsin plants, and micronutrients usually function ascatalysts, cofactors, and inhibitors. Increasing thesupply of an element in deficient or low supplygenerally increases the resistance of plants topathogens.Many factors, interactions, and responses areinvolved in mineral element relationships to diseaseresistance. The effects of mineral elementson plant yield may involve not only the plantrequirements for a specific element, but also theways in which the element may change the host'sdefense mechanism against disease. Mineral elementsmay also have direct toxic effects on invadingpathogens. Lignin and phenol synthesis seemto be more affected by certain elements (N, Cu, B,and Mn) than by others; phytoalexin synthesis alsoappears to be affected by certain other elements(Zn, Fe, and Ni); certain biochemical pathways fordisease defense may also require specific elements(Si, Li, and Ni); competition between hostand pathogen may occur with certain of the elements(Fe); and interactions and toxicities appearwith almost all elements. The mechanisms formineral-element defenses in disease resistanceare multiple, and the function of each element inmetabolism or plant disease resistance processesmust be understood separately. So little is understoodabout the function of mineral elements indisease resistance that similarities of elementfunctions and disease resistance may becoincidental.Mycorrhizae andMineral Element UptakeMycorrhizal fungi play important roles in assuringsufficient and constant supplies of nutrients to hostplants under all conditions, but their importancemay be magnified during drought. The importanceof mycorrhizae in enhancing uptake of mineral elementsbecame evident only in recent years (Tinker1980, Tinker and Gildon 1983). Increased uptake ofN by plants infected with ectotrophic mycorrhizae(ECM) has been suggested, but proof has not beenconclusive. ECM fungi have been found toenhance Zn and K uptake, and their mycelia translocateCa. On the other hand, vesicular-arbuscularfungi (VAM) have been found to enhance P, Zn, Cu,K, Si, and S uptake by host plants, and also totranslocate Ca. VAM fungi are highly involved withenhancing P uptake by plants, especially underconditions of low P. The relationships betweenVAM fungi and P have been the subject of numerousinvestigations since their discovery.Improvement of host plant nutrition by mycorrhizalinfection should occur whenever the uptakerate of the specific element by the host root isrestricted by transport mechanisms of the elementin soils (diffusion and mass flow) below thatrequired for optimum plant growth allowed by theenvironment, if mycorrhizae can absorb andtransfer that particular element. Yield improvementsare difficult to predict, but growth responseshave been large in some cases. For example, theamount of soluble P fertilizer required to give thesame growth response as VAM infection for severalplants was around 100 kg P/ha, and as high as500 kg P/ha for a citrus crop (Menge et al. 1978).90

91Since micronutrients such as Cu, Zn, and Mn havevery low soil mobility, mycorrhizae-enhanced plantuptake has been observed. The mechanisms foruptake and transfer of micronutrients within themycelia are not fully known, but could be associatedclosely with P compound complexes suchas polyphosphate.The beneficial effects of VAM on apparentdrought resistance of plants (Maronek et al. 1981)may result from two sources. Hyphae from VAMinfectedroots extend some distance into the soilmass, effectively increasing the root length densityand thereby reducing the distance water must flowthrough soil (Allen 1982, Gerdemann 1970, Safir etal. 1972). These root extensions could becomeimportant in maintaining high water uptake rates asψ s and H fall due to evapotranspiration. Equallyimportant, however, may be the continued growthof roots made possible by the enhanced uptake ofP described above (Sieverding 1981). Continued orstimulated growth of root axes places larger rootareas in contact with unexplored, wetter soil, therebydelaying the onset of stress. Since mineral nutrientsadded as fertilizers are usually concentratedin the upper 15 cm of the soil profile, mycorrhizalenhanceduptake of mineral elements from soil toodry to support root growth may be very important tocrop health and productivity, and deserves moreextensive study.Influence of Water- andNutrient-Stress Interactionson Disease DevelopmentDeficiencies of both water and nutrients, especiallyN, are the rule rather than the exception in manysorghum-producing regions in developing countries.Even in highly productive dryland systems,water availability has a strong influence on theuptake efficiency and recovery of added nutrientsand may influence management decisions dealingwith the amount and timing of fertilizer applications.The total and seasonal nutrient requirements of asorghum crop have been presented in detail (Laneand Walker 1961, Vanderlip 1972) and will not berepeated here except to point out that large quantitiesof N, P, and K are required during the relativelybrief GS3. For example, at maturity, grain contains67% of the plant's total N, 76% of its P, and 26% ofits K. Much of the grains' total requirement can besupplied by uptake from soil, so long as the surfaceremains moist or is frequently wetted. However, asthe surface dries, root activity is forced to deeperstrata that are normally low in nutrients, and graindemands are met by remobilizing elements storedin leaves, roots, and stalks. Under drought conditionsit is not known whether senescence or firing oflower leaves is triggered by translocation of carbohydratesor mobile nutrients such as N.High grain yields require high plant populationsand large inputs of N, but these conditions alsoincrease disease severity. Sachan et al. (ICRISAT,unpublished data, 1983) found a strong interactionbetween grain yield, N fertility, and stalk rot forsorghum hybrid CSH-6 subjected to water stressafter anthesis with the line source system (Fig. 6).High N fertility resulted in both higher grain yieldand greater incidence of stalk rot. The range ofwater supplies that resulted in a linear increase ingrain yield also resulted in a linear decrease indisease incidence for both fertility levels.Conclusions andResearch NeedsEdaphic factors such as water availability, temperature,and mineral nutrient supply have beenshown to have a large influence on both infectionand disease development by normally weak pathogenscausing root and stalk rots. Fungi are amongthe members of the soil microflora most resistant tolow soil water potentials, making them ideallysuited to the ecosystem of the near-surface soilhorizon. Even mild water stresses trigger changesin host-root resistance, allowing infection at an earlierstage of growth than expected based on symptomexpression. Disease spread in host tissues isassociated with an increasing demand for carbohydratesand nutrients by the developing grain.Since soil water deficits during grain filling mayreduce photosynthate production, greater diseaseincidence observed under these conditions suggestsa causal relationship between the carbohydratestatus of roots and stems and diseaseseverity. The generality of this association has notbeen examined in detail. High supplies of N fertilizeralso promote disease, but are required for highgrain yields.The line-source sprinkler system is an importanttool for screening for resistance to both droughtand disease. It provides a relatively simple meansto establish a dependable, multilevel stress condi-

40060FertilityHigh LowGrain yieldStalk rot30040202000 25 75 125 175Water a p p l i e d (mm)0Figure 6. Influence of nitrogen fertility on the interaction among grain yield, charcoal rot incidence,and water applied after anthesis. Low fertility plots received 20 kg N ha -1 , while high fertility plotsreceived 100 kg N ha -1 . (Source: Sachan et al., ICRISAT, unpublished data, 1983.)tion in the field and overcomes many of the experimentallimitations in studies of soilbornepathogens. Results from the line source systemalso suggest strategies of water management thatmay be effective in disease delay or prevention.Maintenance of high plant water potentials, at leastduring grain fill, are effective in prevention of yieldlosses due to disease and may be achieved by avariety of cultural and water management techniques.The introduction of drought- and diseaseresistantcultivars into farming systems will presentnew opportunities for management for high yield.Several important problems should receiveadded research emphasis. The role of water stressin the production and composition of root exudatesshould be examined in greater detail because ofthe possible importance of this source of organicand mineral nutrients to germination of propagulesand growth of pathogens. Also, stress-inducedchanges in root physiology should be studiedclosely because of the apparent role of even mildstress in the infection process. Root senescence isan almost unexplored area of research that hasimportance to both drought and disease resistance.The total amount of dry matter lost as exudatesand during root degeneration is unknown.Information about the importance of individualmineral nutrient elements to the pathogen and todisease development is badly needed, especiallyfor sorghum. Little is known about interactionsbetween water and nutrient availability near the soilsurface. The importance of root growth in nearsurfaceregions of the profile should be exploredbecause of the large requirements for mineral elementsand their concentration in that region.Finally, the importance of mycorrhizal fungi inenhancing sorghum resistance to drought and nutrientstresses remains to be defined.92

In summary the following is a list of specifictopics for future research:I. Effects of abiotic stresses on the hostA. Optimum root system and rooting pattern1. Define "optimum" in terms of the soilplant-atmospheresystem.2. What is the role of root resistance?3. Determine efficient use of waterresources.B. Root senescence and regeneration1. Determine the effects of low soil waterpotential on growth and survival, especiallyin the near-surface regions of thesoil profile.2. What quantity of root dry matter is lost orremobilized?3. What is the role of root deterioration inmicroflora ecology?4. How much regeneration of roots is necessaryfor efficient water and nutrientuptake?C. Root exudates; quantity and compositionD. Leaf firing1. What is the mechanism—heat or desiccation?To what degree does the retranslocationof carbon and minerals from theleaf affect its longevity?2. Determine genotypic differences.3. Determine progressive vs general firing.E. Floret abortion1. What controls head blasting—-heat stress,growth inhibition due to water stress,involvement of hormones, etc.?2. What are the limits to recovery via seedsize adjustment?F. Capacity and consequences of redistributionof stem and root reserves1. Is there some redistribution under allconditions?2. What is the relationship of reserves toyield under stress?G. Interactions of biotic stressesH. Role of individual nutrient elements andwater x nutrient interactions on host growth,vigor, and senesence.II. Effects of abiotic stresses on pathogensA. Confirmation of synthetic media results insoil system1. Most media studies use osmotic stress.What is the impact of soil water deficitsthrough matric effects?B. Basis for apparent drought resistance1. Investigate stress levels at which propagulesare resistant to heat anddesiccation.2. What is the role of osmoregulation inmaintenance of growth?C. Specific nutrient effectsD. Temperature tolerance at low soil-waterpotential1. What is the effect of high temperaturesnear soil surface?2. Determine growth optimum shifts tohigher temperature as water potentialdecreases in media studies.E. I nvestigate the relation between soil physicalproperties and fungal survivalIII. Host/pathogen interactionsA. Role of root exudates on germination,growth, and pathogenicity of fungiB. Effect of pathogen on exudatesC. Mechanisms of infectionD. Mechanisms for control pf pathogen activityand spread in host tissuesE. Mechanisms for yield reductionIV. Edaphic stress/host stress/pathogen interactionsunder field conditionsA. Inorganic nutrient availability to host andpathogen, including the role of mycorrhizalfungiB. Mechanisms for stress-induced predispositionto infectionC. Direct vs indirect control of pathogen spreadin tissuesD. Separation of effects of abiotic stresses frombiotic stresses on grain yield93

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SCHOENEWEISS, D.F. 1978. Water stress as a predisposingfactor in plant disease. Pages 61 -99 in Vol.5, Waterdeficit and plant growth (ed. T.T. Kozlowski). New York,New York, USA: Academic Press. 323 pp.SEETHARAMA, N., SUBBA REDDY, B.V., PEACOCK,J.M., and BIDINGER, F.R. 1982. Sorghum improvementfor drought resistance. Pages 317-338 in Drought resistancein crops with emphasis on rice. Los Banos, Laguna,Philippines: International Rice Research Institute.SHOKES, F.M., LYDA, S.D., and JORDAN, W.R. 1977.Effect of water potential on the growth and survival ofMacrophomina phaseolina. Phytopathology 67:239-241.SIEVERDING, E. 1981. Influence of soil water regimes onVA mycorrhizae. Zeitschrift fur Acker-und Pflanzenbau150:400-411.SIMPSON, G.M. 1981. Water stress on plants. New York,New York, USA: Prager Press. 324 pp.SMITH, W.H. 1969. Germination of Macrophomina phaseolisclerotia as affected by Pinus lambertiana root exudate.Canadian Journal of Microbiology 15:1387-1391.STOUT, D.G., KANNANGARA, T., and SIMPSON, G.M.1978. Drought resistance of sorghum bicolor: 2. Waterstress effects on growth. Canadian Journal of PlantScience 58:525-533.SULLIVAN, C.Y. 1972. Mechanisms of heat and droughtresistance in grain sorghum and methods of measurement.Pages 247-263 in Sorghum in Seventies (eds.N.G.P. Rao and LR. House). New Delhi, India: Oxford andIBH Publishing Co.SULLIVAN, C.Y., and ROSS, W.M. 1979. Selecting fordrought and heat resistance in grain sorghum. Pages263-281 in Stress physiology in crop plants (eds. H. Musselland R.C. Staples). New York, New York, USA: Wiley-Interscience.TAYLOR, H.M., and KLEPPER, B. 1974. Water relations ofcotton: I. Root growth and water use as related to topgrowth and soil water content. Agronomy Journal 66:584-588.TINKER, P.B. 1980. Role of rhizosphere microorganismsin phosphorus uptake by plants. Pages 617-654 in Therole of phosphorus in agriculture (eds. F.E. Khasawnen,E.C. Sample, and E.J. Kamprath). Madison, Wisconsin,USA: American Society of Agronomy.TINKER, P.B., and GILDON, A. 1983. Mycorrhizal fungiand ion uptake. Pages 21 -32 in Metals and micronutrients:uptake and utilization by plants (PhytochemicalSociety of Europe Symposium No. 21), (eds. D.A. Robband W.S. Pierpoint). New York, New York, USA: AcademicPress.TURNER, N.C., and BURCH, G.T. 1983. The role of waterin plants. Pages 73-126 in Crop water relations (eds. I.D.Teare and M.M. Peet). New York, New York, USA: JohnWiley & Sons.VANDERLIP, R.L. 1972. How a sorghum plant develops.Kansas Agricultural Experiment Station CooperativeExtension Circular 447. Manhattan, Kansas, USA: KansasState University. 19 pp.WILSON, J.H.H., and ALLISON, J.C. 1978. Effects of waterstress on the growth of maize (Zea mays L). RhodesianJournal of Agricultural Research 16:175-192.WILSON, J.M., and GRIFFIN, D.M. 1975. Water potentialand the respiration of microorganisms in the soil. SoilBiology and Biochemistry 7:199-204.YARWOOD, C.E. 1976. Modification of the hostresponses—predisposition. Pages 701-718 in Encyclopediaof plant physiology, New series, Vol. 4 (eds. A.Pison and M.H. Zimmerman). Berlin, Federal Republic ofGermany: Springer-Verlag.QuestionsPartridge:In your conclusion you state that "stress triggerschanges in host root resistance, allowing infectionat an earlier stage of growth than expected...." Doyou have or can you elucidate data to support thisconclusion?Jordan:Reports by Schneider and Pendery [1983] withmaize and Odvody and Dunkle [1979] present evidencethat mild water stress during some periodbefore anthesis promotes colonization of roots byorganisms reported to cause root and stalk rots.Partridge:Do you have or can you elucidate data to supportyour conclusion that "disease spread is associatedwith an increasing demand for CHO...."Jordan:Disease spread (symptom expression in stalk) isassociated with CHO deposition in grain. Theassumption is that the presence of developinggrain creates an increased demand for CHO, but inreality this may just be a competing sink. Diseasespread into the stalk during grain fill of fertile, but notsterile isolines appears to be the best example ofthis presumed increased CHO demand. Referencesare cited in the text.96

Partridge:Dr. Clark, have phytoalexins been demonstrated insorghum, and if so, have they been shown to affectstalk rot?Clark:I saw no literature on phytoalexins in sorghum.However, my literature search was not directed tophytoalexins, but to nutrient elements.97

The Association of Plant Senescencewith Root and Stalk Diseases in SorghumR.R. Duncan*SummaryGrain sorghum (Sorghum bicolor [L.] Moench) generally undergoes sequential senescence inwhich the older leaves near the base of the stalk senesce and die first, followed by a wavelikeprogression of leaf senescence passing up the stem. Senescence is characterized by losses inchlorophyll, carbohydrates, protein, and dry weight, and can result in predisposition to attack byvarious pathogens. The interaction of environment, growth stage, and genetic potential determinesthe levels of endogenous growth regulators which govern senescence. Nonsenescent(indeterminate, "perennialistic," "stay-green") sorghum genotypes maintain more green leafarea and higher stem carbohydrate contents than senescing gehotypes during late reproductivegrowth stages. Since the nonsenescent genotypes supposedly remain physiologicallyactive during the late stages of growth, this characteristic probably contributes to the overallstress tolerance and disease resistance mechanisms in these plants. Environmental stress(drought, high temperature and humidity, and nutritional imbalances) can predispose sorghumto infection by stalk rot pathogens. Many of these organisms are weakly pathogenic orsecondary invaders, while others (e.g., Colletotrichum spp) damage healthy vigorous celltissue. Stalk rotting frequently involves many organisms, and selection within genotypes forspecific resistance mechanisms is often difficult. Concentration of research efforts to developnonsenescing plants that are well buffered against environmental stresses will help to minimizethe predisposing factors leading to stalk rot in sorghum.Sorghum is a versatile plant adaptable to a widerange of environmental conditions. Breedingefforts have centered on development of resistanceto specific disease organisms in a particularenvironment. This paper will present the relationshipbetween senescence/nonsenescence andpotential root/stalk diseases in sorghum. The followingtopics will be discussed in detail: plantsenescence; nonsenescence; host-parasite interactions,including predisposition and infection vssenescence; nonsenescence and potential stalkrot diseases in the southeastern USA; and futureresearch priorities.Plant SenescenceIn the development of plants, senescence is a relativelygross change or series of changes, leadingfinally to the death of the plant. Comfort (1956) hasdescribed senescence as a decrease in viabilitywith an increase in vulnerability. In plants thesechanges can be recognized as decreases ingrowth rates and vigor and increases in susceptibilityto challenge by the environment (water ornutrient shortages) or by pathogens or physicaldisturbance (Leopold 1961). In senescing cells agradual reduction in the capacity for protein syn-*Sorghum Breeder/Physiologist, University of Georgia, Georgia Experiment Station, Griffin, GA 30212, USA.International Crops Research Institute for the Semi-Arid Tropics. 1984. Sorghum Root and Stalk Rots, aCriticalReview: Proceedings of the Consultative Group Discussion on Research Needs and Strategies for Control ofSorghum Root and Stalk Rot Diseases, 27 Nov - 2 Dec 1983, Bellagio. Italy. Patancheru, A.P. 502 324, India:ICRISAT.99

thesis occurs, coupled with degeneration of theendoplasmic reticulum and mitochondria as wellas other organelles and membranes.The rate at which these natural changes occurdepends greatly on the species, the part of the plantinvolved, and the environmental conditions (photoperiod,temperature, soil fertility). Senescencemay take place at about the same time in all parts ofthe plant (whole-plant senescence, which typicallyoccurs following flowering and fruiting), or individualorgans may senesce while the remainder of theplant retains vitality (leaf or fruit senescence).Leaf senescence may be characterized byinvolvement of all the leaves at the same time (i.e.,dropping of leaves in the fall), which is termed synchronousor simultaneous senescence. Or leafsenescence may pass up the stem in a "wave" (inwhich the older leaves at the more basal end of thestem become senescent and die first); this isknown as sequential senescence. Senescence offruits is a late stage in the ripening process, anddoes not generally begin until the developing seedsare fully formed (Leopold 1961; Phillips 1971, pp116-124 and 158-159). Sorghum generally undergoessequential leaf senescence, with the coleoptileand first few leaves senescing and dying duringthe vegetative stage and additional sequentiallyformed leaves continuing this senescence anddeath pattern throughout the reproductive growthstage. During the late reproductive stages, the tip ofthe panicle begins senescing downward. Thissenescence pattern continues into the peduncleand stem, moving toward the base of the stem. Ifenvironmental stress has not terminated the cellsin the crown root region, basal buds will initiate andtillers will grow until stress (frost or water deficits,for example) or disease development kills them.Senescence is clearly a distinct physiologicaland biochemical phase in plant development. Athorough review of plant senescence in general ispresented by Thimann (1980). Its timing is controlledby both internal and external factors. Modelsfor transcriptional and translational control ofsenescence have been summarized by Hoffman(1972). A good general review of the biochemistryof senescence has been presented by Varner(1961). In general senescence is characterized bylosses of RNA, DNA, total nitrogen, chlorophyll, protein,and dry weight (Hoffman 1972, Potter 1971,Spencer and Titus 1972). These changes can beretarded by the addition of certain plant growthregulators.Extensive research has been conducted concerninghormonal regulation of plant senescence(Carr and Pate 1967, Fletcher and Adedipe 1972,Fletcher and Osborne 1965, Garg and Kapoor1972, Leopold 1961, Nichols 1973, Wareing andSeth 1967, and Woolhouse 1967). Fletcher andAdedipe (1972) have proposed a model for hormonalregulation of leaf senescence. They postulatedthat the interplay of environment, time, and geneticpotential determines the levels of endogenousgrowth regulators. These regulators were classifiedinto two broad groups: (a) senescence retardants,which include cytokinins, gibberellins, auxins,and ascorbic acid (Garg and Kapoor 1972); and (b)senescence accelerators, which include abscisicacid, ethylene, and other, unidentified "senescencefactors." The plant species and age governthe effectiveness of any one of the senescenceretardants in delaying senescence. A decline in thelevels of senescence retardants and/or a subsequentrise in those of senescence acceleratorsleads to senescence. The role of senescenceretardants is to maintain the synthesis of macromoleculessuch as chlorophyll, protein, and nucleicacids. This maintenance confers structural integrityand proper partitioning of cell metabolites. Thisis associated with a high photosynthetic rate andan increased turnover of metabolites, accompaniedby an orderly metabolic coordination betweenenergy production and utilization for biosyntheticand growth processes. Conversely, a rise in thelevels of senescence accelerators and/or adecline in senescence retardants results in adecrease in the synthesis or an increase in thedegradation of macromolecules. These changes,accompanied by a loss of membrane integrity,could lead to senescence and ultimately death.The numerous metabolic changes associated withsenescence may be delayed by the exogenousapplication of hormones.Secor et al. (1983) concluded that changes inribulose-1, 5-biphosphate carboxylase activity andchlorophyll content were related to the onset ofsenescence in soybean (Glycine max [L] Merr.)leaves and that a similar mechanism seems to beoperating in leaves that emerge after flowering.Trzebinski et al. (1972) demonstrated a positivecorrelation between the depression of sugar yieldper plant attributable to virus yellows and mosaicinfection and the decrease in chlorophyll (particularlychlorophyll b) content of sugar beet (Beta vulgarisL.) leaves.Harada and Nakayama (1971) have suggestedthat dwarfness in rice (Oryza sativa L.) may be100

elated to leaf senescence. Short rice varieties hadmore chlorophyll per unit leaf area and slow chlorophylldegradation, while tall ones showed less chlorophyllcontent and rapid degradation. Theyconcluded that close relationships exist among thechlorophyll content per unit leaf area, the leaf sdegradation, and the plant type.The removal of flowers or of developing fruits hasbeen observed to delay senescence in a number ofannual plants (Leopold 1961). Moss (1962) foundthat the leaves of maize (Zea mays L) plants onwhich pollination had been prevented were stillgreen towards the end of the season and had ahigher rate of assimilation than the leaves of normalplants, which were by then senescent. Preventionof pollination increased the sugar concentration inthe stalks. Allison and Weinmann (1970) studiedthe relationship between carbohydrate content andsenescence of maize leaves. They concluded thatabnormal concentrations of nonstructural carbohydrates(resulting from pollination prevention orear removal) might interfere with some of the leaffunctions and possibly lead to premature senescencein maize. Mortimore and Ward (1964)showed that high levels of soluble sugars in maizestems at physiological maturity were associatedwith lodging resistance. Papers by McBee andMaranville and Clegg (these proceedings) providemore detailed explanations of carbohydrate metabolismand stalk strength, respectively.Lewis (1953) proposed that host-parasite relationsare governed by a combination of the biochemistryof the host and the nutritionalrequirements of the parasite. Since nutrients in thehost at specific metabolic concentrations sometimesinhibit the parasite, a certain nutrient profilemay be a necessary prerequisite for infection.Schoeneweiss (1975) determined that generallyexcess nitrogen favored infection, excess potassiumreduced infection, and excess phosphorusgave variable results in host-parasite relationships.Jyung (1975) found a close relationship betweenzinc nutrition and leaf senescence as suggested bya rapid decline in total chlorophyll and chlorophylla:b in zinc-deficient leaf discs during aging. As aleaf grows older, its photosynthetic apparatusappears to become markedly less effective, as indicatedby lower photosynthetic rates and depressednet. assimilation rates (Leopold 1961). Criticalchanges occur in the metabolism of leaf carbohydratesand proteins, as well as in respiratory activities.As a result, the chlorophyll pigmentsdeteriorate in favor of the carotenoids and anthocyanins.As these metabolic shifts take place, thereoccurs a gross export of many of the organic andinorganic nutrients from the leaf, until abscissioninterrupts such traffic.Colhoun (1973) stated that interactions amongenvironmental factors and nutrition create problemsin the interpretation of the predisposingeffects of nutrient stresses on plant defense mechanisms.Huber (1978) has written an excellentpaper on mineral nutrition, nutrient imbalances,and disease incidence in plants. Refer to "DiseaseDevelopment and Mineral Nutrition" in the paper byW. Jordan et al. (these proceedings) for a morecomprehensive evaluation of the relationshipsinvolving mineral element stress and stalk/rootrots in plants.NonsenescenceStandard sorghum genotypes undergo a sequentialleaf senescence in which the older leaves at thebase of the stalk senesce and die first. Under environmentalstress conditions, a pattern of leaf senescenceand death progresses in wavelike fashion upthe stem, culminating in overall plant death afterreaching physiological maturity (maximum graindry weight accumulation). In nonstress situations,the plant will senesce most of its leaves, but thebasal and axillary buds are initiated and tillers willgrow until frost or severe stress conditions terminatethem. The phenomenon of green leaf retentionafter the grain has reached physiological maturityhas been termed nonsenescence (Duncan 1977).Senescent (BTx378, RTx7000, RTx2536,S.C0214[IS-1 598C]) and nonsenescent(SC0056[IS-12568], SC0599 [Rio derivative],SC0170[IS-12661]) genotypes were evaluatedduring the reproductive stage of development(Duncan et al. 1981). The nonsenescent (indeterminate,"perennialistic," "stay-green") genotyperequired 2 days longer to reach 50% anthesis,averaged 3 to 4 cm less height, produced 2 to 3more basal tillers per plant, averaged 10% largerstem diameters, maintained 53% higher basal stemsugar concentrations, and produced 11% higherleaf blade chlorophyll contents than did the senescentgenotype. Data involving leaves (green leafnumber and weight, senesced leaf number andweight, leaf area index, leaf area duration [averageleaf area index between two sampling periods as a101

function of time], and leaf area ratio [green leafblade area in relation to the weight of the totalabove-ground dry matter]) favored the nonsenescentgenotype. Since the nonsenescing genotypescontained a higher chlorophyll content for a longerperiod of time, a 20% larger leaf area index, and a23% longer leaf area duration than the senescentgenotypes, the authors speculated that the nonsenescinglines possessed a greater photosyntheticcapacity and possibly greater crop productivity.Leaf area duration was found to be a good indicatorof leaf senescence on the sorghum plant. Thisparameter reflected the ability of the plant to maintaingreen leaf area on a given unit of land throughoutthe life of the crop. Consequently, it revealednot only the growth in leaf area during the vegetativestages, but also the maintenance of green (andsupposedly physiologically active) leaf area overtime during the reproductive stages of development.Since the nonsenescent genotypes remainphysiologically active during the late stages ofgrowth, this characteristic may also contribute tothe overall disease resistance and stress tolerancemechanisms in these plants. The nonsenescentgenotype SC0599 (Rio derivative) has shown verygood dual resistance to Fusarium spp and Colletotrichumspp (Duncan and Sowell 1983).A comparison of rooting patterns of senescentand nonsenescent sorghum genotypes revealedthat the nonsenescent hybrid established itsadventitious root system earlier than did the senescenthybrid (Zartman and Woyewodzic 1979). Rootdensity of both hybrids increased until grain filling,with the senescent cultivars generally exhibitinggreater root density. The root density of bothhybrids decreased after grain filling, with a greaterdecrease noted for the senescent hybrid. Thesenescent hybrid also produced a lower grain yield.McBee et al. (1983) studied the effect of senescenceand nonsenescence on carbohydrates insorghum during late stages of reproductive development.They found that stalk carbohydrates weresignificantly higher in nonsenescent cultivars duringall stages of seed development (grain filling)than in senescent cultivars. Cultivars with thehigher stalk carbohydrates produced panicles withsignificantly more grain weight. Duncan et al.(1981) found 10% higher test weights on grainharvested from nonsenescing genotypes than fromsenescing types. Refer to the paper by G.G. McBee(these proceedings) for a more comprehensiveexplanation of carbohydrates and carbohydratemetabolism in sorghum.Host-Parasite InteractionsPredispositionSchoeneweiss (1975) has defined predispositionas the tendency of nongenetic factors, acting priorto infection, to affect the susceptibility of plants todisease. He proposed that root- and stem-rottingorganisms enter resistant and susceptible hostswith equal frequency in most cases. Whether adisease condition actually develops depends uponthe influence of environmental factors on thegenetically controlled response of the host plant tothe presence of the pathogen or its metabolites, i.e.,a host-environment interaction.Dodd (1977) has proposed the photosyntheticstress-translocation balance concept as beingimportant in maize stalk rots. Several stress-relatedfactors can predispose plants to invasion by certainstalk rot organisms, which could lead topathogenicity (Dodd 1980, Schoeneweiss 1975):hormonal imbalances, nutritional imbalances,environmental extremes, photosynthetic stress,injury, carbohydrate nutrition, and cellular senescence.Refer to the paper by G.G. McBee (theseproceedings) for a more detailed explanation ofthese factors as they relate to senescence.Infection Versus SenescenceMortimore and Ward (1964) stated:Although rotting organisms may invade theroot at a relatively early stage of plant growth,root and stalk rot is essentially a diseaserelated to the onset of senescence and producesno visible symptoms until after theplant has reached physiological maturity. It ispremature degradation of the stalk producedby a range of common decay organisms andappears to be essentially a physiologicalphenomenon. Resistance appears todepend upon the maintenance of a certaindegree of physiological vigor, particularly inthe stalks during the long post-maturityperiod in the autumn when the corn plant isleft standing in the field until the moisture inthe grain is reduced to the desired level. Conversely,susceptibility is due to a lack of vigoras the plant matures.Physiological vigor depends upon asteady respiration rate supported by a continuoussupply of carbohydrate reserves as102

well as an adequate and balanced level ofnutrients. When the vigor of the plant dropsbelow a certain level because of stress conditions,it becomes susceptible to invasion bycertain saprophytes and weak parasites.Farkas (1978) has presented a general discussionof senescence and plant disease, includingseparation of disease-induced senescence andsenescence-induced diseases. He concluded thatnot everything that is stress related will necessarilylead to pathological problems in plants.Mortimore and Ward (1964) determined that highlevels of soluble sugars in the pith of corn (maize)stalks at physiological maturity are associated withresistance to root and stalk rots. A resistant hybridhad a higher sugar content than a susceptiblehybrid when grown using recommended culturalpractices. Treatments that predisposed plants tostalk rots (high population densities and late defoliation)caused a reduction in sugars. Treatmentsthat gave "normal" plant resistance reactions(prevention of kernel development and low populationdensities) resulted in maintenance or increaseof sugars in the pith. Craig and Hooker (1961)theorized that a decrease in the sugar levels ofmaize stalks caused senescence of pith tissue andenhanced susceptibility to diplodia stalk rot.Lewis and Deacon (1982) found that naturalsenescence of the coleoptiles and root cortices ofwheat (Triticum aestivum L.) and barley (Hordeumvulgare L) might increase the establishment ofinfection by the eyespot fungus (Pseudocercosporellaherpotrichoides (Fron) Dei) either directly orthrough the activities of competing microorganismsthat act as biological control agents. Theyproposed that shading decreases the rate of rootproduction, which, in turn, reduces the plant'scapacity to offset pathological infection of theexisting roots by producing new ones. Deacon andLewis (1982) concluded that Cochliobolus sativus(Ito & Kuribay) Drechsler ex Dastur and other weakparasites benefit from the early natural senescenceof wheat root cortex, and that the degree ofsusceptibility or resistance to common root rot is atleast partially determined by differences in corticalsenescence.Hodges and Madsen (1978) established thatDrechslera sorokiniana (Sacc.) Subram. and Jain(= Helminthosporium sorokinianum Sacc. inSorok.) and Curvularia geniculata (Tr. & Earle)Boed. may interact competitively or synergisticallyto decrease or increase the severity of leaf spotexpression on leaves of Poa pratensis L. Theyfound that C. geniculata grew at temperatures (30°C) that were high enough to physiologicallystress P. pratensis. The stress created leaf tissueconditions that were especially susceptible toinfection and proliferation by a weak, primary pathogenwith aggressive saprophytic capabilities athigh temperatures. Hodges and Madsen (1979)subsequently concluded that the synergisticincrease in disease produced by a combination ofD. sorokiniana and C. geniculata at high temperatureswas the result of increased high-temperaturegrowth of the latter organism, which was probablymore saprophytic than parasitic on senescing,heat-stressed leaves and did not reflect a hightemperatureincrease in virulence of this organism.Katsanos and Pappelis (1965) and Pappelis andKatsanos (1966) conducted research on senescenceof sorghum stalk tissue. In an attempt tounderstand the role of living cells in the resistanceto entrance of pathogens into stalks under naturalconditions, they tested the hypothesis that livingcells of sorghum are involved in resistance tospread of several sorghum stalk rot pathogens. Theplants were subjected to root injury, leaf injury, andpanicle removal. The effects of root and leaf injuryincreased the rate of cell death in internode andnodal tissue, whereas the panicle-removal treatmentresulted in a decrease in the rate of cell death.They speculated that if living cells were necessaryin the resistance mechanism, root- and leaf-injuredplants would be more susceptible than "normal"plants, whereas panicle removal would result inplants more resistant than "normal" plants.Gourley et al. (1977) studied the effect of Fusariummoniliforme Sheldon on seedling developmentof sorghum cultivars. The fungus generallyinvades the seedling through insect or mechanicalinjuries, or through roots or stems weakened byother factors, and results in blight or damping off ofsusceptible cultivars. The organism and its toxinreduced primary root length by 53%, number oflateral roots by 25%, and epicotyl length by 32% incomparisons of inoculated and uninoculated juvenileplants.Trimboli and Burgess (1983) found that typicalsymptoms of basal stalk rot and root rot of sorghumwere reproduced in the greenhouse on plants thatwere grown under optimal soil moisture until flowering,then subjected to severe moisture stress,followed by rewetting. Stalk rot did not develop inplants grown under optimal conditions from plantingto maturity, although many of the plants were103

infected and partially colonized by F. moniliforme.The researchers determined that early infectionand establishment of the fungus in the plant maynot be essential for stalk rot development and thatmicroconidia that formed on necrotic coleoptileresidue and on the soil surface may have been theairborne inoculum source.Reed et al. (1983) investigated the fungal colonizationof stalks and roots of sorghum during thegrowing season. Isolation frequency patterns forseveral organisms are presented in Tables 1 and 2.F. moniliforme was the dominant species isolatedfrom stalks, while F. eguiseti (Cda.) Sacc. was mostfrequently isolated from the roots. The colonizationof stalk tissue appeared to coincide with the onsetof anthesis, but roots were apparently inhabited byfungi regardless of the growth stage. Fungi becamemore abundant in both stalks and roots as the cropmatured. The researchers proposed that a balanceexists between fungal activity within plant tissueand the ability of the host to withstand such activity.The balance is then shifted by factors that adverselyaffect the host or by conditions that favorincreased fungal activity. The fungi become destructiveto stalk tissue and lead to the developmentof stalk rot.Odvody and Dunkle (1979) investigated theeffect of environment on host-parasite relationsinvolving sorghum and Macrophomina phaseolina(Tassi) Goid. Charcoal rot occurred when sorghumplants (senescent genotypes) were subjected todrought stress as grain development approachedthe soft dough stage. High soil temperatures andlow soil moisture caused a significant reduction intotal stalk sugars, which correlated with increaseddevelopment of charcoal rot. Nonfertilized malesterilesorghum plants subjected to drought stresswere less susceptible to charcoal rot than fertilizedlines. Root systems of the stressed male-sterileplants were characterized by a high percentage ofroots with latent infections, but no symptoms of rot.Most root infections of both fertile and male-sterilesorghums occurred only after the onset of stressconditions. The researchers also demonstratedthat nutrients increased sclerotial germination andmycelial growth at low osmotic water potentials,which suggests a role for nutrients in overcomingsoil fungistatic factors and promoting infection byM. phaseolina.Doupnik et al. (1975) and Doupnik and Boosalis(1980) investigated the influence of tillage systemson stalk rot incidence in sorghum. F. moniliformewas the major pathogen that caused stalk rot in thesorghum. No-till plots had 72% less stalk rot incidencethan conventionally tilled plots. Sorghumgrain yields were 41 % higher on the no-till than onthe conventional-till plots. The researchers speculatedthat the lower incidence of stalk rot in theno-tillage system was due to increased water conservation,reduced soil temperature fluctuations,Table 1. Pattern of sorghum stalk colonization by various organisms. (Source: Reed et al. 1983.)Isolation frequencyVegetative Reproductive Post-physiologicalOrganism growth growth maturityFusarium moniliforme Sheldon Low High-A LowF. graminearum Schwabe Low Low High-KFF. "roseum" group a Low Low High-KFF. equiseti (Gda.) Sacc. Low Low HighF. tricinctum (Cda.) Sacc. Low Low High-KFF. oxysporum Schlecht. emend. Snyd. & Hans. 'Redolens' Low Low HighF. solani (Mart) Appel & Wr. emend. Snyd. & Hans. Low Low HighAltemaria alternata (Fr.) Keissler Low High-A VariableNigrospora sphaerica (Sacc.) Mason Low High-SD to PM HighTrichoderma viride Pers. ex Gray Low Low LowEpicoccum spp Low Low Lowa. F. scirpi Lambotte & Fautr. var. PM - physiological maturityacuminatum (Ell. & Ev.) Wr.SD = soft doughF. avenaceum (Fr.) Sacc. KF = high incidence of infection after killing frostF. culmorum (W. G. Sm.) Sacc. A = anthesisF.sambucinum Fckl.104

Table 2. Pattern of sorghum root colonization by various organisms. (Source: Reed et at 1983.)Isolation frequencyVegetative Reproductive Post-physiologicalOrganism growth growth maturityFusarium equiseti (Cda.) Sacc. High High HighF. oxysporum Schlecht. emend. Snyd. & Hans. 'Redolens' High Low Very lowF. solani (Mart.) Appel & Wr. emend.Snyd. & Hans. High Low Very lowF. moniliforme Sheldon Very low High-BS to A MediumF. graminearum Schwabe Low High-SD HighF. "roseum" group a Very low High-SD HighF. tricinctum (Cda.) Sacc. Very low Medium HighAlternaria alternata (Fr.) Keissler Medium High-BS to A MediumTrichoderma viride Pers. ex Gray High High MediumNigrospora sphaerica (Sacc.) Mason Very low Very low LowEpicoccum spp Very low Very low High-PMa. F. scirpi Lambotte & Fautr. var. BS = boot stageacuminatum (Ell. & Ev.) Wr. A = anthesisF. avenaceum (Fr.) Sacc. SD = soft doughF. culmorum (W. G. Sm.) Sacc. PPM = physiological maturityF. sambucinum Fckl.and lower mean soil temperatures. Consequently,predisposition to stalk rot was minimized or delayedin a senescent cultivar by a cultural methodreducedtillage.Nonsenescence and Potential StalkRot Diseases in the Southeastern USADuncan and Sowell (1983) have studied the relationshipbetween anthracnose (Colletotrichumgraminicola (Ces.) Wils.) and the Fusarium complexin causing disease problems on sorghum in thehumid southeastern USA. These two organismsworked in tandem to reduce yield and causeserious disease problems in a breeding program inGeorgia (USA) involving susceptible genotypes(Table 3). Other stalk rot organisms are potentialthreats to sorghum production in the Southeast.Charcoal rot generally occurs under conventionaltillage systems without irrigation. Sorghum grown inno-tillage systems tends to have few or no problemswith Macrophomina spp. Pythium stalk rot hasbeen found in the Southeast in isolated fields andhas occurred following rotation after tobacco(Nicotiana tobaccum L.) in the Coastal Plain region.Additional research indicates a possible associationbetween winter cover crops (particularlyannual legumes) and the escalation of diseaseproblems with Pythium spp and other stalk rot orga-Table 3. Potential damage from sorghum root/stalkdiseases and field grain deterioration inGeorgia, USA.Level of damage aOrganism Plants b GrainFusarium moniliforme Sheldon 4-5 5F. "roseum" group (Toussoun & Nelson) 3 3F. semitectum Berk & Rav.Cofletotrichum graminicola (Ces.) Wils.34-531-2Macrophomina phaseolina (Tassi) Goid. 3 0Pythium spp 2 0Altemaria sppPhoma spp1042-3Epicoccum spp 1 2Curvularia spp 0 3-4Helminthosporium spp 0 3-4Periconia circinata (Mangin) Sacc. 1 0Bacteria 1-2 0a. 1 = very little damage; 5=significant damage; 0 = no data available.b. Plants at reproductive stage.nisms in conservation tillage production systems.Current research is focusing on this association.Alternariaspp and Epicoccum spp are generallysecondary invaders of stalks and are apparentlynot competitive with the more dominant Fusarium,Colletotrichum, and Macrophomina stalk rot organismsin this region of the USA.Host-environment interactions are key factors inthe degree of damage caused by Fusarium and105

Table 4. Pathogens isolated from field-grown seed in Georgia, USA, during 1982.Pathogens aPedigree Fusarium Colletotrichum Curvularia Germination (%)Martin 8.75 35.50 2.50 45.0RCY ORO TXTRA 10.00 21.75 700 71.0(SC599 x SC110) 10.50 25.00 7.75 87.0BSC599-6 2.25 2.00 13.00 94.0Funks G-522DR 14.75 10.00 0.00 38.0RTx430 35.00 0.75 0.25 16.5a. Mean number of colonies (4 replications).Colletotrichum on sorghum. Evaluation of seed collectedfrom the field after physiological grainmaturity revealed that Fusarium spp and Colletotrichumspp were dominant genera in reducing germination(Table 4) of breeder seed, BSC599-6(anonsenescent genotype) was the only cultivar thathad a good level of resistance to both pathogens(Tables 4 and 5). Inoculation of the Fusarium susceptible,senescent genotype RTx2536 with thethree Fusarium species that have been isolated inGeorgia revealed substantial seed germinationreductions (Table 6). F. moniliforme reduced germinationthreefold over the check when the plantswere inoculated during the soft dough stage ofseed development. F. roseum and F. semitectumdecreased germination approximately twofoldwhen the plants were inoculated during the harddough stage.Plant genetics, environmental stress, and senescenceinteract in conjunction with the pathogens toaffect the growth and development of the plant.Sorghum yield losses from Colletotrichum spp inGeorgia have been reported as high as 50% (Harriset al. 1964), while fusarium stalk rot and head blighthave caused 40% yield reductions in the JaliscoTable 5. The influence of Fusarium spp. on germinationof field-grown sorghum seed in Georgia,USA, during 1982.PedigreeBSC599-6TP9R02-16(SC599 x SC110)B2219a. Fifty seed samples.Colonies a(mean no.)2.256.7510.5014.25Germinatior(mean %)94.089.587.070.0Table 6. The influence of selected Fusarium spp onseed germination of RTx2536 inoculatedduring reproductive growth.Treatment Germination (%)Check 92Check (atomized with water) 83Fusarium moniliforme Sheldon a 30F. "roseum" group (Toussoun & Nelson) b 52F. semitectum Berk & Rav. b 61a. Treated during soft dough stage.b. Treated during hard dough stage.region of Mexico (Sanchez and Betancourt 1983).Edmunds and Zummo (1975) have indicated thatFusarium spp can reduce sorghum yields up to60%.Future Research PrioritiesEnvironmental stress factors can predisposesorghum plants to infection by a number of pathogenscommonly known as stalk rot pathogens. Theuniversal occurrence of many synergistically reactivemicroorganisms generally leads to multipleorganisminvolvement in stalk rotting (Turner1982), Since many of the pathogens have a relativelywide range of host plants and characteristicallymay be normally weakly parasitic orsecondary invaders, selection within genotypes ofa plant species may not be very productive in locatingunique genes for specific resistance (Van derPlank 1968).Research efforts may need to be concentratedon selection of plants capable of withstanding pre-106

107disposing environmental stresses in an effort tomaintain plant health longer (Turner 1982). Susceptibilityto stresses that may impose irreversiblephysical and/or chemical changes in the plantshould be avoided. Resistance to specific stressesor tolerance to stresses (reversible physical orchemical changes when the stress is removed)should be emphasized. A plant that is well bufferedagainst environmental stresses and that remainsmetabolically and physiologically active (nonsenescent,indeterminate) during late reproductivestages of development should be in a better positionto withstand attack by roots and stalk-rottingorganisms. Improvements in genetic resistance/tolerance mechanisms, especially on the multiplegene level, will help to stabilize plant performance.Several areas of research should be emphasizedduring the next decade:1. Nonsenescence characteristics vs diseasepopulation dynamics.a. Investigation of metabolic activity, nutritionalprofile, and associated internal plantfactors that suppress disease buildup.b. Study of root system dynamics vs diseaseorganism entry and determination of the"triggers" for disease enhancement withinthe plant.c. Evaluation of carbohydrate balance inroots and stems vs stalk disease relationshipsin senescing and nonsenescinggenotypes.2. Multiple gene resistance/tolerance to diseasepathogens.a. Identification of genes and their transfer,and inheritance studies involving senescingand nonsenescing genotypes.b. Continued monitoring of the root and stalkrottingorganisms via international diseasescreening nurseries. Inclusion of senescingand nonsenescing genotypes in thenursery.ReferencesALLISON. J.C.S.. and WEINMANN, H. 1970. Effect ofabsence of developing grain on carbohydrate contentand senescence of maize leaves. Plant Physiology46:435-436.CARR, D.J., and PATE, J.S. 1967. Ageing in the wholeplant. Pages 559-599 in Symposia of the Society forExperimental Biology XXI: Aspects of the biology of ageing.London, U.K.: Cambridge University Press.COLHOUN, J. 1973. Effects of environmental factors onplant disease. Annual Review of Phytopathology 11:343-364.COMFORT, A. 1956. The biology of senescence. NewYork. New York, USA: Rinehart. 414 pp.CRAIG, J., and HOOKER, A.L. 1961. Relation of sugartrends and pith density to Diplodia stalk rot in dent com.Phytopathology 51:376-382.DEACON, J.W., and LEWIS, S.J. 1982. Natural senescenceof the root cortex of spring wheat in relation tosusceptibility to common root rot (Cochliobolus sativus)and growth of a free-living nitrogen-fixing bacterium.Plant and Soil 66:13-20.DODD, J.L. 1977. A photosynthetic stress-transiocationbalance concept of corn stalk rot. Pages 122-130 in Proceedingsof the 32nd Annual Corn and SorghumResearch Conference (eds. H.D. Loden and D. Wilkinson).Washington, D.C., USA: American Seed TradeAssociation.DODD, J.L. 1980. The role of plant stresses in developmentof corn stalk rots. Plant Disease 64:533-537.DOUPNIK, B., Jr., and BOOSALIS, M.G. 1980.Ecofallow—a reduced tillage system—and plant diseases.Plant Disease 64:31 -35.DOUPNIK, B., Jr., BOOSALIS, M.G., WICKS, G.A., andSMIKA, D. 1975. Ecofallow reduces stalk rot in grainsorghum, Phytopathology 65:1021 -1022.DUNCAN, R.R. 1977. Characteristics and inheritance ofnonsenescence in Sorghum bicoior (L.) Moench. Ph.D.thesis, Texas A&M University, College Station, Texas,USA. 70 pp.DUNCAN, R.R., BOCKHOLT, A.J., and MILLER, F.R. 1981.Descriptive comparison of senescent and nonsenescentsorghum genotypes. Agronomy Journal 73:849-853.DUNCAN, R.R.,and SOWELL,G. 1983. The tandem associationbetween anthracnose and the fusarium complexin sorghum grown under Georgia environmental conditions.Page 74 in Proceedings of the 13th Biennial GrainSorghum Research and Utilization Conference, sponsoredby Grain Sorghum Producers' Association (GSPA)and Sorghum Improvement Conference of North America.Available from GSPA, Abernathy, Texas, USA.EDMUNDS, L.K., and ZUMMO, N. 1975. Sorghum diseasesin the United States and their control. U.S. Departmentof Agriculture Handbook No. 468. Washington, D.C.,USA: U.S. Government Printing Office, 47 pp.FARKAS, G.L. 1978. Senescence and plant disease.Pages 391-412 in Plant disease, an advanced treatise,

Vol.3: How plants suffer from disease (eds. J.G. Horsfalland E.B. Cowling). New York, New York, USA: AcademicPress.FLETCHER, R.A., and ADEDIPE, N.O. 1972. Hormonalregulation of leaf senescence in intact plants. Pages 571 -580 in Plant growth substances (ed. D.J. Carr). New York,New York, USA: Springer-Verlag.FLETCHER, R.A., and OSBORNE, D.J. 1965. Regulationof protein and nucleic acid synthesis by gibberellin duringleaf senescence. Nature 207:1176-1177.GARG, O.P., and KAPOOR, V. 1972. Retardation of leafsenescence by ascorbic acid. Journal of ExperimentalBotany 23:699-703.GOURLEY, L.M., ANDREWS, C.H., SINGLETON, L.L., andARAUJO, L. 1977. Effects of Fusarium moniliforme onseedling development of sorghum cultivars. Plant DiseaseReporter 61:616-618.HARADA, J., and NAKAYAMA, H. 1971. Chlorophyll degradationin leaf sections from tall and short varieties ofrice. Journal of Agricultural Science 76:573-574HARRIS, H.B., JOHNSON, B.J., DOBSON, J.W., Jr., andLUTTRELL, E.S. 1964. Evaluation of anthracnose on grainsorghum. Crop Science 4:460-462.HODGES, C.F., and MADSEN, J.P. 1978. The competitiveand synergistic interactions of Drechslera sorokinianaand Curvularia geniculata on leaf spot development onPoa prafensis. Canadian Journal of Botany 56:1240-1247.HODGES, C.F., and MADSEN, J.P. 1979. Leaf senescenceas a factor in the competitive and synergistic interactionsof Drechslera sorokiniana and Curvulariageniculata on Poa pratensis. Canadian Journal of Botany57:1706-1711.HOFFMAN, W.E. 1972. The relationship of amino acidpools, protein synthesis, proteinase activity, and tRNAmethylase activity in senescence of corn tissue. DissertationAbstracts 32:5016.HUBER, D.M. 1978. Disturbed mineral nutrition. Pages163-181 in Plant disease, an advanced treatise, Vol. 3:How plants suffer from disease (eds. J.G. Horsfall and E.B.Cowling). New York, New York, USA: Academic Press.JYUNG, W.H. 1975. A similarity between zinc deficiencyand senescence in navy bean leaves. AgronomyAbstracts 67:72.KATSANOS, R.A., and PAPPELIS, A.J. 1965. Seasonaltrends in density and cell death in sorghum stalk tissue.Phytopathology 55: 97-99.LEOPOLD, A.C. 1961. Senescence in plant development.Science 134:1727-1732.LEWIS, R.W. 1953. An outline of the balance hypothesis ofparasitism. American Naturalist 87:273-281.LEWIS, S.J., and DEACON, J.W. 1982. Effects of shadingand powdery mildew infection on senescence of the rootcortex and coleoptile of wheat and barley seedlings, andimplications for root- and foot-rot fungi. Plant and Soil69:401-411.McBEE, G.G., WASKOM, R.M., III, MILLER, F.R., andCREELMAN, R.A. 1983. Effect of senescence and nonsenescenceon carbohydrates in sorghum during late kernelmaturity states. Crop Science 23:372-376.MORTIMORE, C.G., and WARD, G.M. 1964. Root andstalk rot of corn in Southwestern Ontario, III: Sugar levelsas a measure of plant vigor and resistance. CanadianJournal of Plant Science 44:451-457.MOSS, D.N. 1962. Photosynthesis and barrenness. CropScience 2:366-367.NICHOLS, R. 1973. Senescence of the cut carnationflower: respiration and sugar status. Journal of HorticulturalScience 48:111-121.ODVODY, G.N., and DUNKLE, L.D. 1979. Charcoal stalkrot of sorghum: effect of environment on host-parasiterelations. Phytopathology 69:250-254.PAPPELIS, A.J., and KATSANOS, R.A. 1966. Effect ofplant injury on senescence of sorghum stalk tissue. Phytopathology56:295-297.PHILLIPS, I.D.J. 1971. Introduction to the biochemistryand physiology of plant growth hormones. New York, NewYork, USA: McGraw Hill Book Co.POTTER, J.R. 1971. The effect of senescence on proteinsynthesis and ribosomes in tobacco leaves. DissertationAbstracts 31:5210-5211.REED, J.E., PARTRIDGE, J.E., and NORDQUIST, P.T.1983. Fungal colonization of stalks and roots of grainsorghum during the growing season. Plant Disease67:417-420.SANCHEZ, J.N., and BETANCOURT, A. 1983. Reaction ofselected sorghum lines to fusarium stalk rot and headblight at El Bajio, Mexico. Pages 78-79 in Proceedingsof the 13th Biennial Grain Sorghum Research and UtilizationConference, sponsored by Grain Sorghum Producers'Association (GSPA) and Sorghum ImprovementConference of North America. Available from GSPA,Abernathy, Texas, USA.SCHOENEWEISS, D.F. 1975. Predisposition, stress, andplant disease. Annual Review of Phytopathology 13:193-211.SECOR, J., SHIBLES, R.,and STEWART, C.R. 1983. Metabolicchanges in senescing soybean leaves of similarplant ontogeny. Crop Science 23:106-110.SPENCER, P.W., and TITUS, J.S. 1972. Biochemical andenzymatic changes in apple leaf tissue during autumnalsenescence. Plant Physiology 49:746-750.108

THIMANN, K.V. (ed.). 1980. Senescence in plants. BocaRaton, Florida, USA: CRC Press. 276 pp.TRIMBOLI, D.S., and BURGESS, L.W. 1983. Reproductionof Fusarium moniliforme basal stalk rot and root rot ofgrain sorghum in the greenhouse. Plant Disease 67:891 -894.TRZEBINSKI. J., PAWELSKA-KOZINSKA, K., andWASAG, G. 1972. Studies on the correlation betweenchanges in chlorophyll content of the leaves of sugar beetand tolerance of virus yellows. Plant Breeding Abstracts42:No. 8500.TURNER, M.T. 1982. An update on corn diseases andtheir pathogens. Pages 190-205 in Proceedings of the37th Annual Corn and Sorghum Research Conference(eds. H.D. Loden and D. Wilkinson). Washington, D.C.,USA: American Seed Trade Association.VAN DER PLANK, J.E. 1968. Disease resistance in plants.New York, New York, USA: Academic Press. 206 pp.VARNER, J.E. 1961. Biochemistry of senescence. AnnualReview of Plant Physiology 12:245-264.WAREING, P.F., and SETH, A.K. 1967. Ageing and senescencein the whole plant. Pages 543-558 in Symposia ofthe Society for Experimental Biology, XXI. Aspects of thebiology of ageing. London, U.K.: Cambridge UniversityPress.WOOLHOUSE, H.W. 1967. The nature of senescence inplants. Pages 179-213 in Symposia of the Society forExperimental Biology XXI: Aspects of the biology of ageing.London, U.K.: Cambridge University Press.ZARTMAN, R.E., and WOYEWODZIC, R.T. 1979. Rootdistribution patterns of two hybrid grain sorghums underfield conditions. Agronomy Journal 71:325-328.QuestionsScheuring:How do you relate nonsenescence with juicy anddry-stem sorghums? If you admit that there existdry-stem nonsenescent sorghums, how do youdescribe such plants, since the cortical stem cellsare mostly senesced and dead? According toyours and forgoing discussions, such cells wouldbe vulnerable to colonization by pathogens.Duncan:I really have not been too concerned with whether Ihave juicy- or dry-stemmed nonsenescing sorghums,and we have found both types. Rosenow'swork with charcoal rot has shown basically no significantdifferences in disease ratings between thetwo types. How much actual difference in live anddead cortical stem cells exists between the twostem types in nonsenescing genotypes has notbeen researched to my knowledge. But that is notto say that differences do not exist and pathogeninteractions should not be an importantconsideration.Pande:What is the environmental situation under whichyou have identified lines with the nonsenescenttrait?Duncan:Normal field conditions in any breeding program,but the timing for making selections is at postphysiologicalgrain maturity. If some stress is involvedwith senescence, then the plants may deteriorateand die faster than normal.Pande:Do these lines show consistency for nonsenescenceover a period of time, location, andenvironment?Duncan:I have generally seen consistent reactions overlocations and environments under southeast USAconditions; timing is influenced by interactions withenvironmental stresses and plant genetics.Pande:What scale do you use for quick estimation of nonsenescentlines and the lines that do not showgreen leaves but show only pale green juicy stems.Duncan:After working with the overall nonsenescencecharacter for several years, I now use visual selectionof nonsenescing plants and include leaves,stems, and panicle in the consideration process.Stems and panicle are sometimes split for visualobservation—particularly where disease organisms(C. graminicola and Fusarium in my case)are involved.Henzell:You say that nonsenescence causes stress toleranceand relatively high carbohydrate levels in thestem. What evidence do you have for this causeand-effectrelationship, and would it not be more109

likely that the reverse (i.e., stress tolerance causesnonsenescence) is the case?Duncan:I stated that since nonsenescent genotypes supposedlyremain physiologically active during latestages of growth, this characteristic probably contributesto stress tolerance. I did not intend to sayanything about a cause and effect relationship. Thepoint was that an actively growing, physiologicallyactive plant with perennialistic tendencies may bebetter buffered to withstand stresses such asdrought or acid soils. The nonsenescent characteristicwould only be a portion of the tolerancemechanisms. Jordan has conducted heat anddesiccation tests between senescing and nonsenescinggenotypes and found that nonsenescenttypes were more tolerant to these stresses. I amfinding improved acid soil tolerance in nonsenescinggenotypes, and it is probably tied in with adynamic root system and efficiency in uptake ofmoisture and nutrients.Partridge:What did you mean by "postmaturity" relative toReed et al.? In our research we assume this to beequal to postfrost kill and felt it to be entirely differentfrom host-parasite interactions that existed inthe living host.Duncan:Postphysiological maturity was indeed the postfrostperiod. I agree that the host-parasite interactionsduring this period are probably different thanwhat occurs in the living host, but I was trying toportray the general pattern of disease development,contrasted to that which occurs after frost.The validity of the comparison could be extensivelydebated, but I still think that the trends areimportant.110

Morphological and Physiological FactorsAssociated with Stalk StrengthJ.W. Maranville and M.D. Clegg*SummarySubstantial yield losses occur in lodged crops due to mechanical and physiological alterations.Morphological factors associated with stalk strength reside primarily in the rind. Stalk elasticity,breaking strength, and plant height are somewhat associated with lodging tendency, but stalkdiameter, basal stalk weight, and rind thickness are highly associated. Rind penetrometervalues and crushing strength best integrate the contribution of morphological factors tolodging.Physiological factors contributing to stalk strength reside primarily in the pith. Factors thatenhance plant vigor and well-being contribute to greater stalk strength. Depletion of basal stalkcarbohydrates weakens the plant's ability to resist invasion by stalk rot organisms. Theinvolvement of nitrogen metabolism and enzymes in the breakdown of parenchyma tissue isnot well understood and needs further investigation.Sorghum (Sorghum bicolor (L.) Moench) is anexcellent example of the principle, "for a set ofprescribed biological functions, an organism hasthe optimum possible design with respect to economyof material used and energy expenditureneeded for the performance of the prescribed functions"(Rashevsky 1960). The sorghum stalk istapered throughout its length to maintain strengthin proportion to the load stress that generally isapplied by forces of wind, passage of machinery,and other disturbances. Certain characteristics ofthe stalk determine the degree to which the naturaltaper is effective in resisting the load that tends tolodge it. These are morphological and physiologicalfactors, many of which are inherent to the particulargenotype. However, among the mostimportant characteristics affecting stalk strength isthe plant's ability to withstand, directly or indirectly,the invasion of stalk rot diseases. The followingdescribes some of the plant characteristics mostoften associated with stalk strength, and discussestheir involvement in resistance to lodging.Lodging Effects onYield and QualityThere is general agreement that yield losses fromlodging are due primarily to a disruption in photosynthesisand translocation coupled with mechanicaldifficulties in harvesting the crop. Yieldreductions are more severe if lodging occurs early.As much as 35% of the yield of winter wheat (Triticumaestivum L.) can be lost if lodging occurseither 1 to 2 weeks before heading or 1 to 2 weeksafter heading. This loss is reduced to about 15% iflodging occurs at or just prior to heading (Laudeand Pauli 1956). Weibel and Pendleton (1964)found progressively less yield reduction in wheatfrom heading to the hard dough stages, although upto 12% yield was still lost when lodging occurred atthe hard dough stage. These trends have beensubstantiated in other crops such as maize (Zeamays L.) (Fisher and Smith 1960), barley (Hordeumvulgare) (Day 1957), oats (Avena sativa) (Pen-*Professor and Associate Professor, Department of Agronomy, University of Nebraska, Lincoln, NE 68583-0817, USA,International Crops Research Institute for the Semi-Arid Tropics. 1984. Sorghum Root and Stalk Rots, aCriticalReview: Proceedings of the Consultative Group Discussion on Research Needs and Strategies for Control ofSorghum Root and Stalk Rot Diseases, 27 Nov - 2 Dec 1983, Bellagio, Italy. Patancheru, A.P. 502 324, India:ICRISAT.111

dleton 1954), and sorghum (Larson and Maranville1977).Studies with sorghum in which plants were artificiallylodged indicated that the severity of lodging,as well as the time it occurred, is important to themagnitude of yield reduction (Larson and Maranville1977). Yield was reduced 18% when plantswere lodged at heading by manually forcing overand holding them in place, while breaking the stalkat the same growth stage resulted in a 31 % loss.Progressively less difference in yield reductionoccurred between the two methods the later thetreatments were imposed. Nonetheless, up to 13%yield reductions can occur in sorghum if lodgingoccurs due to stalk breakage as late as the softdough stage, and reductions could reach as highas 30% at this growth stage due to disruption inmetabolism alone. At the hard dough stage, yieldlosses ranged from 0% to 26%.Alterations in grain protein content also occur inlodged grain crops. Generally, the protein concentrationis increased (Laude and Pauli 1956, Esechie1975, Larson and Maranville 1977), probablybecause of interference with carbohydrate assimilation.Protein in cereal grains originates largelyfrom nitrogen, which is accumulated in the foliageprior to heading (Mulder 1954). High grain proteinconcentrations therefore arise from decreasedcarbohydrate deposition, which normally tends todilute protein levels during the grain-fill period.Total protein on a per-area basis, however, is generallyless in lodged portions of a field (Laude andPauli 1956, Larson and Maranville 1977). This is,therefore, another critical loss that is of economicimportance.Morphological Factorsand Stalk StrengthElasticity of the stalk and its resultant breakingstrength are two parameters that have been usedto determine lodging characteristics of somecrops. An instrument for testing the breakingstrength of straw was used in very early researchstudies (Helmick 1915), and its use was later proposedas a means to form a lodging index (Salmon1931). Varying results have been obtained usingbreaking strength as a parameter to judge lodgingtendency. Davis and Stanton (1932) obtained relativelygood agreement between standing ability inoats and breaking strength. Clark and Wilson(1933), however, found no correlation in severalsmall grains, and McAuley (1973) found no correlationbetween breaking strength and lodging insorghum. Breaking strength is apparently dependenton maturity and environmental conditions (Bartel1937).Suggs et al. (1962) were among the first to applycantilever beam techniques to stalks in an attemptto characterize their elasticity. The modulus ofelasticity in several sorghum types was determinedusing a two-point beam-loading technique (Bashfordet al. 1976). This technique involved measurementof the force needed to bend the stalk a certainpredetermined deflection distance. The modulus ofelasticity was calculated from the bending momentequation derived from beam theory. This studyfound that stalk elasticity was not well associatedwith apparent standability in the field. When thestalk was deflected by the instrument until it failed(breakage) there was some correlation. Thosesorghums classified as having a stiff stalk (morelodging-resistant) required more force to effect ,stalk failure. Plants acquired their maximum lodgingresistance somewhere between the dough andphysiological-maturity growth stages if diseasewas not prevalent. The stalk was shown to bestrongest at the base, due, for the most part, to thecontribution of the sheath. Esechie et al. (1977)reported that the weakest point on the sorghumstalk was the top internode immediately below thepanicle. Other work, however, indicated that therewas little difference in bending moment at stalkfailure between the peduncle and the top node(Bashford et al. 1976).Many morphological factors are associated withlodging tendency or resistance, with no single onebeing consistent enough to use in classifyingplants in every situation. Plant height is an exampleof one characteristic related to lodging tendency.Sorghums prone to lodging tend to be taller thanthose that are lodging-resistant (Esechie et al.1977, Bashford et al. 1976). Plant height is so subjectto environmental factors, however, that its useas an index for isolating genotypes should be on arelative basis only. Any consideration of plantheight as a factor in lodging must not overlook theeffect of culm length x maturity interaction (Pinthus1973). An early, short-stalk genotype close tomaturity may be more prone to lodging than a late,long-stalk genotype that at the same time has onlyattained the heading or early dough stage.The relationship between lodging and culm anatomy,particularly that of the basal internodes, hasbeen extensively investigated. Larger basal stalk112

diameters have been consistently correlated withlodging resistance in sorghum (Esechie et al.1977), maize (Twumasi-Afriyie and Hunter 1982),and other small grains (Brady 1934, Hamilton1941). This was also a characteristic of nonsenescentsorghums, which tend to resist lodging (Duncanet al. 1981). Similarly, the weight of a cutsection of stalk can be correlated with lodging.Generally, a basal section is used, although otherportions are satisfactory. Zuber and Grogan (1961)found a correlation of r = -0.73 between lodgingand weight of a second internode of maize. Investigationswith sorghum showed an r = -0.59 correlationbetween lodging and the weight of a basalintemode section, and r = -0.56 between lodgingand the weight of the peduncle node. Stalk sectionweight was better correlated with rind thickness inmany studies, whether rind thickness was determinedmechanically (Twumasi-Afriyie and Hunter1982) or by using the weight/circumference calculation(Esechie 1975, McAuley 1973).Chang et al. (1976) concluded that stalk strengthin maize resides principally in the rind tissue, andthat rind characteristics are better indicators ofstalk strength than those associated with the pith.This view is not shared by all researchers in thefield. Nonetheless, the apparent importance of rindcharacteristics to lodging has led to the use of rindpuncture methods to evaluate the lodging potentialof plants. A penetrometer is often used, and themeasure is determined as force in kilograms forrind penetration to occur (Thompson 1969). Acorrelation coefficient of r =-0.79 for rind punctureand lodging found by Twumasi-Afriyie and Hunter(1982) in maize is typical of the association generallyshown. The method is useful in that it is nondestructiveand obtained quickly at any plantgrowth stage.Rind thickness, which undoubtedly influences orpossibly accounts for rind penetration values,correlates well with plant lodging, but not as well assome other factors. Research in maize showed acorrelation of r= -0.53 between lodging and rindthickness (Twumasi-Afriyie and Hunter 1982).Correlation of lodging with a rind thickness approximationused by Esechie et al. (1977) in sorghumwas only slightly better (r = -0.61). The practicalimportance of rind thickness in maize was quantifiedby Thompson (1963). For every 1.56%increase in lodging due to increases in plant population,rind thickness decreased 0.02 mm. Indirectlyselecting for lodging resistance in anothermaize study resulted in an increase in rind thicknessof 0.09 mm after the fourth selection cycle(Zuber 1973).A method for determining stalk strength that integratesseveral stalk characteristics was developedby Zuber and Grogan (1961). Five-cm stalk sectionswere crushed with a hydraulic press, and theforce required was determined. This "crushingstrength" method has been used extensively inmany lodging studies and is highly correlated withanatomical characteristics associated with lodgingscores, and therefore with lodging per se. The highestcorrelation appeared to be with stalk sectionweight (Zuber and Grogan 1961), although itsassociation with rind thickness, rind weight, andeven rind lignification was strong (Chang et al.1976). The selection of genotypes of maize basedsolely on increased crushing strength resulted in alinear increase in stalk weight, rind thickness, rindpuncture, decreased stalk lodging, and very importantly,improved diplodia stalk rot ratings (Zuber1973).An anatomical feature that appears to have adistinct relationship with lodging is the number ofvascular bundles in the culm. A high number ofvascular bundles has been found in strong stalks ofcereals such as oats (Hamilton 1951) and maize(Chang et al. 1976). There appears to be a similarrelationship in sorghum (Esechie and Maranville,unpublished data, 1977), although this was notconfirmed with actual counts. Hamilton (1951) suggestedthat the number of bundles was directlyassociated with culm diameter, and therefore onlyindirectly with lodging tendency. Correlations ofr = 0.77 between the number of vascular bundlesand the stem diameter in maize have been reported(Martin and Hershey 1934). Positioning of the vascularbundles may be more important. If vascularbundles are considered as giving support to thestem, then bundles that are positioned closetogether and concentrated near the outside of thestem would give added strength. According toHamilton (1951), who compared these factors inwheat and oats, denseness and outside positioningof vascular bundles were major factors in givingwheat superior lodging resistance. Chang et al.(1976) were able to increase the number of vascularbundles in maize by selection for increasedcrushing strength of the stalk, However, this selectioncriterion also increased stalk size and weight.It would appear that several morphological characteristicscontribute to stalk strength, many ofwhich reside in the rind. Crushing strength seemsto integrate these factors best, and this selection113

114criterion has been received favorably byresearchers in the field. Interestingly, in one study,crushing strength of stalks gave a better measureof stalk rot response in infected plants than did rindthickness (Loesch et al. 1962). A selection indexbased on a measure of crushing strength in artificiallyinfected plants might be useful in obtaininggenotypes resistant to the weakening effects ofstalk rot organisms, such as Diplodia maydis inmaize.Physiological Factorsand Stalk StrengthPhysiological factors that contribute to stalkstrength are as numerous, or more numerous, thanthe morphological factors discussed in the previoussection. These factors appear to reside morein the pith tissue than in the rind, but not exclusivelyso. Moreover, the physiological factors associatedwith stalk strength are those that have been associatedwith stalk rot resistance. Some factors, suchas certain cellular constituents, appear to be associatedwith anatomical structure. However, there ismounting evidence that the physiological factorswhich make the greatest contribution to stalkstrength do so by influencing, being directlyresponsible for, or being associated with the overallwell-being of the plant. The following will dealbriefly with anatomical influences, and then withthe more controversial aspects of plant vigor.One of the very early views was that the amountof silica in cells of the culm could determine thelodging tendency of cereals. Davidson and Phillips(1930), however, found more silica and ash inlodging-susceptible wheat than in wheat that waslodging-resistant. Hamilton (1941) concluded thatsilica offered no possibility as an indexto lodging incereals.A deficiency in lignin was considered to be thecause of lodging by some researchers (Welton andMorris 1931). They contended that lignin lentmechanical support to the stalks. Others had contrastingviews (Davidson and Phillips 1930, Hamilton1941 ); their work showed that high rather thanlow lignin contents were associated with lodging.The evidence was so strong in one instance thatselecting for culms with low lignin was proposed asbeing a useful index in breeding for lodging resistance(Hamilton 1941). According to this view, highlignin contents made the culm brittle, and it wasimportant to maintain some degree of elasticity instalks during the selection process, High lignincontents, however, were also associated with highcrushing strength values (Chang et al. 1976), whichhave been strongly associated with lodgingresistance.Stalk mineral content was investigated as adeterminant in lodging tendency for some crops.The element potassium (K) perhaps received themost attention in speculations that it exerted adirect influence on stalk structural components. Apositive correlation between K content and lodgingwas reported by Boswell and Parks (1957) andLeibhardt and Murdock (1965). In contrast, thework of Zuber and Loesch (1966) in maize andEsechie et al. (1977) in sorghum showed that highK values were associated with lodging-prone genotypes.These contrasting views regarding therelationship of K to stalk strength are not surprising,since this element is neither a permanent constituentof the plant nor is it laid down as a part of anyspecific compound. A deficiency of K can apparentlylead to a breakdown in stalk tissue (Liebhardtand Munson 1976) by a direct effect on the parenchyma(Liebhardt et al. 1968). The mechanism bywhich this occurs is thought to be a polar translocationof carbohydrates from the basal stalk portionsto sinks further up the stalk, which triggers parenchymabreakdown in these basal portions. Sincephotosynthate movement and velocity are limitedin the leaves of K-deficient plants (Hart 1969), andtheir lower leaves are an insignificant source ofphotosynthate (Moss and Peaslee 1965), a greaterportion of carbohydrate stored in the lower stalks ofK-deficient plants must be mobilized to fill thedemands of the developing inflorescence or ear.This exhaustive translocation from the lower stalksand roots results in parenchyma breakdown, producinga weaker, lodging-susceptible plant (Liebhardtet al. 1968). Leaf removal has been shown toinduce parenchyma breakdown and typical K-deficient symptoms relating to kernel formation(Liebhardt et al. 1968). These implications may bevaluable in stalk rot studies. For example, high Klevels have been shown to have significant effectsin reducing the incidence of stalk and root rot inmaize (Parker and Burrows 1959).A thorough understanding of the physiologicalphenomenon of pith deterioration should help toexplain aspects of maintaining plant vigor and, veryimportantly, plant reaction to stalk and root rots.Pith condition indices have been developed andused to determine stalk strength (Pappelis and Katsanos1965). The pith rating method has been pop-

ular in stalk rot studies, but its use is not confined tothe incidence of disease infestations. Sorghum, forexample, showed a marked difference in pith conditionbetween lodging-prone and lodgingresistantgenotypes at late stages of growth whendisease was not present (Figure 1). Pith conditionratings were associated with the percentage of livetissue whose cells appeared turgid and hydrated.Pappelis and Smith (1963) demonstrated that pithmoisture content on a volume basis was related tostalk rot incidence, and was most likely a directresult of a high percentage of live, turgid tissue inthe stalk. Their histological observations indicatedthat the spread of Diplodia zeae was limited to deadcells, and that inherent susceptibility was related tothe extent of the dead cells in the stalk. Spread ofthis disease was inhibited by live tissue.Observations such as these have striking implications.Any phenomena, whether natural or artificial,that maintain living tissue in stalks shouldresult in superior stalk quality and reduce thedeleterious effects of rot infestations. Esechie et al.(1977) concluded that lodging-resistant sorghumgenotypes appeared to be more perennial innature, and thus were more resistant to postfreezesenescence than susceptible types. Nonsenescentgenotypes studied by Duncan et al. (1981)were more disease-, drought-, and lodgingresistantthan their senescent counterparts. Anyfactor that enhances the rate of cell death in thestalk increases the plant's susceptibility to disease(Pappelis 1963). Pith condition ratings based onthis premise were developed for several crops inrot studies (Katsanos and Pappelis 1965, Pappelisand Katsanos 1965).Depletion of carbohydrates at maturity appearsto be associated with susceptibility to lodging incrops (Mortimore and Ward 1964, Esechie et al.1977). Maranville (1974) suggested that carbohydratecontent may be only an indirect indication ofthe healthiness and vigor of a plant rather thanhaving a direct relationship to lodging. Certainly,any stress (moisture or mineral, for example)directly affects the plant's well-being. Under idealconditions, plants manufacture sufficient carbohydrateto meet the requirements of both the inflorescenceand the plant, but under stress conditionsthat restrict photosynthesis or alter any of the subsequentprocesses of carbohydrate metabolism,the amount of carbohydrate produced becomesinsufficient to satisfy all demands. Under these circumstances,the requirements of a developinginflorescence are met first, resulting in reduction ofstalk sugar levels. This, apparently, is why weakstalks and stalk rot susceptibilities are more prevalentunder stress. Mortimore and Ward (1964) foundthat by artificially inducing stress, they decreasedtotal sugars in maize stalks at physiological matur-Figure 1. Left, strong: transverse section of the basal stalk of lodging-resistant sorghum linesKS19 x KS21. Right, weak: transverse section of the basal stalk of lodging-susceptible sorghum linesKS21xTX414.115

ity, with a subsequent increase in the incidence ofstalk rot. Stalk rot never occurred, or was minimal,in stalks of a susceptible plant whose sugar levelswere artificially boosted to the same levels as thoseof rot-resistant plants. The relationship of stresscarbohydrateinteractions to disease susceptibilityhas been named the "photosynthetic stresstranslocationbalance (PSTB)'' concept. This concepthas been proposed for both maize (Dodd1977, 1980a) and sorghum (Dodd 1980b), anddeveloped around the hypothesis that predispositionof stalk rot is associated with a carbohydrateshortage in root and lower stalk tissue, which iscaused by the combination of reduced photosynthesisand a translocation of carbohydrate to thedeveloping kernel. This weakens the tissue andallows invasion of rot organisms.Nitrogen/carbohydrate ratios may be importantin stalk quality, as suggested in early work byDeTurk et al. (1937). A decrease in soluble proteinoccurs during parenchyma breakdown (Liebhardt1968), suggesting an internal degradation ofenzymes that is directly associated with senescencein some manner. Aside from inadequatecarbohydrate, a lack of sufficient enzymatic materialneeded for normal metabolism and synthesisreactions would also result in loss of plant vigor.Zuber et al. (1981) showed that the rind tissue wasweakened after invasion by stalk rot. They wereuncertain, however, whether this was a result ofdirect weakening due to enzyme degradation orindirect weakening due to loss of vigor andphotosynthate-producing capacity. The formerwould not necessarily indicate loss of enzymes, butthe initiation of a degradation system. Esechie et al.(1977) found that lodging-resistant sorghums hadlower stalk protein concentrations than susceptibleones in a disease-free environment. They concludedthat a direct relationship between lodgingresistance and stalk protein seemed unlikely. Perhapschanges in protein and enzyme functions onlyappear when stalk rot or other stresses areprevalent.Future Research PrioritiesConsiderable research has been conducted onelucidating the morphological and physiologicaltraits associated with the stalk strength of severalcrops. Many of these investigations have dealtdirectly with the relationship of this factor to stalkrots. Since this relationship has not been fully clarified,future research should be conducted in thefollowing areas:1. Determining the exact influence of yield andmaturity on inheritance and genetic stability ofstalk strength.2. Comparing a broader range of morphologicallyand physiologically different genotypesfor stalk strength characters. A genotype witha high degree of stalk elasticity might be comparedto one with a very stiff stalk, and thesethen evaluated for standability in the presenceof stalk rot.3. Elucidating the chemical and structuralchanges that occur in stalks when environmentalstress is present.4. Integrating studies on the senescence ofleaves, stalks, and roots to better clarify itsrelationship to the incidence of stalk rot.5. Determining the relationship of nitrogenmetabolism to physiological factors influencingstalk quality and stalk rot reaction.ReferencesBARTEL, A.T. 1937. Changes in breaking strength ofstraw from heading to maturity. Journal of the AmericanSociety of Agronomy 29:153-156.BASHFORD, L.L., MARANVILLE, J.W., WEEKS, S.A., andCAMPBELL, R. 1976. Mechanical properties affectinglodging of sorghum. Transactions of the AmericanSociety of Agricultural Engineers 19:962-966.BOSWELL, F.C., and PARKS, W.L. 1957. The effects ofsoil K levels on yield, lodging and mineral composition ofcorn. Soil Science Society of America Proceedings21:301-305.BRADY, J. 1934. Some factors affecting lodging incereals. Journal of Agricultural Science 24:209-232.CHANG, H.S., LOESCH, P.J., and ZUBER, M.S. 1976.Effects of recurrent selection for crushing strength onmorphological and anatomical stalk traits in corn. CropScience 16:621-625.CLARK, E.R., and WILSON, H.K. 1933. Lodging in smallgrains. Journal of the American Society of Agronomy25:561-572.DAVIDSON, J., and PHILLIPS, M. 1930. Lignin as a possiblefactor in lodging in cereals. Science 72:401 -402.DAVIS, L.L., and STANTON, T.R. 1932. Studies on the116

eaking strength of oat varieties at Aberdeen, Idaho.Journal of the American Society of Agronomy 24:290-300.DAY, A.D. 1957. Effect of lodging on yield, test weight, andother seed characteristics of spring barley grown underflood irrigation as a winter annual. Agronomy Journal49:536-539.DeTURK, E.E., EARLY, E.B., and HOLBERT, J.L. 1937.Resistance of corn hybrids related to carbohydrates.Pages 43-45 in Illinois Agricultural Experiment StationAnnual Report No. 49. Urbana, Illinois, USA: University ofIllinois.DODD, J.L. 1977. A photosynthetic stress-translocationbalance concept of corn stalk rot. Pages 122-130 in Proceedingsof the 32nd Annual Corn and SorghumResearch Conference (eds. H.D. Loden and D. Wilkinson).Washington, D.C., USA: American Seed TradeAssociation.DODD, J.L. 1980a. Grain sink size and predisposition ofZea mays to stalk rot. Phytopathology 70:534-535.DODD, J.L. 1980b. The photosynthetic stresstranslocationbalance concept of sorghum stalk rots.Pages 300-305 in Sorghum Diseases, a World Review:Proceedings of the International Workshop on SorghumDiseases, sponsored jointly by Texas A&M University(USA) and ICRISAT. Patancheru, A.P. 502 324, India:ICRISAT.DUNCAN, R.R., BOCHOLT, A.J., and MILLER, F.R. 1981.Descriptive comparison of senescent and nonsenescentsorghum genotypes. Agronomy Journal 73:849-853.ESECHIE, H.A. 1975. Studies of physiological, morphological,and anatomical aspects of lodging in grainsorghum [Sorghum bicolor (L.) Moench]. Ph.D. thesis,University of Nebraska, Lincoln, Nebraska, USA. 145 pp.ESECHIE, H.A., MARANVILLE, J.W., and ROSS, W.M.1977. Relationship of stalk morphology and chemicalcomposition to lodging resistance in sorghum. CropScience 17:609-612.FISHER, F.L, and SMITH, O.E. 1960. The influence ofnutrient balance on yield and lodging of Texas Corn No. 8.Agronomy Journal 52:201 -204.HAMILTON, D.G. 1941. Certain oat culm characteristicsand their relationship to lodging. Science of Agriculture21:646-676.HAMILTON, D.G. 1951. Culm, crown and root developmentin oats as related to lodging. Science of Agriculture31:286-315.HART, C.E. 1969. Effect of potassium deficiency upontranslocation of C 14 in attached blades and entire plants ofsugarcane. Plant Physiology 44:1461-1469.HELMICK, B.C. 1915. A method for testing the breakingstrength of straw. Journal of the American Society ofAgronomy 7:118-120.KATSANOS, R.A., and PAPPELIS, A.J. 1965. Seasonaltrends in density and cell death in sorghum stalk tissue,Phytopathology 55:97-99.LARSON, J.C., and MARANVILLE, J.W. 1977. Alteration ofyield, test weight, and protein in lodged grain sorghum.Agronomy Journal 69:629-630.LAUDE, H.H., and PAULI, A.W. 1956. Influence of lodgingon yield and other characteristics in wheat. AgronomyJournal 48:452-455.LIEBHARDT, W.C. 1968. Effect of potassium on carbohydratemetabolism and translocation. Pages 147-166 inThe role of potassium in agriculture (eds. V.J. Kilmer, S.E.Younts, and N.C. Brady). American Society of Agronomy(ASA) Publication. Madison, Wisconsin, USA: ASA.LIEBHARDT, W.C., and MUNSON, R.D. 1976. Effect ofchloride and potassium on corn lodging. Agronomy Journal68:425-426.LIEBHARDT, W.C., and MURDOCK, J.T. 1965. Effect ofpotassium on morphology and lodging of corn. AgronomyJournal 57:325-328.LIEBHARDT, W.C., STANGEL, P.J., and MURDOCK, J.T.1968. A mechanism for premature parenchyma breakdownin corn (Zea mays L). Agronomy Journal 60:496-499.LOESCH, P.J., Jr., CALVERT, O.H., and ZUBER, M.S.1962. Interactions of Diplodia stalk rot and two morphologicaltraits associated with lodging of corn. CropScience 2:469-472.MARANVILLE, J.W. 1974. What's new in sorghum physiology.Pages 22-28 in Proceedings of the 29th AnnualCorn and Sorghum Research Conference (ed. D.Wilkinson).Washington, D.C., USA: American Seed TradeAssociation.MARTIN, J.N., and HERSHEY, A.L. 1934. The ontogeny ofthe maize plant: The early differentiation of stem and rootstudies and their morphological relationships. Iowa StateCollege Journal of Science 9:489-503.McAULEY, R.L. 1973. The effects of potassium on stressinducedstalk lodging in grain sorghum. M.Sc. thesis, KansasState University, Manhattan, Kansas, USA.MORTIMORE, C.G., and WARD, G.M. 1964. Root andstalk rot of corn in southwestern Ontario, III: Sugar levelsas a measure of plant vigor and resistance. CanadianJournal of Plant Science 44:451-457.MOSS, D.N., and PEASLEE, D.E. 1965. Photosynthesis ofmaize leaves as affected by age and nutrient status. CropScience 5:280-281.MULDER, E.G. 1954. Effect of mineral nutrition on lodgingof cereals. Plant and Soil 5:246-306.PAPPELIS, A.J. 1963. Increased stalk rot susceptibility in117

com following root and leaf injury. Phytopathology 53:24(abstract).PAPPELIS, A.J., and KATSANOS, R.A. 1965. An approachto the study of the physiology of senescence and parasitismin sugar cane. Phytopathology 55:620-622.PAPPELIS, A.J., and SMITH, F.G. 1963. Relationship ofwater content and living cells to spread of Diplodia zeae incorn stalks. Phytopathology 53:1100-1105.PARKER, D.T., and BURROWS, W.C. 1959. Root and stalkrot in corn as affected by fertilizer and tillage treatment.Agronomy Journal 51:414-417.PENDLETON, J.W. 1954. The effect of lodging on springoats yields and test weight. Agronomy Journal 46:265-267.PINTHUS, M.J. 1973. Lodging in wheat, barley, and oats:The phenomenon, its causes, and preventative measures.Advances in Agronomy 25:209-263.RASHEVSKY, N. 1960. Mathematical biophysics, Vol. I.New York, New York, USA: Dover Publications. 293 pp.SALMON, S.C. 1931. An instrument for determining thebreaking strength of straw and a preliminary report on therelation between breaking strength and lodging. Journalof Agricultural Research 43:75-82.SUGGS, C.W., BEEMAN, J.F., and SPLINTER, W.E. 1962.Physical properties of tobacco stalks: Part I. Cantileverbean properties. Tobacco Science 6:146-151.THOMPSON, D.L. 1963. Comparative strength of cornstalk internodes. Crop Science 3:384-386.THOMPSON, D.L. 1969. Selection for stalk quality in corn.Pages 7-14 in Proceedings of the 24th Annual Corn andSorghum Research Conference (eds. J.I. Sutherland andR.J. Falasca). Washington, D.C., USA: American SeedTrade Association.Plant Disease 65:719-722.ZUBER, M.S., and GROGAN, C.O. 1961. A new techniquefor measuring stalk strength of corn. Crop Science 1:378-380.ZUBER, M.S., and LOESCH, P.J. 1966. Total ash andpotassium content of stalks as related to stalk strength incorn (Zea mays L). Agronomy Journal 58:426-428.QuestionsDoupnik:By stalk strength, or standability, are you suggestingthat those genotypes with good (high) resistanceto breakage are also more resistant to stalkrot diseases? Some genotypes with severe stalk rotdisease development can stand very well due torind strength (structural). Isn't this possible?Maranville:The evidence in the literature indicates a verystrong association between high resistance tobreakage and less incidence of disease infection. Idon't know the reason for this strong association—perhaps it's indirect. Your premise that plants canstand in the field even when severely diseased dueto favorable morphological characteristics certainlyshould be true. We see in literature, however,that favorable morphological characteristics arenot conducive to severe disease incidence.TWUMASI-AFRIYIE, S., and HUNTER, R.B. 1982. Evaluationof quantitative methods for determining stalk qualityin short-season corn genotypes. Canadian Journal ofPlant Science 62:55-60.WEIBEL, R.O., and PENDLETON, J.W. 1964. Effect ofartificial lodging on winter wheat grain yield and quality.Agronomy Journal 56:487-488.WELTON, F.A., and MORRIS, V.H. 1931. Lodging in oatsand wheat. Ohio Agricultural Experiment Station BulletinNo. 471. Columbus, Ohio, USA: Ohio State University.ZUBER, M.S. 1973. Evaluation of progress in selection forstalk quality. Pages 110-122 in Proceedings of the 28thAnnual Corn and Sorghum Research Conference (ed. D.Wilkinson). Washington, D.C., USA: American Seed TradeAssociation.ZUBER, M.S., AINSWORTH, T.C., BLANCO, M.H., andDARRAH, L.L. 1981. Effect of anthracnose leaf blight onstalk rind strength and yield in F 1 single crosses in maize.118

Relation of Senescence, Nonsenescence,and Kernel Maturity to Carbohydratesand Carbohydrate Metabolism in SorghumG.G. McBee*SummaryThe sorghum plant produces high levels of carbohydrates. Senescence, nonsenescence, andstage of kernel maturity have been shown to significantly influence concentrations of sucrose,glucose, fructose, and starch within the plant. This paper presents a brief review of factorsaffecting senescence, cell changes, and the associated role of growth regulators. Studies oncarbohydrate production among cultivars varying in rate of senescence are also summarized.Cultivars that are slower in senescing ha ve produced significantly higher levels of all the abovecarbohydrates for relative maturity stages of the plants. This factor also appears to beassociated with improved yields, but more research over a wider land area and longer period oftime is suggested to confirm these findings. Patterns of sugar accumulation within the stemsvary during grain filling; some cultivars exhibit a decrease from anthesis to black layer, and thenrestoration of the stem sugars occurs. Tentative data indicate that sorghum for grain may alsocontain a higher percentage of structural cat bohydrates than forage types. These differences,plus the variations in accumulation patterns for the carbohydrates, may be critical to studies onpathogenesis and represent an area where more research is needed.The sorghum plant (Sorghum bicolor[L.] Moench)produces tissue composed of high percentages ofcarbohydrates. By careful attention to management,including specific cultivar selection and culturalmodifications, it is possible to significantlyinfluence the structural and nonstructural carbohydratecomposition within the plant. Due toincreased interest in use of the biomass for energy,more attention has been directed to the levels andtypes of carbohydrates produced by cultivars.Because of the association between higher nonstructuralcarbohydrate content in stems (primarilysucrose, glucose, and fructose) and potentiallyincreased grain yields (McBee et al. 1983), breedersare devoting more attention to developing cultivarswith sweeter stems. This may altersusceptibility or resistance of sorghum plants to thevarious pathogens attacking them. These changesin stem carbohydrate content warrant attention,since "all plant pathogens have the ability to producepolysaccharide-degrading enzymes" (Albersheimand Anderson-Prouty 1975).Two factors that appear to influence levels ofnonstructural sugars within the stems are theinherent rate of progressive senescence and stageof kernel maturity at the time of sampling. Sinceplants senesce in various ways, the process shouldbe defined. Bidwell (1979) defines senescence as"the latter part of the developmental process,which leads from maturity to the ultimate complete*Professor of Plant Physiology, Department of Soil and Crop Sciences, Texas A&M University, College Station, TX 77843-2474, USA.International Crops Research Institute for the Semi-Arid Tropics. 1984. Sorghum Root and Stalk Rots, a CriticalReview: Proceedings of the Consultative Group Discussion on Research Needs and Strategies for Control ofSorghum Root and Stalk Rot Diseases, 27 Nov - 2 Dec 1983, Bellagio, Italy. Patancheru, A.P. 502 324, India:ICRISAT.119

120loss of organization and function." Further, he describestypes of senescence, particularly progressivesenescence where older parts of the plants diewhile the younger parts in the juvenile stage remainactive. This appears to be the type that typifiessorghum. "Reduced progressive senescence"would, then, more accurately describe thosesorghums referred to as nonsenescent.then be regarded as a delay in senescence, or adelay in the physiological processes of senescence,which are discussed later. This effect wouldbe much less significant for adapted cultivarslocated at increased distances from the equator,since the plants have tended to become lessphotoperiod-sensitive.Mineral NutritionEnvironmental and Other FactorsInfluencing SenescenceThere are several factors that may influence normal,regulated plant senescence. These should bedistinguished from the normal changes that occuras the plant matures or abnormal changes due togenetic inheritance. Such factors include light,mineral nutrition, temperature, water, pathogens,insects, physical restrictions, growth regulators,and wind. These factors will be briefly discussed,primarily in relation to monocots. Investigatorsshould be careful to consider them when ratingsorghum for the degree or completeness ofsenescence.LightQuality, duration, and intensity of light affect senescence(Thomas and Stoddart 1980). Plants aresensitive to changes in the quantity of light, andcontinued darkness results in chlorophyll loss orelse the failure to synthesize it. Light delays leafsenescence (Thimann et al. 1977) and probablyexerts its effect by photoproduction of adenosinetriphosphate.Phytochrome may also have aneffect on the tendency to senesce. Red lightappears to delay senescence, whereas illuminationwith far-red light overcomes this effect, thusimplicating phytochrome (Beevers 1976, Mishraand Pradhan 1973). Additionally, sensitivity to photoperiodis a contributing factor. Schwabe (1970)has shown that senescence rates in Kleinia spp aredetermined by the daylength prevailing during earlygrowth; daylengths adverse to flowering tended toenhance senescence. The reverse has beenobserved to occur in photoperiod-sensitive sorghums,which tend to be short-day plants (Martin1970, p 18). Photoperiods that are either too shortor too long to induce flowering tend to stimulatevegetative growth. The delay in flowering couldThe effect of mineral nutrition level is closelyrelated to the growth, development, and maturity ofthe plant. Deficiencies often result in chlorophylldegradation, subsequent necrosis, and perhapssenescence. Initially, it was suggested by Molisch(in Bidwell 1979) that nutritional deficiencies maybe the cause of senescence, but later studies havenot supported this theory. Since certain elements,such as nitrogen, phosphorus, and potassium, aremobile (Williams 1955) and may be translocatedfrom old to younger tissue within the plant, senescencewithin those particular tissues may occurearlier than normal as a result of translocation or ofthe deficiency. Additionally, senescence occurs inannual plants such as maize (Zea mays L) aftergrain maturity, even when large applications of fertilizerhave been previously applied.TemperatureSince most plants can be characterized as exhibitingoptimum growth within a certain range oftemperatures, high or low extremes result inadverse effects. Frierabend and Mikus (1977) havenoted that supraoptimal temperatures tend toinhibit chloroplast ribosome synthesis. Thomasand Stoddart (1980) have proposed that althoughheat stress may not be the total reason for senescence,it can adversely affect various pathways,producing effects typical of aging. Sullivan andRoss (1979) have noted that direct hightemperatureinjury occurs even in relatively tolerantcrops such as sorghum. Such injury could thenbe expected to contribute to premature, localized,or partial senescence.WaterDrought resistance and water relations in sorghumhave been discussed by Blum (1979). At critical

levels of moisture stress, stomata close (Turnerand Begg 1973) and growth approaches zero.Upon watering, growth resumption depends on therecovery potential of that genotype. Prematuresenescence and leaf firing may occur, thus suggestingthat progressive senescence is alsorelated to the drought resistance of the sorghumgenotype. Inherent drought resistance and the varyingdegrees of drought to which the plant has beensubjected must both be considered when evaluatingplants for progressive senescence.PathogensAttack by bacteria or viruses may result in eitherreduced or accelerated senescence of plants. Asis known, symptoms may range from small, green,photosynthetic areas ringed by chlorotic haloes(Shaw 1963, Wood 1967, pp 393-397) to large,necrotic areas. Wheeler (1975) states that plantpathogens may employ enzymes, growth regulators,or toxins in pathogenesis. Both Wheeler(1975) and Albersheim and Anderson-Prouty(1975) present evidence that plant pathogens canproduce polysaccharide-degrading enzymes. Infact, the latter authors state that together theseenzymes can degrade all known glycosidic linkagesoccurring in primary plant cell walls.Reduced senescence in localized areas is sometimesattributed to the ability of the pathogen toproduce cytokininlike substances, possibly anauxin or a gibberellin. The total effect on the plant,however, is generally premature senescence asdistinguished from normal senescence exhibitedby a healthy plant.InsectsVarious categories of insects and mites can berelated to accelerated senescence of the sorghumplant. Piercing, sucking types such as the greenbug(Schizaphis graminum), other aphids (Siphaspp) and spider mite (Oligonychus spp) are prominentamong those that produce significant destructionof sorghum blades (Hoelscher and Teetes1981). Due to injection of toxin by the greenbug andthe persistence of these various pests throughoutthe growing season, care should be taken to distinguishbetween normal senescence and thatinduced by these pests.Physical RestrictionsThere are various other factors that contributedirectly or indirectly to senescence. We should alsoconsider plant populations and consequences ofphysical constraints (Thomas and Stoddart 1980).It may be noted that the lower leaves of manycurrently planted sorghum cultivars tend tosenesce when cultured in normal row patterns. Partof the initiation of senescence in the lower leavescan be attributed to darkness or to competition forlight. With the more nonsenescent plant typesbeing released, the lower leaves tend to remaingreen for a much longer period of time. A definiteexplanation for the lower leaves remaining green isnot yet available. The answer may lie within thephytochrome and growth regulator complex.Photoperiod-insensitive sorghum plants produceapproximately 20 leaves on the main culm duringthe growth cycle but contain only 7-10 (excludingside branches and tillers) at maturity. Normal morphologicaldevelopment will explain the senescenceof the lower leaves of many monocot plants,especially sorghum. As the culm enlarges, thesheaths of leaves developed early are ruptured,thus resulting in their death (Vanderlip and Reeves1972).Growth RegulatorsThe influence of growth regulators within the plantmay also explain some of the variations in thedegree of senescence by plants (Bidwell 1979,Sacher 1973, Thomas and Stoddart 1980). Cytokineshave been demonstrated to play a role, andsome scientists propose that an antisenescencehormone translocated from the roots is a cytokininor a group of them. Other growth regulators thathave been shown to be active in promoting orretarding senescence are the gibberellins, auxins,and ethylene. These will be discussed in moredetail later.ThigmomorphogenesisAnother environmental factor associated with plantresponses and senescence and rarely discussedis thigmomorphogenesis. Jaffe and Biro (1979)have discussed such effects. They includemechanical perturbation that may result from suchfactors as wind, raindrops, and machinery. Such121

studies have indicated relationships to plantresponses such as stem elongation, electrical resistance,ethylene production, and some resistanceto stress. Certainly, incorporation of adequate lodgingresistance to excessive wind and some delay ofsenescence are critical factors in sorghum cultivardevelopment.Degenerative Cell ChangesSeveral excellent reviews, chapters, and articles(Thomas and Stoddart 1980, Sacher 1973, Beevers1976, Forward 1983, Bidwell 1979, Butler andSimon 1971) have been published on the regulatedprocesses exhibited within plants during senescence.Most investigators agree that senescencefollows an orderly process and the cell does notsimply "collapse." Basically, most of the referencesindicate a sequential effect or change in chlorophyll,chloroplasts, ribosome content,mitochondria, RNA, proteins, lipids, and finally thenucleus. There are, of course, variations in patterns,such as between monocots and dicots aswell as annuals and perennials.Knowledge of normal cell degradation processesthat occur during senescence may bedesirable, and a generalized sequence (Butler andSimon 1971, Thomas and Stoddart 1980) has beendescribed. During the early stages, chlorophylldegradation is evident, and, concurrent with this, adecrease in ribosome populations and chloroplastbreakdown occurs. The process of chlorophyllbreakdown is still not clearly understood, anddoubts exist that it involves an enzymatic process.Chloroplast destruction apparently involves twosystems, one of which acts on the stroma complexand the other on the thylakoid components. Thestroma disappear, thylakoids swell and burst, andthen a massing of osmophilic globules is apparent.During this period or soon thereafter, the endoplasmicreticulum swells and disintegrates or disappears,as do the Golgi dictyosomes. Other factorsthat occur include breakdown of the tonoplast, followedby the plasmalemma. Evidence indicatesthat there is a distortion of the mitochondria duringthe changes outlined above, but they tend to persistuntil the latter stages. Apparently the nucleus isstable until the last stage, when the nuclear membranebreaks down, the chromatin disappears, andthe cell dies.Other effects observed during stages of cellsenescence, as described above, include adecline in protein synthesis. Within a leaf, turnoverof protein is expected, but in a senescing leaf,protein synthesis is retarded and amino acids tendto accumulate (Beevers 1976). Some evidenceexists, however, that not all proteins are degradedsimultaneously. Thomas and Stoddart (1980) reasonthat a sensing reaction may occur as a result ofreduced protein synthesis. The resulting gradualdecrease in protein synthesis along withdecreased chloroplast components may thentrigger the sequential senescence steps throughdecreased export of metabolites to the cytoplasm.Concurrent with declines in chlorophyll, chloroplasts,and protein, there is a decline in RNA (Thomasand Stoddart 1980, Beevers 1976, Bidwell1979). This is based on a decline in incorporation ofprecursor into total RNA. Additionally, this has beenexplained as a failure of DNA to transcribe a templatefor RNA synthesis (Osborne 1962). Such findingssupport the idea that senescence is controlledat the transcriptional level. Concurrent with RNAdecline, a decrease in ribosome content occurs.Although this would result in decreased proteinsynthesis, study of some works (Balz 1966, Matile1968) also suggests that the content of remainingribosomes may function to produce hydrolyticenzymes. Simultaneously with the previously describeddecreases, a decline also occurs in lipids.Not all lipids degrade at the same rate (Draper1969), but lipid hydrolysis does occur during thisperiod of degradation.Growth RegulatorsThe relationship of growth regulators to senescencehas been extensively studied, and numerousreferences are included in reviews of thissubject (Thomas and Stoddart 1980, Bidwell 1979,Sacher 1973). A summary of the results, perhapsoversimplified, indicates that the cytokinins, auxins(particularly indoleacetic acid [IAA]), and gibberellins(GA) are associated with the prevention, retardation,or reversal of senescence, whereasabscisic acid (ABA) and frequently ethylene areassociated with enhancement or promotion ofsenescence.The interactive processes of these regulatorshave been described in various studies, but stillmany questions remain to be answered. Sacher(1973) states that cytokinins and GA are prominentas retardants of senescence in citrus fruit. In areview by Thomas and Stoddart (1980), several122

eferences are cited to indicate that cytokinins aregenerally the most effective class of senescenceretardinghormones. Bidwell (1979) states that acytokinin or group of cytokinins produced andtranslocated from the roots prevents or reversessenescence. Degradation of RNA during celldegeneration has been previously described, andsome scientists propose that cytokinins may protectagainst such degradation. Thomas and Stoddart(1980) also present evidence that cytokininsfunction in sustaining the metabolic state and normalphotosynthate-exporting phase of matureleaves. This in turn would prevent a decline belowthe threshold for senescence initiation (for example,reduced protein synthesis and amino acidaccumulation). Ambler et al. (1983) have shownthat cytokinin levels in the less senescent sorghum77CS2 were about three times those of a moresenescent entry, RTx7000. In addition to the cytokinineffects presented, Sacher (1973) proposesthat auxin declines at about the time that ABAbegins to increase. He further cites evidence toindicate that ABA enhances the hydrolyticenzymes and acts antagonistically with auxin, GA,or cytokinin. Additionally, Cracker and Abeles(1969) have reported that ABA enhances ethyleneproduction. Not all plants respond in the same wayto hormones, but apparently cytokinins areinvolved in the regulation of senescence in sorghums.Many of the reviewers above have cited referencesto experiments that detail the processes ofenhancement or reversal of senescence by hormones.A detailed discussion of these processes,however, is beyond the scope of this paper.An interesting observation is that photosynthesisdecreases (Woolhouse 1967) and respiration continuesat a fairly normal rate until the final phases ofsenescence (James 1953). With the degradation ofchloroplasts and decrease in chlorophyll content, adecrease might be expected in the rate of photosynthesis.Although respiration proceeds as describedabove, changes have been recorded in therespiratory quotients. Protein degradation productsmay supply the respiratory substrate during senescence,thus partially explaining why we do notobserve declines in respiratory rates until near theend of the senescence process.From the previous discussion, it may be notedthat senescence is a strictly controlled degradationprocess, and ultrastructural changes in the cellproceed in a reasonably defined sequence (Butlerand Simon 1971). This begins with a decrease inribosomes and chloroplast degradation, followedby a somewhat orderly process: mitochondriachange, tonoplast rupture, organelle degeneration,and finally plasmalemma and nucleusdeterioration.Senescence and ReducedProgressive Senescencein SorghumSince initiation of the sorghum conversion program(Stephens et al. 1967), more emphasis is beingplaced on various studies comparing senescent tononsenescent sorghum genotypes. Distinguishingcharacteristics have been described for both categories.Duncan et al. (1981) noted that the nonsenescenttypes produce higher leaf-bladechlorophyll content and retain green leaves for alonger period of time after grain maturity.One of the major factors we have observed in ourstudies on the comparison of senescent to nonsenescentsorghum cultivars is a larger relative quantityof total nonstructural carbohydrates within thestems of the latter types. Several factors should beconsidered, however, in evaluating a sorghum cultivarfor patterns of sugar development and correlationwith the biochemistry of pathogenesis.Significant among these factors is correlationbetween the maturity stages of the sorghum plantand concentration of nonstructural carbohydrates.Minimum differences in nonstructural carbohydrateshave been obtained prior to heading in boththe senescent and nonsenescent cultivars studied.Webster et al. (1948) determined sugar compositionin several cultivars of sorghum with selectionsfrom sorgo, kafir, milo, feterita, and others. Theyreported little difference in the percentage of sugarin the juice from the different entries prior to heading.After heading, significant differences in stemsugar levels began to develop among the entries.McBee and Miller (1982) observed a similarresponse in studies comparing Combine Kafir-60(CK-60) and Rio at the preboot and early anthesisstages of maturity. As shown in Figure 1, the percentageof total nonstructural carbohydrates wasvery similar for the two cultivars at the prebootstage. After the beginning of anthesis, percentagesincreased significantly in both entries, with theincrease being much larger for Rio. Starch is frequentlyhigher in the stems during the prebootstage than during anthesis or grain fill, but thiswould not suffice to account for the significantly123

403530CK-60ANTHESIS - 10 cm spacingANTHESIS - 40 cm spacingPREBOOT - 10 cm spacingPREBOOT - 40 cm spacingRIO252015105040353025201510500730 1045 1330 1630 1930 2400 0730 1045 1330 1630 1930 2400Time of dayFigure 1. Percentage of total nonstructural carbohydrates over diurnal cycle in upper and lowerculm sections of CK-60 and Rio during preboot and early anthesis stages at two plant spacingswithin rows. Values are mean ± SE.124

higher levels of sugars produced after panicleemergence and anthesis.Plant population will apparently affect partitioningof nonstructural carbohydrates regardless ofthe senescent or nonsenescent influence. Amongthe first reports on this was a study conducted byEilrich et al. (1964). They found the percentage ofcarbohydrates to be higher in sorghum planted inrows than in a drill system. It may also be noted inFigure 1 that plant spacing within rows significantlyinfluenced the percentage of total nonstructuralcarbohydrates. More closely spaced plants containeda higher percentage of these sugars. Rowswere spaced 100 cm apart in this study (McBeeand Miller 1982).Distribution of the nonstructural carbohydrateswithin the plant will vary somewhat. Janssen et al.(1930) noted that the central portion of the stem insorgo contained the highest amount of soluble sugars,followed in sequence by the lower and uppermostsections. Ventre (1939) found more glucosein the lower portion of the stalk and more sucroseand starch in the upper portions. In general, wehave noted lower glucose levels in the upper portionof the sorghum stem and rather uniform distributionfor sucrose. Starch may vary some, butgenerally, more starch has been found in upperparts of the stems of closely spaced plants, whereasthe quantities are sometimes higher in the basalpart of widely spaced plants. This may be partiallydue to partitioning of carbohydrates into structuralforms where more spacing exists between plants.Leaf position definitely has an influence on thequantity of carbohydrates produced by the particularleaf. As previously stated, earlier senescenceoccurs in the first four or five leaves produced. Thismay result from a combination of factors such ascompetition for light, nutrient translocation, andrupture of the sheath due to stem enlargement.Various workers (Stickler and Pauli 1961, Goldsworthy1970, and Fischer and Wilson 1971) havestudied the effect of the remaining leaves onassimilate production. Goldsworthy (1970)reported that, for the cultivars used, the top leavessenesced more slowly than the middle leaves andmuch more slowly than those on the bottom of theplant. All of the investigators showed that the upperleaves contributed most to grain yield. Fischer andWilson (1971) found that 93% of the grain yield wasdue to assimilation by the head and upper fourleaves.As the plant approaches maturity or the laterstages of senescence, levels of glucose, fructose,sucrose, and starch within the plant will change.Webster et al. (1954) have noted that total sugars,especially sucrose in extracted sorghum juice,increased to a maximum after the soft dough stage.Ventre et al. (1948) reported that sucroseincreased with maturity in sorghum, and Eilrich etal. (1964) stated that nonreducing sugarsincreased in forage sorghum after anthesis forabout 7 weeks and then decreased. We (McBee etal. 1983) observed a significant increase in stemsugars after anthesis, with variable patternsobtained for the different cultivars (Figs. 2,3). Theeffect of the kernel maturity stage was very significant,as is shown in the figures.As may be noted, nonstructural carbohydrateproduction was greater in the nonsenescententries. Variations in stem concentrations should4003002001000PAPanicle removed atblack l a y e r stage6RP56537M a t u r i t y stagesMaturity stages:PA = 15 days postanthesisBL = black layerPBL = 15 days postblack layerPBLCultivars used:37 (senescent) = ATx378 x RTx70006R (nonsenescent) = ATx623 x RioP5 (nonsenescent) = APurl x R74CS538865 (nonsenescent) = ATx623 x R74CS5388Figure 2. Effect of kernel maturity on sucroselevels in culms of four sorghum cultivars.Values are mean ± SE.BL125

302520151050Panicle removed atblack l a y e r stage,6RP56537PA BL PBLM a t u r i t y stagesMaturity stages:PA = 15 days postanthesisBL = black layerPBL = 15 days postblack layerCultivars used:37 (senescent) = ATx378 x RTx70006R (nonsenescent) = ATx623 x RioP5 (nonsenescent) = APurl x R74CS538865 (nonsenescent) = ATx623 x R74CS5388Figure 3. Effect of kernel maturity on starchlevels in culms of four sorghum cultivars.Values are mean ± SE.be noted, however. Both P5 and 65 exhibited higherlevels of sucrose and starch at PA, decreased atBL, and then increased. This appears to be a patternthat is followed by other nonsenescent cultivars(Clark 1981). Hybrid 6R exhibited an upwardtrend in stem levels at all kernel maturity stages.Apparently the supply of sugar was sufficientlygreater than the sink demands so that no decreaseoccurred during the peak demand of the kernels.Lengyel and Annus (1960) noted that sorghumfor forage possesses less cellulose and hemicellulosethan sorghum for grain. We have obtainedsimilar results in our laboratory; however, thesestudies are in the preliminary stages. My preliminarydata indicate that nonsenescent sweet sorghumscontain about 20% hemicellulose and 2 1 %cellulose, whereas a nonsenescent grain sorghumcontains 24% hemicellulose and 23% cellulose.Information about variations in the structural fractionsduring development of the sorghum plant isvery limited. Bettini and Proto (1960) reported thatthe percentage of crude cellulose content does notvary significantly as the plant progresses throughits growth cycle.Concentrations of cytokinins were approximatelythree times greater in a nonsenescentsorghum line than in a senescent one (Ambler et al.1983). Major cytokinins in the stem exudate duringthe postblack-layer stage, were, in order ofdecreasing concentrations, trans-zeatin riboside,trans-zeatin, and isopentyl adenosine. This wouldsubstantiate the previous statement (see "GrowthRegulators'' above) that cytokinins are one of themost effective classes of hormones in retardingsenescence. F.R. Miller (Texas A&M University,Soil and Crop Sciences Dept., USA; personal communication,1983) reported that leaves on nonsenescentsorghum lines remain green longer and donot senesce on lower parts of the plant until significantlylater than the more senescent entries. Theseobservations together with the higher cytokininsconcentrations indicate that this group of growthregulators is associated with delayed senescencein sorghum.ConclusionsBased on the previous discussion, it can be proposedthat reduced progressive senescence isgenetically controlled (Butler and Simon 1971).Sorghum exhibits a somewhat uniform and typicalpattern of senescence in the first leaves produced,due to sheath rupture. Sequentially, the lowerleaves senesce, followed at a later period by theupper ones and subsequently by the stem. Thepattern may be influenced by alterations in factorssuch as nutrition, light, etc., but reduced progressivesenescence has also been shown to be associatedwith genetic inheritance. Under normalconditions, some controlled senescence occurs inthe plant, as illustrated by the organized death ofcells to form xylem tissue and naturally programmedleaf and chloroplast senescence (Woolhouse1967, 1978; Butler and Simon 1971). Areview by Heslop-Harrison (1967) also proposedthat developmental changes in plants are based onchanging patterns of gene repression and derepression.Evidence is also offered by Butler andSimon (1971) that DNA in the chloroplasts, mito-126

chondria, and nucleus is involved. The evidenceindicates that the rate of senescence in sorghum isgenetically controlled and that the growth regulators,especially the cytokinins, are involved.I ncreased levels of sugar accumulation at comparativematurity stages in stems of various sorghumcultivars have been associated with delayedsenescence. Accumulation of sugar in stems afterblack layer in the kernel is evidently due to thereduction in sink volume and continued photosynthesisresulting from incomplete senescence insome of the sorghum cultivars described. This factorappears to be important for improved yields andshould be carefully observed for any correlationswith pathogenesis.Future Research Needs1. Studies to determine conditions that influencepartitioning of photosynthates between structural(SC) and nonstructural carbohydrates(NSC) at different plant growth stages.2. Studies to obtain data for inherent levels of SCand NSC expected for various genotypes andcultivars.3. Techniques to manipulate carbohydrate partitioningfor improved quality of biomass.4. Determination of the relationships of aboveitems to resistance or susceptibility of plants todiseases.5. Correlation of higher concentrations of NSC incultivars to disease susceptibility orresistance.ReferencesALBERSHEIM, P., and ANDERSON-PROUTY, A..J. 1975.Carbohydrates, proteins, cell surfaces, and the biochemistryof pathogenesis. Annual Review of Plant Physiology26:31-52.AMBLER, J.R., MORGAN, P.W., and JORDAN, W.R. 1983.Cytokinin concentrations in xylem sap of senescent andnonsenescent sorghums. Plant Physiology Supplement72(1):168.BALZ, H.P. 1966. Intracellular localization and function ofhydrolytic enzymes in tobacco. Planta 70:207-236.BEEVERS, L. 1976. Senescence. Pages 771 -794 in Plantbiochemistry (eds. J. Bonner and J.E. Varner). New York,New York, USA: Academic Press.BETTINI, T.M., and PROTO, V. 1960. [Chemical compositionof some hybrid sorghums.] Annali delta SperimentazioneAgraria 4:957-974 (in Italian).BIDWELL, R.G.S. 1979. Plant physiology. New York, NewYork, USA: Macmillan Publishing Co. 726 pp.BLUM, A. 1979. Genetic improvement of drought resistancein crop plants: a case for sorghum. Pages 428-445in Stress physiology in crop plants (eds. H. Mussell andR.C. Staples). New York, New York, USA: John Wiley andSons.BUTLER, R.D., and SIMON, E.W. 1971. Ultrastructuralaspects of senescence in plants. Advances in GerontologicalResearch 3:73-129.CLARK, J.W. 1981. The inheritance of fermentable carbohydratesin stems of Sorghum bicolor (L.) Moench.Ph.D. thesis, Texas A&M University, USA. 88 pp.CRACKER, L.E., and ABELES, F.B. 1969. Abscission:roles of abscisic acid. Plant Physiology 44:1144-1149.DRAPER, S.R. 1969. Lipid changes in senescingcucumber cotyledons. Phytochemistry 8:1641-1647.DUNCAN, R.R., BOCKHOLT, A.J., and MILLER, F.R. 1981.Descriptive comparison of senescent and nonsenescentsorghum genotypes. Agronomy Journal 73:849-853.EILRICH, G.L, LONG, R.C., STICKLER, F.C., and PAULl,A.W. 1964. Stage of maturity, plant population, and rowwidth as factors affecting yield and chemical compositionof atlas forage sorghum. Kansas Agricultural ExperimentStation, Technical Bulletin No. 138, Manhattan, Kansas,USA. 23 pp.FISCHER, K.S., and WILSON, G.L. 1971. Studies of grainproduction in Sorghum vulgare: I. The contribution ofpre-flowering photosynthesis to grain yield, II. Sitesresponsible for grain dry matter production during thepost-anthesis period. Australian Journal of AgriculturalResearch 22:33-47.FORWARD, D.S. 1983. Senescence. Pages 468-481 inVol. 7, Plant physiology: a treatise (eds. F.C. Steward andR.G.S. Bidwell). New York, New York, USA: AcademicPress.FRIERABEND, J., and MIKUS, M. 1977. Occurrence of ahigh temperature sensitivity of chloroplast ribosome formationin several higher plants. Plant Physiology 59:863-867.GOLDSWORTHY, P.R. 1970. The sources of assimilatefor grain development in tall and short sorghum. Journal ofAgricultural Science 74:523-531.127

HESLOP-HARRISON, J. 1967. Differentiation. AnnualReview of Plant Physiology 18:325-348.HOELSCHER, C.E., and TEETES, G. 1981. Insect andmite pests of sorghum—management approaches.Texas A&M University, Bulletin No. 1220, College Station,Texas, USA. 23 pp.JAFFE, M.J., and BIRO, R. 1979. Thigmomorphogenesis:The effect of mechanical perturbation on the growth ofplants, with special reference to anatomical changes, therole of ethylene, and interaction with other environmentalstresses. Pages 25-59 in Stress physiology in crop plants(eds. H. Mussell and R.C. Staples). New York, New York,USA: John Wiley and Sons.JAMES, W.O.1953. Plant respiration. London (U.K.) andNew York, New York (USA): Oxford University Press. 282PP.JANSSEN, a, MCCLELLAND, C.K., and M E T Z G E R , W.H.1930. Sap extraction of sorghum and the localization ofjuice and sugars in internodes of the plant. Journal of theAmerican Society of Agronomy 22:627-639.LENGYEL, P., and ANNUS, S. 1960. [Domestic (Hungarian)plants suitable for pulp manufacture, IV]. Papiripar4:100-105 (in Hungarian).MARTIN, J.H. 1970. History and classification of sorghumSorghum bicolor (Linn.) Moench. Pages 1 -27 in Sorghumproduction and utilization (eds. J.S. Wall and W.M. Ross).Westport, Connecticut, USA: AVI Publishing Co.MATILE, P.H. 1968. Lysosomes of root tip cells in cornseedlings. Planta 79:181-196.McBEE, G.G., and MILLER, F.R. 1982. Carbohydrates insorghum culms as influenced by cultivars, spacing, andmaturity over a diurnal period. Crop Science 22:381-385.McBEE, G.G., WASKOM, R.M., III, MILLER, F.R., andCREELMAN, R.A. 1983. Effect of senescence and nonsenescenceon carbohydrates in sorghum during late kernelmaturity states. Crop Science 23:372-376.MISHRA, D., and PRADHAN, P.K. 1973. Regulation ofsenescence in detached rice leaves by light, benzimidazoleand kinetin. Experimental Gerontology 8:153-155.OSBORNE, D.J. 1962. Effect of kinetin on protein andnucleic acid metabolism in xanthium leaves duringsenescence. Plant Physiology 37:595-602.SACHER, J.A. 1973. Senescence and post harvest physiology.Annual Review of Plant Physiology 24:197-224.SCHWABE, W.W. 1970. The control of leaf senescence inKleinia articulata by photoperiod. Annals of Botany 34:43-55.SHAW, M. 1963. The physiology and host-parasite relationsof the rusts. Annual Review of Phytopathology1:259-294.STEPHENS, J.C., MILLER, F.R., and ROSENOW, D.T.1967. Conversion of alien sorghums to early combinegenotypes. Crop Science 7:396.STICKLER, F.C., and PAULI, A.W. 1961. Leaf removal ingrain sorghum: I. Effect of certain defoliation treatmentson yield and components of yield. Agronomy Journal53:99-102.SULLIVAN, C.Y., and ROSS, W.M. 1979. Selecting fordrought and heat resistance in grain sorghum. Pages263-281 in Stress physiology in crop plants (eds. H. Musselland R.C. Staples). New York, New York, USA: JohnWiley and Sons.THIMANN, K.V., TETLEY, R.M., and KRIVAK, B.M. 1977.Metabolism of oat leaves during senescence. Plant Physiology59:448-454.THOMAS, H., and STODDART, J.L. 1980. Leaf senescence.Annual Review of Plant Physiology 31:83-111.TURNER, N.C., and BEGG, J.E. 1973. Stomatal behaviorand water status of maize, sorghum, and tobacco underfield conditions. Plant Physiology 51:31-36.VANDERLIP, R.L. and REEVES, H.E. 1972. Growth stagesof sorghum [Sorghum bicolor (L.) Moench]. AgronomyJournal 64:13-16.VENTRE, E.K. 1939. Jellying and crystallization of sirupsmade from different parts of the sorgo stalk at differentstages of maturity. Journal of Agricultural Research59:139-150.VENTRE, E.K., BYALL, S., and CATLETT, J.L. 1948.Sucrose, dextrose and levulose content of some domesticvarieties of sorgo at different stages of maturity. Journalof Agricultural Research 76:145-151.WEBSTER, J.E., BENEFIEL, D., and DAVIES, F. 1954.Yield and composition of sorghum juice in relation to timeof harvest in Oklahoma. Agronomy Journal 46:157-160.WEBSTER, J.E., SIEGLINGER, J., and DAVIES, F. 1948.Chemical composition of sorghum plants at variousstages of growth, and relation of composition to chinchbug injury. Oklahoma Agricultural Experiment Station BulletinT-30, Stillwater, Oklahoma, USA. 32 pp.WHEELER, H. 1975. Plant pathogenesis. New York, NewYork, USA: Springer-Verlag. 106 pp.WILLIAMS, R.F. 1955. Redistribution of mineral elementsduring development. Annual Review of Plant Physiology6:25-42.WOOD, R.K.S. 1967. Physiological plant pathology.Oxford/Edinburgh, U.K.: Blackwell. 570 pp.WOOLHOUSE, H.W. 1967. The nature of senescence inplants. Symposia of the Society for Experimental Biology21:179-214.WOOLHOUSE, H.W. 1978. Cellular and metabolicaspects of senescence in higher plants. Pages 83-99 in128

129The biology of aging (eds. J.A. Behnke, C.E. Finch, andG.B. Moment). New York, New York, USA: Plenum Press.QuestionsMaranville:Regarding the slide in your presentation thatshowed the source-sink relationship when the topdidn't fill: if there was no environmental stress andthe head fills from top to bottom, why didn't the topfill and the bottom become depleted if only thesource was limiting?McBee:Lack of complete kernal fill occurred at the top ofthe panicle in those plants with a"high-sink/lowsource"treatment. Preliminary data indicate theplant was producing insufficient carbohydrate duringthe period of fill. Apparently proximity was thereason that lower kernels filled first, because as thephotosynthate was translocated acropetally, thelower kernels received the photosynthate at theexpense of the upper ones.Scheuring:You commented on the hydrolysis of sucrose at theplacental sac site. That's the deposition end ofcarbohydrate mobilization. Please comment on thestarting point of carbohydrate mobilization, i.e.,from cortex cells into vascular tissue: Does hydrolysisoccur at that time? If so, might there beimplications for pathogen nutrition and growth?McBee:I know of no work on hydrolysis of polysaccharidesat the cellular level in sorghum for grain. There arereports for sugarcane. Those authors state andshow data to support the fact that gradient levels ofinvertase are controlled by auxin. Consequentlysucrose is hydrolyzed and moved symplasticallyfrom cell to cell as glucose and fructose and apoplasticallyin the vascular system. I would think themonosaccharides would be more conducive togrowth of some pathogens. I might add, however,that as fructose and glucose are transported, theplant tends to combine them into sucrose again forease of transport.

Sorghum Sensitivities to Environmental Stresses*J.D. Eastin, C.Y. Sullivan, J.M. Bennett,A.M. Dhopte, T.J. Gerik, V.A. Gonzalez-Hernandez,K.-W. Lee, V. Ogunlela, and J.R. Rice**SummarySorghum is relatively insensitive to heat and water stress during the vegetative stage. Stresshas variable effects during panicle development, with the most sensitive times being about 3 to6 days after floret differentiation (i.e., during microsporogenesis) and 7 to 11 days after floretdifferentiation (at megasporogenesis). Yield and seed number losses at 5°C above ambientnight temperatures can easily be on the order of 30%. A marked loss of stomatal control occursabout 3 days after anthesis. Stress 7 to 10 days after anthesis can limit seed size, presumablybecause of cell division or cell wall elasticity problems in the endosperm. Sizeable shifts in thepolarization of assimilate transport to grain at the expense of roots may predispose sorghum tocharcoal rot and other root-stalk lodging problems during grain fill.Other contributions at this symposium contain aptreviews of stresses imposed by pests,, includingreferences to stresses from pathogens and insectfeeders. Our purpose is to consider the plant'schanging sensitivities to environmental stresses(heat and water) at various growth stages so thatpathologists may better consider the sometimescompounding negative effects of pathogens ongrain yield.The sensitivity of a plant to an environmentalstress may relate to its predisposition to diseases.Yarwood (1959) defined predisposition as the tendencyof nongenetic factors (such as heat andwater stress), acting prior to infection, to affect theplant's susceptibility to disease. This implies aneffect on the host (plant) rather than on the pathogen,which is what we wish to consider. Schoeneweiss(1975) discussed this topic at length.Environmental stresses do force shifts in assimilatesnormally available for developing grain, whichresults in reduced grain production. Therefore, it isappropriate to consider the times and nature ofsorghum sensitivity to environmental stresses asthey relate to grain yield and its seed size and seednumber components. This amounts to an exercisein both developmental physiology and, to somedegree, process physiology. Developmental physiologyis a vehicle for analyzing grain-yield reductionsin terms of the seed weight and seed numbercomponents of yield. This establishes the timeframework within which yield reductions occur, dueto either stresses or diseases. Investigators may*Contribution of the Nebraska Agricultural Experiment Station, Lincoln, Nebraska, USA.**J.D. Eastin - Professor of Agronomy, C.Y. Sullivan - Professor of Agronomy, USDA-ARS; K.-W. Lee - ElectronMicroscopist, School of Life Sciences; A.M. Dhopte - Agronomy Graduate Assistant, University of Nebraska, Lincoln, NE68583-0817, USA. J.M. Bennett - Assistant Professor of Agronomy, University of Florida; T.J. Gerik - Assistant Professor,Texas A&M University; V.A. Gonzalez-Hernandez - Postgraduate College, Chapingo, Mexico; V. Ogunlela - AssistantProfessor of Agronomy, Ahmadu Bello University, Zaria, Nigeria; J.R. Rice -Plant Breeder, Cargill, Inc., Plainview,Texas,USA.International Crops Research Institute for the Semi-Arid Tropics. 1984. Sorghum Root and Stalk Rots, a CriticalReview: Proceedings of the Consultative Group Discussion on Research Needs and Strategies for Control ofSorghum Root and Stalk Rot Diseases, 27 Nov - 2 Dec 1983, Bellagio, Italy. Patancheru, A.P. 502 324, India:ICRISAT.131

then consider physiological processes that mayhelp them understand developmental limitations.We will not attempt an exhaustive coverage of theliterature. The simple growth stage terminology ofEastin (1972) will be used for discussion. Morecomplex growth stage terminology utilizing informationgathered since 1972 would probably beuseful in crop modelling.Vegetative D e v e l o p m e n t ( G S 1 )Whiteman and Wilson (1965) withheld water fromsorghum to the point of suppressing all growth for 2,3, and 4 weeks prior to panicle initiation andobserved no adverse effects on panicle developmentwhen stress was relieved. General observationsin the field seem to support their results, solong as growth is good enough to insure reasonablyadequate leaf-area development prior to panicleinitiation. Stressing plants during panicle development,however, can reduce yields drastically.Floral D e v e l o p m e n t ( G S 2 )Seed number per unit of land area usually correlatesmore positively with grain yield than doesseed size (weight) (Stickler et al. 1961; Kambal andWebster 1966; Blum 1967, 1970; Quinby 1963Doggett and Jowett 1967; Beil and Atkins 1967Fischer and Wilson 1975; Eastin and Sullivan 1974;Ogunlela 1979). The seed size component of yieldmay become relatively more important as the levelsof environmental stress increase (Eastin et al.1983, Heinrich et al, 1983, Eastin 1984). Considerationof both yield components follows.Vegetative-floral CompetitionEastin (1972) reported yield comparisons of 2-, 3-,and 4-dwarf RS 626 isogenic height hybrids (Table1). Grain yields did not differ, but seed weights andtotal dry matter production did. Seeds were about30% larger in the tall 2-dwarf hybrids. Since yieldswere the same, the seed number was proportionatelylower. The reason for the higher seed numberin the short hybrids (3x3 and 4x3 dwarfs) is probablyexplained by the comparative total dry weightfigures. The tall hybrid produced 16% more total dryweight than the 3x3 dwarfs and 19% more than the4x3 dwarfs. Since the heights of the hybrids wereindistinguishable at panicle initiation, the extravegetative dry weight was produced while the paniclewas developing. Apparently competitionbetween the simultaneously expanding panicleand vegetative parts for available assimilates wassufficient to reduce seed number. Panicles in the2x3-dwarf hybrid were noticeably shorter, and thelarge bold seed could be discerned by eye. Panicledevelopment is definitely influenced by otherassimilate demands during GS2. Assimilatedemands by insect vectors and diseases may befactors.Panicle DevelopmentPaulson (1962) and Lee et al. (1974) illustratedapex transformation when sorghum goes fromvegetative to floral status (Fig. 1 a-c). Relativelyphotoperiod-insensitive temperate sorghumsreach the panicle initiation (PI) stage about whenthe 10th to 13th leaf blade tip emerges from thewhorl. The floral status is signalled by the appearanceof primary panicle branch primordia, whichTable 1. Comparative production data for tall (2x3-dwarf), normal (3x3-dwarf), and short (4x3-dwarf) RS 626sorghums grown under irrigation at Mead, Nebraska, USA (1970). Germination to maturity was 106days. Dry matter is adjusted to 14% moisture. (Source: Eastin 1972.)Dry wt (kg/ha)GrainstoverHeight ratio a Grain Total2dw3dw4 dw0.761.141.087741 179407988 150807528 14501Dry matter/day (kg)%of2 dw Grain Total100848173.375.471.0169142137a Ratio is higher than normal due to leaf loss in a heavy unseasonal snow before final harvest.%of2 dwtotal1008481%ofSeed 2 dwwt over(g/1000) others29.322.7 2922.5 30132

Figure 1. The vegetative and floral apices of Sorghum bicolor (L.) Moench.(Eastin and Lee 1984.)a. Leaf primordium (Lp) and shoot apex (A) of a 3-week-old seedling.b. Enlargement of the apex before floral development.c. Initiation of primary branch primordia (Pb) on the floral apex; secondary branch primordium(Sb) starts to form before primary branch primordia are completely formed at the apical dome.d. Enlargement of floral apex due to the formation of more branch primordia of higher order.e. Initiation of the outer glume primordia (O) on both sessile (S) and pedicellate (P) spikelets.f. Sterile lemma (SI) and lemma (L) are initiated on floret enclosed by outer (O) and inner (I)glumes.g. Initiation of stamen primordia (St) in florets.h. Both stamen (St) and pistil (Pi) primordia are initiated in the florets of the sessile (S) andpedicellate (P) spikelets.133

134subsequently differentiate into higher order paniclebranches, as shown in Figure 1 d. The appearanceof glume ridges (Fig. 1 e) signals the formation ofspikelet primordia. Figure 1 f illustrates the lemmaand sterile lemma. Anthers are differentiated andsurround the pistil primordium, which appearsslightly later (Fig. 1g,h). Glumes then quicklyenclose the stamens and pistil. A. Dhopte of ourlaboratory stripped away the glumes to get scanningelectron microscope prints illustrating subsequentstamen expansion and development of thebilobed pistil (Fig. 2a-c) terminating in the stigmaticstructures (Fig. 2c).Regarding developmental timing for temperatelyadapted sorghum at Lincoln, Nebraska (USA), spikeletprimordia (Fig. 1 e) differentiate about 10 daysafter PI, floret differentiation (FD) proceeds at about2 weeks after PI, and bloom occurs from about 30Figure 2. Pistil and anther development in Sorghum bicolor (L.) Moench. (Source: A.M. Dhopte.)a. Glumes removed, exposing the three anthers surrounding the bilobed pistil primordium.b. Anthers surrounding the developing pistil.c. Pistil with stigmatic structures.d. Mature stigmas.

to 35 days after PI. Lengths of the various periodsare very temperature-sensitive and are also influencedby daylength in photoperiod-sensitive plants(Lane 1963).Sensitive PeriodsData from several sources relate to sensitivity tostress during GS2. Musick and Grimes (1961) firstshowed that the period approaching boot in theirtreatments was the most sensitive, while Shipleyand Regier (1970) found the period from heading tobloom to be slightly more sensitive than mid-to-lateboot. Lewis et al. (1974) used treatments thatshowed boot through bloom to be the most sensitiveperiod.Castleberry (1973) attempted to expand knowledgeof sorghum's reaction to environmentalchanges by a series of thinnings that altered theamount of light energy available per plant. Hethinned sorghum weekly and noted the effects ongrain yield and its seed number and seed sizecomponents. Yields did not decrease until thinningswere done past the FD stage. While plantpopulation was decreased by one-fourth, the seednumber per head increased sufficiently to maintainyields until FD (about 2 weeks after PI, Fig. 1 g). Atthat point the plant could not compensate in termsof seed number per unit of land area, and theincrease in seed size was insufficient to offset theseed number loss, so yields declined.Building on Castleberry's results, Ogunlela(1979) elevated night temperatures in the field 5°Cabove ambient during weekly intervals, beginningat PI. The results in Table 2 show that the week afterFD begins is the most sensitive. Note that yield perhead was reduced proportionately to seed numberper head. The obvious times to study mechanismsresponsible for yield reductions are during antherand pistil development prior to anthesis. Ogunlelaisolated these time periods more specifically thanwere indicated by the work of Downes (1972) andEastin et al. (1976).Dhopte of our laboratory is currently working ondefining events causing seed number reductions.Weekly night-temperature treatments similar tothose of Ogunlela have been used, plus growthchambertreatments of 35/17°C, 35/23°C, and35/29°C (day/night). He has sampled florets at FD,FD + 3, 7, 10, 14, 21, and 25 days (FD + 20 wasanthesis). Field and growth-room results are similar.Therefore only growth-room results will be discussed,considering a 23°C night as normal, 29°Cas high, and 17°C as cool for the hybrid RS 671.Microsporogenesis was affected adversely atboth 17° and 29°C. Cell vacuolation in the tapetumwas somewhat premature. Meiosis was normal;however, meiotic division of the pollen mother cellwas occasionally tangential to the tapetum, ratherthan perpendicular as in control plants. This abnormalrelationship with the tapetum probably causednutritional problems. Microspores past the tetradstage were dissociated from the tapetum to a substantialdegree. Those at 17°C were detached andshrivelled, while those at 29°C were detached butnot shrivelled, Nonviability was high in both types.Structural changes occurring at this time appear tocause later pollen abortion.Structural changes and functional behavior alsochanged in the tapetum. Vacuolation in the tapeturnapparently led to incomplete engorgement ofthe microspores, leaving unfilled or partially filledmicrospores by the time microsporogenesis washalf completed. Mitotic division was generally normalat all temperatures, except for an increasingfrequency of vegetative nuclei positioning themselvesaway from the annulus, which is not ideal forpollen germination. An increase of about 50% inpollen sterility resulted.Table 2. Influence of night temperature on yield andother characteristics of RS 671 grainsorghum at Lincoln, Nebraska, USA, in1979. Night temperatures (field) were regulatedat 5°C above ambient. (Source: Ogunlela1979.)Grain/ 1000- Grain/GS3 aplant Seed seed day/plantTreatment (g) no. wt(g) (g)Control 66.9 2659 26.6 2.09bPl 1 to Pl 7 59.3 2333 27.2 1.85dPl 8 to FD 1(-11) c (-12) (+2) (-11)53.4 2174 27.8 1.71(-20) (-18) (+5) (-18)DF 1 to FD 7 48.0 1855 29.7 1.49(-28) (-30) (+12) (-29)eFD 8 to BL 1 52.7 2176 27.8 1.66(-21) (-18) (+5) (-21)BL 1 to BL 7 55.9 2223 25.5 1.80(-16) (-16) (-4) (-14)a. GS3 = Grain filling stage.b. PI = Panicle initiation (subscripts are days).c. Values in parentheses are percent change from the control.d. FD = Floret differentiation (stamen and pistil primordia).e.BL = Bloom.135

60C-46 RS 67150403020100 days4 days6 days w/oi r r i g a t i o n02000100003025201530 35 40 30 35 40Day temperature (°C)Figure 3. Grain yield (A), seed number (B), and seed size (C) of two sorghum hybrids grown in soil,as affected by temperature and drought stress imposed for 0, 4, and 6 days at the floret differentiationstage. LSDs(0.05) were 2.3 for (A), 576 for (B), and 8.6 for (C). (Source: Gonzalez-Hernandez 1982.)136

Megasporogenesis was also affected adversely.Embryo sac development was normal, as was differentiationand development of the egg apparatus,synergids, polar nuclei, and antipodals. Abortionwas preceded by separation of the integuments atthe micropylar end and degeneration of nucellartissue. Widening intercellular spaces led to collapseof the ovule, while the ovary wall remainedintact. Of a sample of 30 florets, half had a poorlydeveloped pistil with shrivelled stigmas, and 30% ofthe ovules were aborted. Results were similar in the17°C treatments. Seed number per plant wasappreciably reduced in both treatments.The night-temperature elevation treatments ofOguniela (1979) and Dhopte were very modest butwere, nonetheless, very effective in reducing seednumber, as described by Dhopte above. There wasno sign of stress in the plants. One then wonderswhether the effects of early infection by stalk- androot-rot organisms may be equally subtle but stilldeleterious to yield.Gonzalez-Hernandez (1982) compared a stressresistanthybrid (C-46) with a normal hybrid (RS671) in 11 -liter greenhouse pots. Plants were transferredto growth rooms set at 30/22°C, 35/22°C,and 40/22°C. Beginning at FD, water was withheldfor 0, 4, and 6 days. Plants were then watered fullyuntil maturity. These experiments are of particularinterest because the genotype C-46 is a DeKalbstress-resistant and charcoal-rot-resistant hybrid,while RS 671 is a normal hybrid and is charcoal-rotsusceptible. Figure 3 illustrates the extreme grainyield stability of C-46 compared to instability in RS671. Note the distinct temperature x water stressinteractions for RS 671 when water was withheldfor either 4 or 6 days. The 40°C temperature inconjunction with water stress was particularlydeleterious. Note also that damage was largely afunction of seed number reduction. Seed size compensationwas adequate to maintain grain yield athigh temperatures and low water levels in C-46 butnot in RS 671, where seed number losses weremore severe.Photosynthesis (PS), transpiration, and stomataldiffusive resistance were monitored in an effort todiscover the mechanisms of stress resistance inC-46 (Fig. 4). Curves for the three plant propertieswere strikingly similar, except that PS appeared todecline at a slightly higher percentage of soil moisturein RS 671. Photosynthesis, transpiration, anddiffusive resistance properties do not help much inexplaining yield differences. Growth characteristicsdid show some differences. The number of newmature leaves that expanded did not appear usefulin relating to yield differences (Table 3). In fact, leafexpansion during the 6-day stress period appearsto be slightly better for RS 671. However, the relativechanges (%) in functional leaf area per plantmay be revealing. Note in Table 4 that the relativedecline in functional leaf area at 40/22°C underboth water stress levels was on the order of three tofour times greater in RS 671. DeKalb C-46 apparentlyhas osmotic adjustment characteristicsunder stress, which permit it to persist. This mayrelate also to the lower seed number reductionunder stress (due to either floret abortion or lack ofsynthesis of florets). Dhopte's observations regardingtapetum vacuolation, poor development of floraltissues, abortion, etc., may result partially fromosmoregulation inadequate to maintain cellular turgor.Blum and Sullivan (University of Nebraska,personal communication, 1983) showed that, ofseveral physiological characteristics measured,only osmotic adjustment correlated with droughtTable 3. Number of new mature leaves expanded by sorghum hybrids C-46 and RS 671 grown in soil, as affectedby temperature and drought stress imposed for 6 days during floret differentiation. (Source: Gonzalez-Hernandez 1982.)Temperature (day/night, in °C)DroughtC-46 RS 671period(days) 30/22 35/22 40/22 Mean 30/22 35/22 40/22 Mean0 4.54 3.26 0.7Mean 2.8LSD (0.05) = 1.08 leaves;3.53.20.72.5CV = 30.0%3.71.51.02.13.92.60.83.03.52.22.93.22.72.02.72.5 2.92.2 2.81.5 1.92.1137

35C-46 RS 6713025201510530/22°C35/22°C40/22°C02.01.00.010050030 25 20 15 10 5S o i l moisture (%)30 25 20 15 10 5Figure 4. Net photosynthetic rates (A), transpiration rates (B), and stomatal diffuse resistances (C)of two sorghum hybrids as affected by temperature and soil moisture stress imposed at the floretdifferentiation stage. (Source: Gonzalez-Hernandez 1982.)138

Table 4. Relative changes (%) in functional leaf area per plant of sorghum hybrids C-46 and RS 671 grown insoil, as affected by temperature and water deficits imposed for 6 days during floret differentiation.(Source: Gonzalez-Hernandez 1982.)Temperature (day/night, in °C)DroughtC-46 RS 671period(days) 30/22 35/22 40/22 Mean 30/22 35/22 40/22 Mean0 79.9 63.74 19.8 45.46 6.0 -5.4Mean 35.3 34.6LSD (0.05) = 29.0%; CV = 83.6%56.917.7-16.819.366.827.7-5.470.035.9-2.234.557.732.8-4.028.836.5-9.1-47.1-6.654.719.8-17.8resistance in sorghums evolved along a geographicalrainfall gradient in India, Mali, and Sudan.Jordan et al. (1983) suggested that osmoregulationmay permit lowering the threshold value of availablesoil water at which numerous turgor-dependentessential processes can occur. There is some evidencethat the root systems of sorghums related toC-46 do have a high capacity to extract water.In that respect Hultquist (1973) compared theperformances of RS 626 and DeKalb C-42Y(female parent similar to C-46) under greenhousestress conditions. RS 626, like RS 671, has poorstress tolerance and high charcoal rot susceptibility.When water-stressed during panicle development,the stress-resistant C-42Y transported arelatively greater proportion of its assimilates to thedeveloping panicle than to the roots and lowernodes. C-42Y produced some grain under extremewater stress, whereas RS 626 translocated availableassimilates to the roots while the aerial part ofthe plant died back. Regrowth occurred from thebasal nodes when stress was relieved. By contrast,when C-42Y was stressed hard enough for thepanicle to die back, the plant died. The growthpattern of RS 626 is geared to survival, while thegrowth pattern of C-42Y is geared to produce grainin the Great Plains environment of the USA, whererainfall is intermittent and unpredictable but thesoils are often deep, with good water-holdingcapacity. Extensive water extraction capability isessential to production by C-42Y sorghums grownin season-limited and water-limited temperateenvironments, in contrast to some tropical environments.Concerning this, Hultquist (1973) notedthat, while RS 626 exported a greater percentage ofits photosynthetically fixed 14 CO 2 to the roots, theroot hairs (presumably the active sites) in C-42Yhad a higher specific activity, suggesting that theywere more active under stress. Perhaps a greaterportion of the 14 C translocated to RS 626 roots wasstored to be used for regrowth once water stresswas relieved.Rice (1979) compared production of C-46 andRS 671 in hydroponics and measured root growthand respiration from panicle initiation to the harddough stage. Figure 5 shows root dry-matteraccumulation to be slightly higher in G-46 duringpanicle development up to bloom, but differenceswere not great. By contrast, the root respiration ratein RS 671 was appreciably higher. The matter ofroot production efficiency then becomes a concern,since evidence given earlier suggests competitionbetween simultaneously expandingabove-ground vegetative and floral parts.Average RS 671 root production day -1 divided bymg O 2 consumed per unit of dry weight day -1 = 1.30mg root dry matter produced per mg O 2 consumedper gram of root dry weight. A comparable value forC-46 was 2.48. The division 2.48/1.30 suggeststhat C-46 was 1.9 times more efficient in root drymatterproduction. This would appear to be a significantfactor contributing to stability in seed numberand yield under stress and in predisposition todiseases.Another related C-46 characteristic appearsinteresting during grain fill. Note (Fig. 5) that fromsoft dough to maturity, when seed assimilatedemand may be declining somewhat, the respirationrate in C-46 roots increased sharply while rootrespiration in RS 671 stayed flat or declined slightly.Just preceding and during this period, RS 671expressed severe charcoal rot susceptibility, while139

101.291.080.870.6650.40.240321Root r e s p i r a t i o nRoot DM accumulationRS 671C-460.20.40.6Paniclei n i t i a t i o nBoot Bloom SoftdoughHarddoughFigure 5. Root respiration and daily root dry-matter (DM) accumulation in RS 671 and DeKalb C-46grain sorghum, under controlled conditions, from panicle initiation through the hard dough stage ofdevelopment (Source: Rice 1979.)C-46 was charcoal rot resistant. The ability of C-46to maintain metabolic activity (exhibit perennialtendencies) must relate to its stalk-rot-resistancetendencies.Bennett (1979) found sorghum sensitivities towater stress in hydroponics very similar to thoseshown by Hultquist (1973), Ogunlela (1979), andGonzalez-Hernandez (1982). Bennett also noted arelatively high level of sensitivity right at bloomcompared to slightly later.Grain D e v e l o p m e n t ( G S 3 )The sensitivity that Bennett (1979) recorded wasboth in loss of stomatal control about 3 days afterbloom and in loss of seed number from stress rightat bloom. Dickinson (1976) tested for sensitivityduring grain fill by placing plastic bags over paniclesevery 3 days after anthesis and leaving themfor different time periods. Temperature elevationsfor varying times created different stress levels.Seed abortion was generally modest. Effects onseed size limitations, however, were substantial.Stress applied 7 to 9 days after anthesis reducedseed size drastically. The influence could havebeen the inhibition of endosperm cell division,decreasing cell-wall elasticity, or other processesrelated to cell division and/or cell expansion.Physiological relationships between stalk rotsand grain-fill events are not well understood. It isclear that simultaneous heat and water stress, generallyduring the first 2 weeks of grain fill, are necessaryfor a serious attack of charcoal rot. Eastin(1972) showed that substantial14 C-labelled photoassimilateswere translocated to roots up tobloom. After that, increasingly larger percentagesof labelled assimilates were translocated to thedeveloping seeds. Whether or not lesser quantitiesof assimilate render roots more susceptible to invasionand damage by stalk rot organisms is notclear. As pointed out earlier, Rice's (1979) data doshow that root respiration in C-46 (stalk rot resist-140

ant) more than doubles between the soft dough andhard dough stages, while the respiration rate in RS671 falls slightly, The increased root activity mayrelate to charcoal rot resistance in C-46. Thehigher respiratory efficiency of C-46 may also be apositive factor when photoassimilates are low dueto water and heat stress.The matter of temperature influence on respirationrate and its potential influence on the efficiencyof respiratory energy utilization is intriguing. Thesuggestion that temperature may influence the efficiencyof respiratory energy utilization comes frompreliminary data in our laboratory. The test systeminvolved seedling growth in the dark. Seeds of severalgenotypes were weighed and germinated (radicleappearance) at 22°C, and subsequently splitinto lots and grown in the dark for 5 to 7 days at20°C, 25°C, 30°C, 35°C, and 40°C. The growth wasthen separated from the seed remnant, and bothwere dried and weighed. The ratio of grams ofgrowth per gram of seed weight lost was used as anindex of metabolic or growth efficiency. Most genotypeswere similar at 30°C, but divergence at 5 to10°C on either side of 30°C revealed significantdifferences. Some genotypes had high efficienciesat cool temperatures and some had high efficienciesat high temperatures, suggesting that oneshould be able to choose a genotype with anappropriate temperature response to fit a giventemperature environment.Given this generality, plus the notion that respirationis tightly coupled to many of the syntheticprocesses dictating plant growth, Gerik (1979)checked to see what kind of genotype variability inrespiratory response to temperature might exist inthe field. He checked respiration rates in the field insorghum panicles in a random-mating population(fertile S 1 heads) during three different times of dayto get three different temperatures. Table 5 showsthe responses. First, temperature had a markedeffect on respiration rate, as expected, in the 50panicles sampled. Second, and more importantly,the ranges in respiration rates at each respectivetemperature were 1 to 2 times greater than themean respiration rates. Results were confirmed inother populations. Obviously, great variabilityexists in respiration rates at any given temperature.Therefore, if temperature response is important inmaximizing metabolic or growth efficiency, asappears to be the case (see Fig. 3), one should beable to select appropriate genotypes to fit varioustemperature environments and minimize stresseffects.Table 5. The mean, range, and coefficient of variationfor panicle dark respiration at 17, 21,and 24°C for 50 randomly selected plants inthe random-mating grain sorghum population.(Source: Gerik 1979.)Dark respiration(mg CO 2 evolved(g dry wt) -1 hr -1 ) CoefficientTemperature 50-plantofvariation(°C) means Range(%)17 0.51 0.21-0.90 30.721 0.72 0.36-1.18 39.524 1.20 0.50-2.75 33.9Future Research PrioritiesSome of the factors bearing on future research arethat sorghum is relatively insensitive to heat andwater stress during the vegetative stage. Stresshas variable effects during panicle development,with the most sensitive times being about 3 to 6days after FD (i.e., during microsporogenesis) and7 to 11 days after FD (at megasporogenesis). Postanthesissensitivities occur at 7 to 9 days, whendifficulties can cause restrictions in seed size. Substantialheat and drought stress after anthesis predisposessorghum to charcoal rot. This coincideswith the time when increasing proportions of photoassimilatesare transferred to the developinggrain and decreasing amounts of assimilates go tothe roots. One charcoal-rot-resistant hybrid retainsa high level of root respiration during the doughstages, which may relate to stalk rot resistance.High metabolic efficiency in root growth may alsobe a factor contributing to stress resistance in general.Plant response to temperature may have abearing on metabolic efficiency and predispositionto diseases.Future research should be concerned withosmoregulation as it might relate to soil waterextraction and turgor maintenance in florets duringmicrosporogenesis and megasporogenesis, Partitioningof photoassimilates among competing plantparts and/or organisms may influence osmoregulationor be influenced by it. Differences in plantmetabolic efficiency or dry-matter production efficiencyat different temperatures need to be consideredin relation to possible predisposition of plantsto diseases. Consideration should be given to141

selecting genotypes with appropriate temperatureresponses to fit a given environment.Several types of investigation were cited to illustratethe sensitivities of grain sorghum to water andtemperature stress. Similar types of experimentsshould be done superimposing stalk and root rotorganisms on water and temperature treatments.Genotype x disease x environment interactionsneed to be defined, the mechanisms responsiblefor damage exposed, and the information used todevise cultural and/or genetic solutions for eitheravoiding or tolerating stalk and root rot diseases.AcknowledgmentsResearch reported in this paper was partially supportedby the International Sorghum and MilletConsultative Research Project (U.S. AID) and theNebraska Water Resources Center.ReferencesBEIL, G.M., and ATKINS, R.E. 1967. Estimates of generaland specific combining ability in F 1 hybrids for grain yieldand its components in grain sorghum, Sorghum vulgarePers. Crop Science 7:225-228.BENNETT, J.M. 1979. Responses of grain sorghum(Sorghum bicolor (L) Moench) to osmotic stressesimposed at various growth stages. PhD. thesis, Universityof Nebraska, Lincoln, Nebraska, USA.BLUM, A. 1967. Effect of soil fertility and plant competitionon grain sorghum panicle morphology and panicle weightcomponents. Agronomy Journal59:400-403,BLUM, A. 1970. Heterosis in grain production by sorghum.Crop Science 10:28-31.CASTLEBERRY, R.M. 1973. Effects of thinning at differentgrowth stages on morphology and yield of grain sorghum(Sorghum bicolor (L.) Moench). Ph.D. thesis, University ofNebraska, Lincoln, Nebraska, USA.DICKINSON, T.E. 1976. Caryopsis development and theeffect of induced high temperatures in Sorghum bicolor(L) Moench. M.Sc. thesis, University of Nebraska, Lincoln,Nebraska, USA.DOGGETT, H., and JOWETT, D. 1967. Yield increasefrom sorghum hybrids. Nature (London, U.K.) 216:798-799.DOWNES, R.W. 1972. Effect of temperature on the phenologyand grain yield of Sorghum bicolor. AustralianJournal of Agricultural Research 23:585-594.EASTIN, J.D. 1972. Photosynthesis and translocation inrelation to plant development. Pages 214-216 in Sorghumin seventies (eds. N.G.P. Rao and L.R. House). New Delhi,India: Oxford & IBH Publishing Co.EASTIN, J.D. [1984.] Sorghum development and yield. Inproceedings of the Symposium on Potential Productivityof Field Crops under Different Environments (ed. SYoshida), Los Banos, Laguna, Philippines. 22-26 Sept1980. Los Banos, Laguna, Philippines: International RiceResearch Institute, (in press.)EASTIN, J.D., BROOKING, IAN, and TAYLOR, S.A. 1976.Influence of temperature on sorghum respiration andyield. Page 71 in Agronomy Abstracts. Madison, Wisconsin,USA: American Society of Agronomy.EASTIN, J.D., CASTLEBERRY, R.M., GERIK, T.J., HULT-QUIST, J.H., MAHALAKSHMI, V., OGUNLELA, V.B., andRICE, J.R. 1983. Physiological aspects of high temperatureand water stress. Pages 91 -112 in Crop reactions towater and temperature stresses in humid, temperateclimates (eds. C.D. Raper, Jr., and P.J. Kramer). Boulder,Colorado, USA: Westview Press.EASTIN, J.D., and LEE, K.-W.[1984.] Sorghum bicolor (L)Moench. in Handbook of flowering (ed. A.H. Hallevy) BocaRatan, Florida, USA: Chemical Rubber Co. Press (inpress).EASTIN, J.D., and SULLIVAN, C.Y. 1974. Yield considerationsin selected cereals. Pages 871 -877 in Mechanismsof regulation of plant growth (eds. R.L. Bielski et al.),Bulletin No. 12. Wellington, New Zealand: Royal Society ofNew Zealand.FISCHER, K.S., and WILSON, G.L 1975. Studies of grainproduction [Sorghum bicolor (L) Moench]: V. Effect ofplanting density on growth and yield. Australian Journal ofAgricultural Research 26:31-41.GERIK, T.J. 1979. The relationship of photosynthesis anddark respiration in grain sorghum [Sorghum bicolor (L.)Moench] to yield, yield components, and temperature.Ph.D. thesis, University of Nebraska, Lincoln, Nebraska,USA.GONZALEZ-HERNANDEZ, V.A. 1982. Sorghumresponses to high temperature and water stress imposedduring panicle development. Ph.D. thesis, University ofNebraska, Lincoln, Nebraska, USA.HEINRICH, G.M., FRANCIS, C.A., and EASTIN, J.D. 1983.Stability of grain sorghum yield components acrossdiverse environments. Crop Science 23:209-212.HULTQUIST, J.H. 1973. Physiologic and morphologicinvestigation of sorghum [Sorghum bicolor (L.) Moench]:I. Vascularization; II. Response to internal drought stress.Ph.D. thesis, University of Nebraska, Lincoln, Nebraska,USA.JORDAN, W.R., DUGAS, W.A., and SHOUSE, P.J. 1983.Strategies for crop improvement for drought proneregions. Agricultural Water Management 7:281-299.142

KAMBAL, A.E., and WEBSTER, O.J. 1966. Manifestationof hybrid vigor in grain sorghum and the relations amongthe components of yield, weight per bushel and height.Crop Science 6:513-515.LANE, J.C. 1963. Effect of light quality on maturity in themilo group of sorghum. Crop Science 3:496-499.LEE, K.-W., LOMMASSON, R.C., and EASTIN, J.D. 1974.Developmental studies on the panicle initiation insorghum. Crop Science 14:80-84.LEWIS, R.B., HILER, E.A., and JORDAN, W.R. 1974. Susceptibilityof grain sorghumto water deficit at three growthstages. Agronomy Journal 66:589-591.MUSICK, J.T., and GRIMES, D.W. 1961. Water managementand consumptive use of irrigated sorghum in WesternKansas. Kansas Agricultural Experiment StationTechnical Bulletin No. 113. Manhattan, Kansas, USA:Kansas State University. 20 pp.OGUNLELA, V.B. 1979. Physiological and agronomicresponses of grain sorghum [Sorghum bicolor (L.)Moench] hybrid to elevated night temperatures. Ph.D.thesis, University of Nebraska, Lincoln, Nebraska, USA(Diss. Abstr. 80:10871).YARWOOD, C.E. 1959. Predisposition. Pages 521-562 inVol. 1. Plant Pathology (eds. J.G. Horsfall and A.E Diamond).New York, New York, USA, and London, U.K.:Academic Press. 674 pp.QuestionsPartridge:In your paper was any cognizance made of thepresence, absence, or pathogenicity of any internalparasite and/or their potential role affecting yourconclusions?Eastin:Tests for the presence of pathogens were notmade. Plants were green and healthy in appearance.Pathogenicity was not considered in thesepresumed normal plants.PAULSON, I.W. 1962. Embryology and seedling developmentto floral transition of Sorghum vulgare Pers. Ph.D.thesis, Iowa State University, Ames, Iowa, USA.QUINBY, J.R. 1963. Manifestation of hybrid vigor insorghum. Crop Science 3:288-291.RICE, J.R. 1979. Physiological investigations of grainsorghum [Sorghum bicolor (L) Moench] subjected towater stress conditions. Ph.D. thesis, University ofNebraska, Lincoln, Nebraska (Diss. Abstr. 40(1 -2): 527B).University Microfilm no. 7918697, Ann Arbor, Michigan,USA.SCHOENEWEISS, D.F. 1975. Predisposition, stress, andplant disease. Annual Review of Phytopathology 13:193-211.SHIPLEY, J. and REGIER, C. 1970. Water response in theproduction of irrigated grain sorghum, High Plains ofTexas, 1969. Texas Agricultural Experiment Station ProgressReport No. 2829. College Station, Texas, USA:Texas A&M University. 24 pp.STICKLER, F.C., PAULI, A.W., LAUDE, H.H., WILKINS,H.D., and MINGS, J.L. 1961. Row width and plant populationstudies with grain sorghum at Manhattan, Kansas.Crop Science 1:297-300.WHITEMAN, P.C., and WILSON, G.L. 1965. Effects ofwater stress on the reproductive development ofSorghum vulgare Pers. University of Queensland Papers(Queensland, Australia) 4:288-289.143

Physiological and Environmental Factorsin Root and Stalk Rot DiseasesSummary and SynthesisD.F. Schoeneweiss*The excellent papers presented in this section providea wealth of information on physiological andenvironmental factors associated with lodging,senescence, and root and stalk rot diseases inmonocot grain crops. Much of the information hasbeen derived from studies on maize and extrapolatedto sorghum because of the similarity of thetwo species. In most cases, results obtained fromresearch on maize appear to apply to sorghum aswell, but such interpretations should be confirmedbefore they are accepted as valid. Although patternsof growth, senescence, nutrient transport,and source-sink relations are similar and basicallythe same pathogens are involved in root and stalkrots of maize and sorghum, the two species not onlydiffer genetically but are often grown in differentareas of the world under different cropping practices.It seems questionable Whether high managementapproaches to control disease in maize (i.e.,breeding for narrow-based genetic characters,modifications in row spacing, and tillage practicesor soil fertility management) can be incorporatedinto marginal sorghum cropping systems in developingcountries in the semi-arid tropics. Sorghumlines that produce satisfactory yields under highlyvariable, marginal growing conditions will need topossess broad-based genetic tolerance to physicaland environmental stresses that are involved inpredisposition to root and stalk rot pathogens.There appears to be a consensus amongresearchers that any factor that contributes to plantvigor, particularly to a retardation of senescence ofpith parenchyma cells, enhances resistance to rootand stalk rots. Unfortunately, the mechanisms ofresistance or defense reactions of parenchymacells to pathogen attack in grain sorghum areessentially unknown. The weight of evidencestrongly indicates that the amount and distributionof nonstructural carbohydrates are closely correlatedwith stalk rot resistance, as summarized in thephotosynthetic stress-translocation balance conceptproposed by Dodd (1980). Physiological andenvironmental factors that predispose sorghum tostalk rots cause either a reduction in synthesis ofcarbohydrates or a depletion in nonstructural carbohydratesdue to uneven transport to the grainsink. Since carbohydrate metabolism is involved inmost physiological processes in higher plants,many hypotheses could be advanced to explainthe role of carbohydrates in host resistance. Albersheimet al. (1969) stated that high levels of glucoserepress the synthesis by fungal pathogens ofpolysaccharide-degrading enzymes that are universallyinvolved in plant pathogenesis. The closeassociation between sugar levels and predispositionto stalk rot fungi in grain sorghum supports thisconcept and merits further research.Wavelike or sequential senescence from base totop is characteristic of grain sorghum. In genotypespossessing nonsenescence or delayed progressivesenescence characters, carbohydrate levelsremain high longer and parenchyma cells remainphysiologically active into later stages of plantmaturity. After black layer formation in the kernel,*Plant Pathologist, Illinois State Natural History Survey and University of Illinois, 607 E. Peabody Drive, Champaign, IL61820, USA.international Crops Research Institute for the Semi-Arid Tropics. 1984. Sorghum Root and Stalk Rots, a CriticalReview: Proceedings of the Consultative Group Discussion on Research Needs and Strategies for Control ofSorghum Root and Stalk Rot Diseases, 27 Nov - 2 Dec 1983, Bellagio, Italy. Patancheru, A.P. 502 324, India:ICRISAT.145

Pappelis:I believe this lack of contact will occur only in asevere disease situation.McBee:The model would need to have a phenology componentin that susceptibility to stress may vary withstage of development, e.g., pre- or postanthesis.Drought ResistanceMughogho:In my experience at ICRISAT the model is supported.However, a question arises from this: Is adrought-resistant plant (i.e., one that resists damagein the absence of a pathogen even under largestress) also resistant to disease?Duncan:In sorghum, Rosenow considers that there are twotypes of drought-resistance: one expressed duringpreflowering and the other during postflowering.We need to consider the latter in relation to stalk rotpathogen resistance. There is genetic variation forboth types Of drought stress, but no known genotypesare resistant to both.Jordan:There may not be much energy loss due to tissuedestruction by the pathogen since very little additionalmaterial would be moved to the grain in theabsence of the pathogen.Schneider:I would like to make a point here that with fusariumor charcoal rot where invasion is primarily into deadcells there is probably no energy loss, but in thesituation with Colletotrichum, which invades livingtissue, there will be a net energy loss.Temperature EffectsMaunder:I'd like to hear a discussion of temperature as wellas moisture deficits.Jordan:We don't know the role of temperature in the model.Partridge:Pathologists have information on the effect oftemperature on fungal growth. The problem is findingthe effect of temperature on the interaction ofthe host and pathogen. One problem is finding acontrol, i.e., an uninfected plant.Yield Reductions/Energy LossJordan:Dr. Mughogho, you say you accept the model. Whatexplanation do you have for the increased grainyield reduction caused by the pathogen?Mughogho:Literature suggests that the reduction is throughdecreased grain size, but the same literature doesnot separate the effects of the pathogen from theeffects of the predisposition factors, although Mayersin Australia has some data which show thatthere is an added reduction in yield in stalk-rottedplants and that it is due to reduction in both grainsize and number.Eastin:What are the energy costs to the plant from fungalinvasion?Nutrient EffectsMaunder:Are plants subjected to a sudden moisture stressmore likely to develop stalk rot than those grownunder continuous, low-level stress, and is it truethat high nitrogen will induce greater stalk rotincidence?Clark:Yes, there is a relationship between N and stalk rot.Schneider:Leaf area/root ratio is high in N-fertilized wheatplants, and these therefore are more likely to runinto stress.Pappelis:We've shown that cell senescence is increased byhigh N.Partridge:I don't know of any evidence suggesting that plantscan outgrow fungi in response to nutrition.148

Jordan:We have data that show that both grain yield andstalk rot increase with N.NonsenescenceSeetharama:Nonsenescence is associated with a cost, and thatis the production of extra roots. This is of little use inthe Indian situation where soils are shallow.Secondly, I do not consider that all drought resistantgenotypes are charcoal rot resistant.Rosenow:Dr. Duncan, please comment on your stated associationof nonsenescence with anthracnose.Duncan:Yes, there seems, in our environment, to be anassociation; for example, in sorghum lines SC-170,SC-56, and SC-599.Scheuring:Please comment on the genotype x environmentinteraction problem with expression ofnonsenescence.Duncan:We don't have this problem in southeastern USA.Rosenow:In Texas we do get the genotype x environmentproblem in evaluating nonsenescence. It's probablyrelated to the cause of the senescence; forexample, the cause is moisture stress in WestTexas, whereas in other areas it may be leaf disease,insecticide burn, etc.Maunder:What does the F 2 look like in a senescent x nonsenescentcross?Rosenow:In some crosses nonsenescence acts as a recessivecharacter and in others the opposite. We needto know more about this.Stalk QualityPappelis:The sorghum people must not lose sight of the twoaspects of the lodging problem: stalk rot resistanceand stiff stalk characteristics.Maunder:Where does morphology fit into breakage of stalks?Maranville:I would like to ask another question. Are the anatomicalcharacters associated with lodging resistancealso found in the nonsenescent types? Iwould also like to comment that it appears thatselecting for stalk quality characters, for example,crushability, also carries along resistance to stalkrots.Duncan:We found larger stem base diameter in nonsenescenttypes.Rosenow:We select simultaneously for both characters.Zummo:The variety Brandes is an exceptionally goodstander—no one knows why. Certainly there is noapparent anatomical reason for it. Its disease resistance,I consider, is not the cause.Pappelis:There are problems in using crushability: for example,stem segments high in sugar when dried underheat will turn out like bricks; these should be consideredartifacts.McBee:The variety Giza, which has a very stiff stalk, has avery high lignin content in the stem.Maranville:Crushing strength correlates with rind puncture—r = 0.98.Pappelis:In maize, rind puncture taken at preflowering is avery useful tool. I think it should be adopted bysorghum workers.Maunder:Most sorghum breeders would agree that selectingfor stalk quality is an important component ofselecting for lodging resistance.Partridge:I agree that significant progress has been made in149

maize in selecting for lodging resistance via stalkmorphological characters, but I make a plea thatbreeders do not neglect the pathological aspects ofthis problem.Mughogho:I would like to support Dr. Partridge in that, insorghum, lodging resistance based on physiological/pathologicalcharacters will at times breakdown, and it's then that stalk quality characters willassume importance.Carbohyclrate RelationshipsRosenow:Dr. McBee, your data reported today were collectedunder well-watered conditions.—Do youhave any from moisture-stress situations?McBee:Dr. Fred Miller [Professor, Texas A&M University,College Station, USA] had a student who found thatATx623 x RTx423 yielded very well under droughtconditions—there is some correspondence.Schneider:You reported a plant spacing effect. What wasthat?McBee:Plants spaced closely in the row had a higher percentageof nonstructural carbohydrates in thestems in both senescent and nonsenescent types.Schneider:So spacing affects translocation patterns? In maizethere is good evidence that spacing affects stalk rotdue to Fusarium and Verticillium spp. Maybe yourfinding provides an explanation for this.McBee:This seems relevant, and as a result of this meetingI'm going to take much more notice of pathogens inthe stalk. The distribution of carbohydrate may beof importance. For example, the sucrose leveltends to be uniform all along the stalk; but theglucose level is high in the top early in plant development,and then later there is more glucose in thebase.Schoeneweiss:Very rarely has it been demonstrated that pathogengrowth is limited by host nutrients. More likely highCHO has a suppressant effect on pathogen growth.Pappelis:The sugar level in maize stalk tissue is irrelevant.The question is whether it's dead or not, You mustlook at the cell level.Grain Yield RelationshipsRosenow:Dr. Eastin, in your presentation you talked aboutdifferences in drought resistance with respect tograin yield. Is this average yield or yield understress conditions?Eastin:Average yield over a wide range of environments.Environment/TemperatureSeetharama:I would like to show data from an experiment involvingone genotype and four planting dates and theresponse in yield and stalk rot incidence as it isaffected by the environment, specifically temperature.The first planting in September was inferiorand the fourth planting in November was superior,both in highest yield and lowest stalk rot incidence.Early growth was affected by temperatureextremes in all cases, but in the fourth plantinggrowth was very fast after flowering. This was atime of increasing temperature, which was alsocritical for this important grain-filling period. Thisillustrates the importance of environment during aperiod of high grain filling.Carbohydrate Relations to StressPartridge:Dodd's photosynthetic stress-translocation concepthas been often quoted in papers prepared forthis meeting. It's been out now for 6 or 8 years.Does anyone have any experimental evidence tosupport or refute it?Mughogho:Chamberlin's Ph.D. degree thesis does not supportit in that his research did not indicate that mobilizationoccurred in response to stress.Partridge:I take it then that Dodd's hypothesis is notsupported.150

Mughogho:No, not entirely, because Chamberlin looked atonly two genotypes.Henzell:I believe that the crux of Dodd's hypothesis is thatthe shortage of carbohydrate in the stem and rootsresults in cell death and consequent predispositionto pathogen attack. If Dodd is saying that reallocationof assimilate in response to stress contributesto this CHO shortage in the stem, then Chamberlin'swork does not support this part of hishypothesis.Scheuring:This kind of discussion on CHO content of stemshas problems unless we can talk about CHO contentat the cellular level.Henzell:Dodd considers this purely hypothetical.Pappelis:This is not hypothesis: it cannot be tested andtherefore it is pure speculation. Let's call it what it is.Partridge:I agree with Dr. Pappelis.151

Experience with Root andStem Rots of CropsOther than Sorghum

The Maize Root Rot, Stalk Rot,Lodging SyndromeA.J. Pappelis and J.N. BeMiller*SummaryStudies of diplodia and gibberella stalk rots of maize and related breeding programs wereadvanced by the recognition that stalk rot resistance is associated with living parenchyma cellsand stalk rot susceptibility is associated with dead cells. Anthracnose stalk rot of sorghum has asimilar etiology.In maize, injury to roots, stalks, or leaves and water stress accelerate the expression ofparenchyma cell death in roots and stalks. Root rot pathogens spread upward into the stalks asareas of dead cells in these are linked. Hence, one way to prevent (or delay) root and stalkrotting is to prevent (or delay) parenchyma cell death. We established that nuclear andnucleolar degeneration, loss of tRNA methylase activity, abnormal protein synthesis, andincreased synthesis and activity of nucleases and proteases precede cell death. We proposethat research (cytological, biochemical, physiological, pathological) needs to be continued todetermine the effects of genes and environment on the expression of cell death patterns, todevelop practical methods to delay cell death (related to disease responses), and to determinethe nature of resistance and susceptibility to major fungal pathogens that incite root rot, stalkrot, and lodging in maize and sorghum.The root rot, stalk rot, lodging (RSL) syndrome iseconomically more important than any other diseaseof maize. Annual world losses due to the RLSsyndrome exceed 1 billion bushels. Thirty yearsago, the nature of resistance to the RSL syndromewas considered too difficult to solve and unimportantin that period of surplus. However, in 1954, ateam effort was begun by A.L. Hooker, A.J. Pappelis,and F.G. Smith to seek a physiological basis forresistance to diplodia stalk rot. This effort led to thediscovery that susceptibility to the disease was dueto parenchyma cell death (pithiness); resistance tospread was associated with living cells. Theseresearch efforts resulted in a change in attitude.Data now exist that permit a better understandingof the nature of resistance and susceptibility ofmaize to several stalk rot pathogens that play acentral role in the RSL syndrome. We haveextended these principles to similar diseases insorghum.Information on the sequential diseases of maizeshould not be separately analyzed, since a combinationof diseases causes a reduction in fieldstands, reduced health and vigor of plants survivingseedling stages of growth, root and stalk rotting andlodging in developing and maturing plants, and areduction in yield and grain quality at maturity. Theinterrelationships between parasitic organisms, thegenetic constitution of the host, the expression ofhost and pathogen genes, cultural practices, andthe age and physiological state of the host must beconsidered as a function of variations in environmentthroughout the season. A number of reviewarticles present various aspects of the problem,state some of the major contributions to this field ofstudy, and give a sense of direction to the present*Professor, Department of Botany, and Professor, Department of Chemistry and Biochemistry, Southern Illinois Universityat Carbondale, Carbondale, IL 62901, USA.International Crops Research Institute for the Semi-Arid Tropics. 1984. Sorghum Root and Stalk Rots, a CriticalReview: Proceedings of the Consultative Group Discussion on Research Needs and Strategies for Control OfSorghum Root and Stalk Rot Diseases, 27 Nov - 2 Dec 1983, Bellagio, Italy. Patancheru, A.P. 502324, India:ICRISAT.155

esearch (Bruehl 1983; Christensen and Wilcoxson1966; Hooker 1976,1978; Koehler 1960; Pappeliset al. 1971; Schneider and Pendery 1983; Shurtleff1980; Thompson 1970; Twumasi-Afriyie and Hunter1982a, 1982b; Ullstrup 1961,1977; White et al.1979).Root rots that begin during seed germination, oras seedlings develop, can predispose stalks tostalk rot. Pathogens from rotted roots spreadupward and eventually penetrate the crown(below-ground internodes and nodes). Crown rotmay remain quiescent for weeks. If rotting extendsupward through brace roots, basal stalk rot maybecome severe. Severe root rotting can cause rootlodging, and thus cause direct yield loss.In addition to spreading from roots to stalks, stalkrot pathogens can penetrate the mature stalkdirectly and through corn [maize] borer tunnels.Several stalk-rotting fungi penetrate nodes. Othersattack the rind. Extensive spread in the stalk mayresult in stalk lodging or breakage that interfereswith machine harvesting, thus causing indirectyield loss.By producing maximum disease response (orpredicting it) at any geographic location,researchers have improved our understanding ofthe underlying causes of disease resistance andsusceptibility. Because of the importance of thesemethods to maize breeding, we will briefly describetheir use. We will, in particular, discuss the pithcondition rating system, based on the distribution ofdead parenchyma cells. In doing so, we will reviewresearch on stalk rots incited by Diplodia maydis(Berk.) Sacc., Gibberella zeae (Schw.) Petch, andFusarium moniliforme Sheld. These three pathogenscan incite seed rot, seedling root rot andblight, root and stalk rot of maturing plants, root andstalk lodging, shank rot, and ear rot. The factors forresistance to diplodia and gibberella stalk rots areconsidered to be the same or closely related(Hooker 1956). Fusarium stalk rot is difficult to distinguishfrom gibberella stalk rot (Shurtleff 1980,Ullstrup 1977). We propose that parenchyma celldeath in root and stalk tissue predisposes maize toroot and stalk rots incited by these fungalpathogens.R S L S y n d r o m eIt is generally believed that stalk rot infections startfrom roots (Britton and Hooker 1963, Craig andHooker 1961, McKeen 1953, McNew 1937, Pappelis1970a, Pappelis and Boone 1966b, Schneiderand Pendery 1983, Whitney and Mortimore 1957)and through nodes of the lower stalk (Durrell 1923,Pappelis and Boone 1966b). Susceptibilityincreases in all plants with time after flowering.Late-maturing cultivars are more resistant to naturallyoccurring basal stalk rot than those maturingearlier (Koehler 1960).Incidence of diplodia stalk rot has been shown tobe highly correlated with susceptibility to artificialinoculation, as is the incidence of natural infectionwith broken stalks (Smith et al. 1938, Cloninger etal. 1970, Horrocks et al. 1972). Methods of inoculationwere reviewed by Koehler (1960). Althoughstalk-lodging resistance has been improved overthe past four decades, stalk breakage and stalk rotcontinue to be a maize production problem (Zuber1983).Hooker (1957) found a progression in internodesusceptibility to stalk rot following inoculation: thelowest elongated internode above the uppermostbrace roots were the least susceptible, and the fifthinternodes above the uppermost brace roots werethe most susceptible. He recommended that similarinternodes be inoculated to measure comparativeresistance to stalk rot among maize plants orvarieties. Inoculation of the first (basal) or secondelongated internode above the ground between 1and 3 weeks after silking was recommended asmost satisfactory for this purpose, with stalk rotratings preferably made 4 weeks after inoculation.This procedure classifies inbreds and hybrids intodisease-response groups that are highly correlatedwith natural stalk rot observations. In susceptiblecultivars, the rate of spread of the inoculum israpid in the first 2 weeks after inoculation. In cultivarsof intermediate resistance, the rate of spread isless rapid but constant during the 4-week intervalfollowing inoculation. In resistant cultivars, nospread occurs after the 1 st week following inoculation.However, later in the season the rate of spreadchanges and all cultivars become susceptible(Pappelis 1957).Parenchyma Cells andResistance to RSL PathogensPappelis (1957, 1965) and Pappelis and Smith(1963) were the first to relate resistance to thespread of D. maydis and G. zeae with living parenchymacells of nodal and internodal tissue, andareas of susceptibility to these pathogens with156

areas of stalk tissue composed primarily of deadparenchyma. These observations also apply toanthracnose stalk rot of sorghum incited by Colletotrichumgraminicola (Cesati) Wilson (Katsanosand Pappelis 1965, 1966a, 1966b, 1967, 1968,1969a, 1969b; Pappelis and Katsanos 1966) andred rot of sugar cane incited by Physalospora tucumanesisSpeg. (Bare et al. 1971; Pappelis and Katsanos1965a, 1965b; Schmid et al. 1966). As plantsof these three species undergo developmentalchanges associated with flowering, the number ofdead stalk parenchyma cells increases greatly.Areas of dead cells in internodes are observed aswhite tissue between vascular bundles. In eachspecies, the patterns of stalk cell death vary frombasal to upper internodes. Discoloration associatedwith stalk rot response following inoculationoccurs where living cells are present along thevascular tissue, rind, and in the nodes. Injuringplants during this developmental period changesthe rate of cell death in stalks: cutting roots orremoving leaves increases the rate and removal ofthe ear of maize and inflorescence of sorghumdelays it. There is much additional support for theconceptual scheme of host-pathogen interactionin maize involving D. maydis and G. zeae (Gates1970; Kang et al. 1974; Pappelis 1970a, 1970b;Pappelis and Boone 1966a; Pappelis et al. 1971,1973a; Pappelis and Katsanos 1969).Rating Systems forPith Condition and Stalk RotPappelis (1957) and Hooker (1957) used the samediplodia stalk rot rating system for inoculated maizeplants. The pith-condition system developed byPappelis (1957) was based on the same numericalrating units used for tissue discoloration followinginoculation, but was limited to one internode. Theserating systems and the high correlations betweenthem were described by Pappelis and Smith(1963). The two systems were expanded toimprove both ends of the rating scales (Pappelis1963, 1965, 1970a, 1970b; Pappelis and Boone1966b). Cell death in nodal tissue (after massivecell death in internodes) was highly correlated withnaturally occurring stalk rots that spread from rottedroots and penetrated the stalk through nodes. Ifno cell death occurs in the pith tissue, the pathogendoes not spread in the inoculated internode.The improved diplodia stalk rot rating systemwas as follows: 0.0 = less than 1% of inoculatedinternodes discolored; 0.5 =1-12.5% discolored; 1= 12.6-25%; 2 = 26-50%; 3 = 51 -75%; 4 = 76-100%;4.5—like 4, with less than 50% of the adjacentinternode discolored; 5—like 4, with more than 50%of the adjacent internode discolored; 5.3 = discolorationof three internodes (including the inoculatedinternode); 5.4 = discoloration of four internodes;5.5 = discoloration of five or more internodes; and 6= premature death of plant. The report of Hooker etal. (1962) contained a modification of the improvedsystem.The improved pith-condition rating system wasas follows: 0.0 = no white, fluffy pith in rated internode;0.1 = less than 1 % white; 0.5 = 2-12.5% white;1 = 12.6-25% white; 2,3, and 4, as described above;4.1 —like 4, with dead cells between intercalarymeristem and node and/or in the nodal plate; 5—like 4, with dead parenchyma cells in node linkingareas of dead cells in adjacent internodes; and6—like 5, with premature death of plant, no greencolor in leaves or rind.When rapid cell death occurs in previously resistantinternodes, the spread of D. maydis or G.zeae may require 1 or 2 weeks to reach living cellsalong the rind and in nodes, where additional discolorationcan occur. Thus, late-season stalk rotratings may not be well correlated with pithconditionratings (Abney 1964).Pappelis and Boone (1966b), using the 4.1 and5.0 pith-condition ratings, predicted the spread ofstalk rot pathogens from rotted roots into the lowerstalk and penetration of the pathogen into the uppernodes from infected leaf sheaths. They concludedthat the physiological changes in the stalk reportedby McNew (1937), McKeen (1953), and Whitneyand Mortimore (1957,1961) to occur prior to penetrationof stalk-rotting organisms appear to berelated to cell death in internodal and nodal tissueof the stalk, especially the latter. We have madefurther improvements in the pith-condition ratingsystem as follows: 4.1 —like 4, with dead cellsbetween node and nodal plate (intercalacy meristem);4.5—like 4.1, with dead cells in the nodalplate, as well as between the node and the nodalplate; and 5.3,5.4, and 5.5 indicate that dead cellsare linked from the first through the third, fourth, andfifth internodes above the uppermost brace roots,respectively.Sorghum stalk-rot and pith-condition rating systemswere also developed (Katsanos and Pappelis1965, 1966a). The pith-condition rating systemsuggested for sorghum stalk tissue is as follows:0.0 = no white, fluffy tissue composed of dead157

parenchyma in the internode; 0.1 = less than 1%white; 0.5 = 2-12% white; 1.0 =13-25% white; 2.0 =26-50% white; 3.0 = 51 -75% white; 4.0 = 76-100%white; and 6.0 = plant dead. The letter "T" is addedto the internode when cell death in the upper nodelinks dead cells in adjacent (upper) internodes. Thestalk-rot rating system for plants inoculated with C.graminicola uses the same 0.0 through 6.0 ratingunits and the letter T, but the area of discoloration israted, rather than the area of white tissue. As withmaize, the pith-condition ratings were highly correlatedwith stalk rot ratings.Pappelis (1963) rated parenchyma cell death incortical and stelar tissue of maize roots after determiningthat cells in the root that appeared whitewere dead and others were living (neutral redplasmolysis-deplasmolysis method). The extent ofdead cells in roots is difficult to quantify, but celldeath patterns in adventitious roots can be documented.As dead cells in the adventitious roots linkwith areas of dead cells in the stalk, root-rottingpathogens spread into the stalk because there isno barrier of living cells in the root-stalk junction.These predictions can be recorded with basalinternode pith-condition ratings by adding the lettersRS.Root and Stalk Rot Symptomsand InoculationIn severely root-rotted plants, stalk rot and lodgingmay occur concurrently with the premature deathof plants. Severely affected plants show suddenchanges in leaves similar to those caused by earlyfrost. The green color of the lower stalk fades. Earsbecome chaffy. Stalk pith tissue is discolored andhas a shredded appearance (Ullstrup 1961,1977).After some success in inducing stalk rot symptomsby cutting roots (Pappelis 1970a, 1970b),Pappelis (1963) was able to reproduce all thesymptoms ascribed to stalk rot by cutting the rootsof maize inbreds B2, C103, 38-11, and Os420before tasseling. The development of the followingsymptoms varied in each inbred: stunting, areas ofgray on leaves lighter green in color than those ofnormal plants, wilting of lower leaves followed bydeath, drooping of developing tassel, death of twoto three upper leaves around tassel, inhibition ofleaf expansion (width) associated with potassiumdeficiency symptoms, reduction in ear size andnumber (plants normally having two ears developedone stubby ear), ears generally chaffy, andpremature death of some plants. Growth of newsecondary roots past the point of root cutting wasobserved often in plants of B2 and C103 (resistantto stalk rot and least affected by root cutting), occasionallyin 38-11 (intermediate; severely affectedby root cutting), and seldom in Os420 (susceptible;very severely affected by root cutting—manyplants died prematurely). Root cutting induced allthe symptoms of stalk rot without any basal stalkrot, crown rot, or root rot evident in either controlplants or those whose roots were cut. However, astime passed, the latter developed severe root rot(stalk-rot-resistant plants showing less than stalkrot-susceptibleplants); and in susceptible inbreds,spread of the pathogen into the stalk through theroot-stalk junction followed. The death of root corticalparenchyma and stelar parenchyma precededthe spread of root rot pathogens (this was determinedusing the neutral red plasmolysisdeplasmolysismethod), and the death of internodalpith parenchyma at the root-stalk junction-precededthe spread of the pathogen into the stalk.The root and stalk rots were similar to those incitedby G. zeae, and the diseased tissues subsequentlybecame invaded by the charcoal-rot pathogen,Macrophomina phaseolina (Tassi) Goid. Cuttingroots always increased susceptibility to diplodiaand gibberella stalk rot following inoculation. Thesefindings have disease implications with respect tocultivation practices and root worm damage.Stalk rot results obtained using the single inoculationmethod with first and fourth internodes werehighly correlated with results obtained using a doubleinoculation method (both first and fourth internodesinoculated within the same plant) (Pappelis1965,1970a). The results were as follows: D. maydis-1957, r = 0.95 and 0.98; 1960, r = 0.98; and G.zeae - 1960, r = 0.98. The diplodia and gibberellastalk rot ratings obtained in these tests were alsohighly correlated with pith-condition ratings for thefirst and fourth internodes of control plants: D, maydis-1957,r = 0.95 and 0.99; 1960, r = 0.95; and G.zeae-1960, r = 0.95.Inoculations with D. maydis and G. zeae to producestalk rot in breeding plots at maturity aretraditionally made in the first elongated internodeabove the brace roots. The reports that internodesabove this location are susceptible have notcaused changes in the plant breeder's routine.However, the study of two internodes within thesame plant is attractive. Inbreds can be selected toprovide resistant first and susceptible fourth internodesfor study at the time of flowering and for158

several weeks thereafter. This eliminates geneticdifferences encountered when a number of inbredsshowing a wide range of stalk rot responses arestudied for differences at maturity. Similarly, it is notnecessary to study resistance at flowering andsusceptibility at maturity within the same inbred(first internodes), thus eliminating seasonal variations.The variables of leaf size, photosynthesisrates, translocation patterns, ear development,mineral nutrition, and drought stress can all beincluded for study within the same plant. A modelnow exists to relate physiological changes tochanges in parenchyma cell death within the sameplant. Methods to select appropriate inbreds forstudy have been described (Pappelis and Williams1966, Pappelis et al. 1975).In the past, as maize breeders improved yield,they were also unknowingly selecting for cell deathin roots and stalks (as evidenced by the continuingproblems of the RSL syndrome). By including celldeath ratings as an important trait in breeding programs,breeders can now improve disease andlodging resistance as well as yield and other agronomicallydesirable traits.Cell Death PatternsGas spaces (aerenchyma) in the root cortex ofmaize seedlings grown in water culture were firstreported by Norris in 1913 (McPherson 1939).Dunn (1921) confirmed and extended the findingsto include wheat. In 1934, Bryant reported that thesame condition existed in barley roots when seedlingswere grown in nonaerated solutions, but notwhen they were grown in aerated solutions(McPherson 1939).Dunn (1921) observed cortical aerenchyma inmaize seedlings grown in sphagnum, sand, or soilculture under summer greenhouse conditions butnot winter conditions. She suggested that the rateof root growth (temperature effect) and oxygensupply seemed to be the factors determining thetime of the appearance of aerenchyma, not seedlingage. Gas spaces were largest in the upperpart of the root (4 cm below the seed) and smallest3 cm from the root tip (roots 10 to 12 cm long).McPherson (1939) studied the progressivechanges in the cortex of maize roots that wererelated to aerenchyma formation (cell death anddegeneration). Nuclear degeneration preceded theloss of cytoplasmic streaming and failure of the cellto plasmolyze. Cell walls collapsed near the root tipand degenerated in the area of cell elongation. Theaerenchyma was surrounded by dead corticalcells. When roots 15 cm long with no dead Corticalcells were placed in unfavorable conditions, celldeath was extensive and aerenchyma formationensued both in the mature tissue formed beforetransference and in newly formed cortical tissue. Afew rows of cells adjacent to the epidermisappeared to resist deterioration, but sometimes allcortical cells died. Roots grown in well-aeratedsoils were not as severely affected. Roots of plantsgrown for half a season in the field contained aerenchymacells in the cortex. Relatively dry soils ledto smaller and fewer air spaces than water-ladensoils. In the latter, aerenchyma formed within 4days (at 20°C). The rate of aerenchyma formationincreased as the temperature increased. Oxygenprevented or greatly reduced cell death in all cultureconditions. Poorly aerated roots and soils haverecently been shown to cause increases in ethyleneand ethylene trapped in roots induces theformation of lysigenous cortical cavities (aerenchyma)due to cell death (Konings 1982). The identicalcourse of aerenchyma development wasobserved in roots of maize, wheat, barley, and oats(McPherson 1939).Cytochemical tests revealed that the cell walls ofyoung cells in maize root tips contained cellulose,pectic acid, and protein (McPherson 1939). Ascells became older, the cell-wall proteins were lost,pectic acid decreased, and insoluble pectinincreased. Endodermal cell walls became lignified.Cell death patterns in the epidermis and cortex ofwheat and barley have been reported (Holden1975, 1976; Deacon and Henry 1978a, 1978b,1980). Root hairs and cortical cells died at a fasterrate in wheat than in barley over the first 4 weeks ofgrowth. Cell death in cortical tissue first occurrednear the epidermis and then progressively towardthe endodermis. Pathogens grew into tissue composedof dead cells and induced discoloration ofadjacent living cells. Several types of host reactionswere observed in response to parasitism; corticalcell walls thickened; cell walls became brown(with or without thickening); and living cells oftenproduced lignitubers (fingerlike wall ingrowths surroundinginfection hyphae). Xylem pluggingoccurred in advance of hyphae growing up thestele. The methods used to study root rots of wheatand barley may have application in the study of r6otrots of maize and sorghum. D. maydis has beenreported to induce lignitubers in cells of the maizeroot (Craig and Hooker 1961), Schneider and159

160Pendery (1983) reported reduced water uptake followingmaize root rot.We discovered that death of parenchyma cells inthe lower nodes was delayed in no-till andconservative-tillage plots (unpublished data,1970). This may explain the observation by Mock(1982) that less stalk rot occurred in no-till plots.No-till plots contain 20 to 30% more water, moreorganic matter (due to reduced aerobic microbialoxidation and increased anaerobic activities), areseveral degrees colder than plowed soil (Doran1982), and are devoid of any root damage fromcultivation.Mechanisms of ResistanceRecurrent selection has enabled breeders toimprove yield, root and stalk strength, and stalk rotresistance (Miles et al. 1980, Smith 1983, Thompson1982, Zuber et al. 1980). Quantitative methodshave been developed to evaluate stalk strengthand to determine the contribution of rind and pith tostrength (Twumasi-Afriyie and Hunter 1982a,1982b; Zuber and Kang 1978; Zuber 1983). Rootvolume was found to be highly correlated with rootpullingresistance (Zuber et al. 1971). Methods thatcould be used to study this aspect of the syndromewere reviewed by Donovan et al. (1982), Ariharaand Crosbie (1982), and Peters et al. (1982). Selectionfor size of the root system is not expected toreduce grain yield. Methods to study root morphology(Maizlish et al. 1980) may be helpful in testingfor root rot resistance. Fungal population studieshave been completed by many researchers (Kommedahlet al. 1979). Hornby and Ullstrup (1967a,1967b), using methods to study fungal and nematodepopulations on maize roots, reported highermicroflora populations on susceptible plants thanon resistant plants. Similarly, ear-rot screeningmethods have been improved (Sutton 1982, Suttonand Proctor 1982). These new research methodsand reports should guide pathologists, physiologists,and biochemists through resistance mechanismstudies.Physiology, Biochemistry,and Cytology of RSLSenescence and Cell DeathWhen it became evident that the way to maintainfield resistance to diplodia and gibberella stalk rotswas to keep a barrier of living parenchyma cells innodes, internodes (especially along the rind), andadventitious roots, we began to explore the eventsrelated to senescence and cell death. We definedthe moment of cell death as that time when thecytoplasmic membrane becomes irreversibly permeableand cellular senescence as irreversibledegeneration that leads to cell death. We definedcellular autolysis as the degenerative events thatoccur following cell death. (Some of our early studiesalong this line have been reviewed: Pappelis etal, 1971). Biochemical changes in senescing cobparenchyma tissue, stalk pith tissue, and first developedleaf of maize were examined (BeMiller et al.1969a, 1970, 1972/73, 1973, 1976a, 1976b;BeMiller and Hoffmann 1972), and characteristicsthat make each of these tissues useful for studiesof senescence were described and evaluated(BeMiller et al. 1972/73, 1976a).Because pith tissue included both parenchymacells and vascular tissue, the relationship betweenchanges in concentrations of components in thesample and cellular senescence and death wasnot clear. Although parenchyma cells of the stalkdied, many cells around vascular tissue remainedalive, and the vascular tissue continued to function.For this reason, BeMiller et al. (1969a) used maizecob parenchyma tissue, free of vascular bundles,as a model for study of senescence. BeMiller et al.(1970) concluded that the only valid basis for comparingcell constituents in stalk and cob parenchymatissue was the per-cell basis.In a 3-week study beginning at silking, BeMiller etal. (1970) determined changes in concentrations ofvarious nutrients that might give a clue to changesin membrane integrity and compared the data withthose of previous studies. They found that K, Si, P,Fe, and Co concentrations per cell increased duringthe 1 st week (period of greatest cell elongation),then decreased slowly as the cells senesced anddied. There were continuous accumulations of Sr,Cu, crude fiber, and ether-soluble substances percell over the study period. Mo per cell increasedduring the 1st week, then remained constant. Zn,Ba, and B per cell increased until the 2nd week,then decreased. Mg and total N per cell remainedconstant during the study period. There was noindex that appeared to forecast cell senescenceand death.BeMiller and Hoffman (1972) determined the80% ethanol-soluble carbohydrate content ofmaize cob tissue (parenchyma cells) on a per-cellbasis before and during the period of cellular

senescence and death. In four of the five populationsstudied, a period of cell elongation was followedby a decrease in the amounts of total andreducing sugars per cell. Before cells died, at least90% of the total sugars were reducing sugars,Within a day or two after the drop in the per-cellsugar contents, many cells in the tissue died. Afterthis period, the total sugar content increased to amaximum, then decreased (and in some populationsincreased again). Changes in per-cell contentof D-glucose, D-fructose, sucrose, and total sugarwere also calculated. Glucose and fructose contentalmost paralleled each other throughout thestudy in all varieties. When cells died, the reducingsugars had declined to 10% or less of the maximumlevel. The sucrose content, however, was very lowuntil after the 1 st week, at which time it began toincrease (at the same time massive cell death wasbeginning in all cultivars).Betterton (1963), using pith tissue from fully elongatedfirst and fourth internodes and expressing hisdata on a volume basis, did not observe the earlyabrupt decrease of total and reducing sugars to avery low level, followed by an increase as cellsdied. On the contrary, he found that sucrose content,and thus total sugars, increased as cells in thetwo locations were dying, and only reducing sugarsdecreased. His data showed that water content ofthe tissue decreased before the decrease in reducingsugars, suggesting that leakage occurs as aresult of senescence and cell death rather than asa cause of these events. Using both water andsugar content data (per cc of tissue), he found thatfirst-internode pith tissue generally containedgreater amounts of reducing sugars and sucrosethan did fourth internodes, but the molar concentrationsof these in the two locations were similar.The data from cob tissue (BeMiller and Hoffman1972) showed similar relationships; i.e., decreasesin reducing sugar content per cell were correlatedwith senescence and cell death (densitydecreases), while sucrose and total sugar contentper cell were not. The soluble carbohydrates thatwere lost from stalk parenchyma cells were probablytransported to ears to increase yield.The literature on carbohydrate synthesis, distribution,and utilization in maize is vast and needscritical evaluation since the bases of data comparisonsdiffer widely and can result in misleadingviews about physiological trends. Attempts torelate some of the data to stalk rot resistance weremade by Schneider and Pendery (1983) and Dodd(1980). Many additional considerations of the physiologicalbaste of genetically controlled increasesin yield, with emphasis on control and improvementin distribution and storage of photosynthetic assimilates,were discussed by Gifford and Evans (1981).Hoffmann (1968) reported a drop in the per-cellphenylanine content to zero and an increase intotal amino acid (especially aspartic acid) contentpreceding the onset of cell death in cob parenchymatissue. The content of total fatty acids didnot appear to be correlated with anything else, butthe highest fatty-acid content occurred at the timeof lowest sugar content, just prior to water loss (celldeath). Two unknown acids peaked in contentshortly after silking, then disappeared; subsequently,one was identified as aconitic acid(BeMiller and Hoffman, unpublished data, 1969).In searching for changes in the per-cell contentof potential regulatory molecules in stalk internodalpith tissue, we obtained the following results. Theputrescine:spermidine ratio (per-cell basis) in stalkpith tissue decreased with distance from the intercalarymeristem, increased sharply to the originallevel just below the region in which cells werebeginning to die, and then decreased in the regionin which cells were dying (Curran 1971). In cobparenchyma tissue the putrescine:spermidine ratioincreased continuously during the period of cellelongation and senescence preceding cell death.Spermine was either absent from or at very lowlevels in the tissues sampled.Recent literature on polyamines (biosynthesis,precursors, ubiquitous distribution, involvement invarious growth processes, and senescence) hasbeen reviewed by Altman (1982). Among theirother physiological effects, polyamines areinvolved in the control of several stress-relatedphenomena. Exogenous application of polyaminesand related precursors retard the progressivesenescence of oat leaf protoplasts, stabilize themagainst lysis, and support a higher incorporation ofuridine and leucine. These events may be due tothe effect polyamines have on preventing chlorophyllloss and preventing the rise of RNase andprotease, and the stabilizing effect they have onboth nucleic acids and membrane function duringsenescence. Because polyamines were highlyeffective in retarding protease and RNase activityprior to chlorophyll loss, Altman concluded thatpolyamines affect early senescence-linked eventsthat are not light-dependent. While their modes ofaction are not known, the cationic nature of thesecompounds may produce an effect similar to that ofcalcium (stabilization of chloroplast thylakoids, sta-161

ilization of membranes against leakage, and inhibitionof RNase and protease).Curran (1971) in our laboratory, found thatsenescence of cells in the first leaf, cob parenchyma,and stalk pith tissue of maize is accompaniedby considerable loss of total polyamines.Research in our laboratory (Liu 1972) also showedthat the 3', 5'-cyclic adenosine monophosphate(cAMP) content (per-cell basis) decreased slightly,but not significantly, in the first three sectionsabove the intercalary meristem (young elongatingcells), then increased as the mature cells aged; thispattern exactly parallels those of protein synthesis,RNA synthesis, RNase activity, and DNase activity,and is the inverse of the total RNA pattern. In cobparenchyma tissue, the cAMP content decreasedfor the first 7 days after silking, then increased,though not significantly, as cell death began. Inthiscase, the pattern was the inverse of that of proteinsynthesis and RNase activity, patterns and paralleledRNA synthesis. Therefore, correlations ofcontents of possible regulatory molecules and celldevelopment and senescence were obtained. Thisis not surprising since senescence of higher plantsis known to involve a series of highly synchronizedevents under hormonal control, but it is not yetpossible to use these data to develop a unifiedconcept of plant cell senescence and death.Decreases in the amount of soluble protein percell were observed during senescence in cobparenchyma, but not in senescing stalk parenchyma(BeMiller et al. 1972/73). Associated withthe decrease in soluble protein in cob parenchymacells was an increase in the free amino acid contentof the cells. However, as the number of deadcells increased in the tissue, the free amino acidcontent began to decline rapidly. In both cob andstalk tissue, protein synthesis (incorporation oflabeled leucine) decreased with tissue age untillate in the senescence period, when there was alarge increase in synthesis. The increased synthesiscould be reduced with actinomycin D. Theamount of free leucine per cell increased withsenescence, indicating that the increase in proteinsynthesis was not simply an apparent increaseowing to an increase in specific activity of thelabeled leucine because of a smaller pool of leucine.The nucleic acid content of cob parenchymatissue (volume basis) dropped to less than 20% ofthe original value as cells elongated, underwentsenescence, and died (BeMiller et al. 1969a).In a later study in our laboratories, Fong (1973)found that different cultivars appeared to have differentpatterns of age-related metabolic changes.In general, there was an increased synthesis of aprotein fraction during tissue senescence. In bothcob parenchyma and stalk pith tissue of Pioneerhybrid 314, it was high-molecular-weight proteinmolecule(s) or particle(s) whose synthesisincreased, but synthesis of this fraction wasunchanged in both cob parenchyma and stalk pithtissue of WF9 x 38-11 single cross. In stalk pithtissue of both Pioneer hybrid 314 and WF9 x 38-11,synthesis of a low-molecular-weight proteinincreased with age. In cob parenchyma tissue ofboth cultivars, synthesis of this fraction decreasedwith age. In Pioneer hybrid 314, there was anincreased synthesis of intermediate-molecularweightproteins with age. RNA synthesis in bothtissues of both cultivars, if it changed at all,increased. Ribonuclease activity also increased,indicating an increasing rate of RNA turnover.Cob and stalk parenchyma cell senescence anddeath also involved decreases in total RNAcontent(primarily a loss in RNA which preceded a loss inDNA) and in RNA synthesis, and a sharp increasein nuclease activity a few days prior to cell death(BeMiller et al. 1976b). Based on additional cytochemicaldata from our laboratories (with theemphasis on a per-cell basis extended by analyticaland quantitative cytology), BeMiller et al.(1976b) proposed that early decreases in DNA anddegeneration of nucleoli were indicators of cellsenescence in maize stalk and cob parenchymatissue.tRNA methylase activity of cob parenchymatissue, stalk pith tissue, and the first developed leafof maize disappeared or declined to low levels ascells senesced preceding death (BeMiller et al.1973). The fact that similar changes in tRNA methylaseactivity were found in all three tissues suggeststhat the decrease in activity is a generalcharacteristic of senescence in maize tissue. Measurementsof the cob parenchyma tissue began onthe day of silking and continued until cell deathabout 10 days later. Maize stalk tissue was takenfrom the fourth internode before tassel elongation(plants about 1.22 m tall), when parenchyma celldeath was beginning to occur in the upper part ofthe internode (sections from pith cores were analyzed;the pith cores were from the intercalary meristemthrough the area containing deadparenchyma cells). Leaf tissue (2nd- and 3rd-cmsections from the tip) was coltected on the 8ththrough the 20th days after planting. The undermethylationor nonmethylation of tRNA in senesc-162

ing tissue could account for changes in the cellularcontent of specific enzymes, perhaps by misreadingof codons. Decreases in essential enzymescould then cause senescence. The breakdown offidelity of protein synthesis could result both inenzymically inactive proteins and in an increasedrate of synthesis of particular proteins affected bymisincorporation of amino acids into polypeptidechains via feedback mechanisms.These studies support the idea that gene-levelactivity such as RNA synthesis (BeMiller et al.1976a) and protein synthesis (BeMiller et al.1976b) continues, but in such a way that errors inpolypeptides accumulate, causing senescenceand death of cells. The increase in nuclease andprotease activities may simply indicate an increasein turnover as cells try to make correct polypeptidesequences.Several people in our laboratories have usedquantitative Feulgen cytochemistry to determinechanges in DNA during cell growth, development,maturation, and senescence, and quantitativeinterference microscopy to determine changes innuclear and nucleolar dry mass and size. Commean(1974) found that nuclear and nucleolar drymass and size increased during parenchyma celldevelopment and elongation in both maize stalkand cob tissue (attributed to increases in nuclearproteins and RNA), then declined during senescence(often rapidly). The DNA content in cobparenchyma cells remained constant through theearly period of cell elongation and declined as cellssenesced and died.Bhattacharya and Pappelis (1983) reported thateight nuclear traits (total nucleic acid, DNA, RNA,total nuclear protein, histone protein, nonhistoneprotein, protein-bound arginine, and protein-boundlysine) decreased as cell senescence occurred intwo models in onion bulb leaf base tissue. In thesequential leaf-senescence model, tissue wasselected from similar sites in young and older (physiologicaland chronological) leaves. Cells in youngleaves had the least amounts of the macromoleculesmeasured, and those in older, normal leaveshad four to five times these amounts due to polyploidy.Cells in the oldest, dying leaves had little orno measurable amounts of macromolecules. Webelieve that a similar "all-or-nothing" effect wasencountered in maize, using the random selectionmethod in cross sections of tissue.In the apical-cell senescence model in individualonion leaf bases, normal cells were encounteredwithin 3 mm of dead cells (Bhattacharya and Pappelis1983), and drastic decreases in the eightnuclear traits were obtained when successive,contiguous cells were studied. We believe that thissampling method should be used in future studies.We concluded that the models we selected forstudy could be improved by measuring multiplenuclear and nucleolar traits, selecting successive(contiguous) cells from dead to normal types formeasurements, and selecting cells of the samesize (normal and polyploid cells within the sampleshould not be mixed). The same methods shouldbe used to study the host-pathogen interactions.Using quantitative interference microscopy,Pappelis et al. (1973b) found that D. maydisinduced increases in nuclear dry mass, nuclearsize, and nucleolar size in parenchyma cells of thefirst internodes of two single-cross maize hybrids.Similar results were obtained using inoculatedcobs from one of these hybrids. This may be aninhibition response of all living parenchyma cells.Since the multigenic mechanisms that controlthese responses are not known, they represent animportant starting point that should be applied tothe study of inbreds. It may be that other fungalpathogens have the opposite effect on host cells(killing in advance of spread into tissue). We haveobtained data on induced host-cell senescenceand death in several studies of onion pathogens(Kulfinski and Pappelis 1976, Bhattacharya andPappelis 1982).Karagiannis et al. (1984) characterized thenucleolar enlargement when quiescent onion cellsare activated without pathogens. Small, roundnucleoli enlarge to form elongated and dumbbellshapednucleoli within a few hours. As nucleolienlarge, nucleolar vacuolarization occurs. This isindicative of transcriptional activity in the nucleolarorganizer regions and represents a significant physiologicalchange. Karagiannis and Pappelis(unpublished data, 1983) have found that manygrowth-regulating substances cause nucleolaractivation, as well as inhibition of this process.The use of quantitative interference microscopyto measure loss of dry mass during fungal sporegermination was first accomplished with twocelledspores of D. maydis (Pappelis et al. 1979).We extended that work with studies of asexualspores of G. zeae (Mumford and Pappelis 1978).We expected and found dry-mass losses in bothcases. In addition, we found that both accumulateddry mass after germination, suggesting that thisprocess in water is not merely a utilization of endogenousspore reserve. The dry-mass increases163

could be accounted for by the uptake of secreted orleached substances from the spores that did notgerminate. Murphy et al. (1976) found that sporesof D. maydis contained relatively large amounts ofSi, P, CI, and K; smaller amounts of S and Ca; andtrace amounts of Mg and Al. K and CI were concentratedin the cells without a germ tube, and Mg andP were concentrated in the germinating cells. X-rayimage maps revealed that K and CI were locatedtogether at one end of the spore. No such studieshave been conducted with spores in inoculatedhost tissue. These methods may be very helpful instudying highly resistant varieties of maize that maykill germinating spores following inoculation, andalso in bioassay studies of fungistatic and fungitoxicsubstances from maize.Murphy (1977) examined the infection processof D. maydis in maize stalk tissue using both transmissionand scanning electron microscopy. Usinga technique to detect cellulase activity, she studiedcellulose degradation in culture and in penetrationof the host-cell wall (Murphy et al. 1973, 1974,1976, 1977, 1980). Before penetration of deadparenchyma cell walls in inoculated stalk tissue,hyphal "flattening" occurred and adhesion materialwas secreted. As hyphal constriction occurred, therelease of cellulase was detected and penetrationfollowed. The frayed appearance of the host-cellwalls occurred only where there was direct contactwith hyphal surfaces and where cellulase activitywas detected. The spread of the pathogen in deadhost cells appeared to be random. Cellulase wasdiscovered to be constitutive (i.e., the enzyme wasassociated with vesicles in the cytoplasm and onthe wall of the pathogen and did not require induction).These studies supported earlier findings byBeMiller et al. (1969b) that the release of cellulasefrom hyphae did not occur when the pathogen wasgrown in the presence of glucose.Studies of the relationship of the nutrient elementcontent in maize parenchyma cells to senescencein field-grown plants (BeMiller et al. 1970, Imbambaet al. 1966, Pappelis and Boone 1966a) wereexpanded, with studies of plants grown in a gravelnutrientculture using high-low NPK nutrient solutions(Meyer 1966, Pappelis and Liu 1966, Pappeliset al. 1967). Cell death in internodes was hastenedand stalks lodged when plants were grown in lowpotassiumsolutions. When gravel beds wereinfested with G. zeae, severe root and stalk rotswere produced in a susceptible inbred; moderateroot and stalk rots in an intermediate inbred; andtrace amounts of root and stalk rots in a resistantinbred. Because the results were comparable inevery way with results obtained with these inbredsin field studies, we concluded that the gravel culturemethod would be the best possible way tostudy agronomic stresses and their interaction withthe RSL syndrome.It was obvious from our field studies (Pappelisand Myers 1970, Miller and Myers 1974) thatgenetic control of cell death (associated with susceptibility)and genetic control of physiologicalactivities in living cells (associated with resistance)were separate phenomena. Evidence that celldeath is controlled by one or few genes wasobtained. The number of genes that control theproduction of fungistatic and fungitoxic compoundsfound in living cells is not known (BeMillerand Pappelis 1965a, 1965b; BeMiller et al. 1967;Dabler et al. 1969).Water Stress and Cell DeathProbably the most exciting development that willlead to the long-sought cause of cell death intissues of the stalk and other organs of maize andsorghum has come from research on water stress.Petiole pithiness in celery was shown to developrapidly after the plants were subjected to a shortperiod of water stress (Aloni and Pressman 1979)and could also be induced by treatment with abscisicacid (ABA) solutions. Additional research(Aloni and Pressman 1981) demonstrated waterstress-inducedwilting of younger leaves of tomatoand the nonreversible onset of pithiness in stems.Increasing the duration of water stress increasedthe extent of pithiness. ABA applied through theroot system induced the same effect with or withoutwater-stress treatments, using polyethylene glycolto obtain an osmotic potential of -2.0 bars. Kinetinenhanced pithiness only after water stress hadoccurred. Pithy cells in water-stressed plants(white tissue) lost their stainability with 2, 3, 5-triphenyltetrazoliumchloride (no staining = senescingor dead cell).Ackerson (1983) found that leaves of waterstressedplants contained higher-than-normalamounts of ABA, and he discussed his findings inrelation to earlier reports of ABA accumulation andother physiological indices in leaves of waterstressedcotton, maize, wheat, and pearl millet.Durley et al. (1983) and Kannangara et al. (1983)were able to evaluate genotype drought resistanceto a given stress treatment in sorghum by examin-164

ing ABA and phaseic acid (PA) concentrations inleaves. PA is a principal metabolite of ABA. ABAlevels were increased and PA levels reduced bystress, lndole-3-acetic acid levels could not berelated to stress. Kannangara et al. reviewed earlierwork with hormones and water stress in relation towork in their laboratories and concluded that leafABA levels are a sensitive indicator of the degreeand type of drought stress for sorghum plants.Increases in ABA levels were also correlated withmarked leaf senescence, decline in plant height,and reduced yield. Leaf area development wasmore sensitive to stress than stem elongation.Water stress was associated with increased leaftemperature.Eze et al. (1983) demonstrated that leaf temperatureextremes did not induce changes in ABA levelsif plants were not water-stressed. However,under conditions of water stress, leaf temperaturedid affect ABA levels (the highest increase wastenfold at 25°C). ABA has also been shown toinhibit sucrose uptake by leaf tissue; i.e., it inhibitsphloem loading (Vreugdenhil 1983). Although oneplausible explanation of the inhibition of phloemloading by ABA might be that ABA diminishes thetransmembrane proton gradient that is coupled toand drives this process (Giaquinta 1983), Vreugdenhil(1983) found no such effect. He suggestedan alternative explanation: ABA could induce oractivate a passive sucrose leak and result in stimulatedfruit and seed import.Water stress is a major predisposing factor tostalk rot of maize (Koehler 1960, Schneider andPendery 1983, Ullstrup 1955). Ullstrup (1955)observed that the severity of diplodia stalk rot wasincreased by wet weather near the end of the growingseason, especially when preceded by unusuallydry weather. Schneider and Pendery (1983)verified this experimentally. Late-season stalk rot(incited by F. moniliforme) in early water-stressedplants was more than twice that of control plants.Pith density in water-stressed plants was significantlylower than that in control plants. Also, pithtissue in water-stressed plants was more spongelikeand white. Root senescence in the upper soilstrata was inferred from increased root infectionsand systemic colonization. Root infections resultedin inefficient water uptake. Schneider and Penderyinferred that chronic water stress may follow suchconditions and result in (a) the remobilization ofstored assimilates from roots and stalks thatenhance yields, (b) senescence and cell death inroots and stalks, and (c) root and stalk rotsusceptibility.Schneider and Pendery (1983) also observedthat although postpollination water stress causedlittle or no change from the control treatment (diseaseresponse), water stress at grain fillingreduced the incidence of naturally occurring stalkrot. They did not attempt to explain this observation.Whether parenchyma cells in the upper roots andlower nodes remain alive longer by enduring such abrief period of stress remains to be determined.Possibly ear-filling ceased under these conditions.The relationship between root and stalk rot wasclear. Pith condition ratings would have greatlyaided interpretation of the data.ConclusionsWe conclude that many of the symptoms of earlystalk rot (retarded leaf development, stunting, wilting,reduction in ear size and number, chaffy ears,etc.) may be caused by a hormone imbalanceinduced by severe early-season water stress. Celldeath in roots predisposes them to root rot. Rootrots predispose the stalks to an increased rate ofparenchyma cell death and stalk rot, and root rotpathogens spread into the lower internodes whenareas of dead cells in roots are linked to areas ofdead cells in stalks. The roles of ABA, ethylene, andcytokinin in cell death and patterns of cell deaththroughout the plant need to be studied. If ABAeffects membrane leakage, glycosides (BeMillerand Pappelis 1965a, 1965b) may leak fromvacuoles, their cytotoxic (fungistatic) aglyconesmay be released enzymically into the cytoplasm,and cell death may follow.We agree with Zuber (1983) and Mahon (1983)that the next big breakthrough in disease resistance,water-stress tolerance, standability, andyield is likely to be related to physiological/biochemicalresearch.Future Research Needs1. Patterns of parenchyma cell death in roots andstalks of sorghum should be determined in thescreening programs designed to select sourcesof resistance to root and stalk rots.2. The inheritance of parenchyma ceil deathpatterns should be determined sincegenetically-controlled variability in this trait is165

expected to be related to disease-responsevariability.3. Inoculation procedures should be developedthat predict disease responses in disease nurseries.The results of inoculation trials shouldbe studied in relation to parenchyma cell deathpatterns in sorghum.4. Cell death patterns in midribs of sorghumleaves have been reported to predict pithinessin stalks. This may be an important trait to usein disease nursery studies of stalk rot resistanceand susceptibility, and thus the relationshipsbetween these traits should be studied.5. Gravel culture methods should be developedfor sorghum to enable researchers around theworld to study a wide range of variables undersimilar conditions.6. Cytological, physiological, and biochemicalstudies on the nature of resistance and susceptibilityto root and stalk rots of sorghummust be given high priority. Included should bestudies on the mechanism(s) of cellularsenescence, death, and autolysis; studies onfungitoxic substances in living cells that inhibitthe spread of fungal pathogens; and studies onthe mechanism(s) of induced host cell deaththat are associated with the spread of somefungal pathogens in nonsenescing sorghumtissue; and the effect of water stress on allthese phenomena.7. The effects of soils and soil environments onthe longevity of parenchyma cells in roots andstalks of sorghum should be determined andrelated to tillage methods and cultural practicesused in sorghum production.8. Pathogen variability needs to be studied toprevent unexpected worldwide productionproblems.ReferencesABNEY, T.S. 1964. Seasonal trends in total nitrogen contentof corn stalk tissue in relation to stalk rot resistance.M.Sc. thesis, Southern Illinois University at Carbondale,Carbondale, Illinois, USA. 48 pp.ACKERSON, R.C. 1983. Comparative physiology andwater relations of two corn hybrids during water stress.Crop Science 23:278-283.ALONI, B., and PRESSMAN, E. 1979. Petiole pithiness incelery leaves: Induction by environmental stresses andthe involvement of abscisic acid. Physiologia Plantarum47:61-65.ALONI, B., and PRESSMAN, E. 1981. Stem pithiness intomato plants: The effect of water stress and the role ofabscisic acid. Physiologia Plantarum 51:39-44.ALTMAN, A. 1982. Retardation of radish leaf senescenceby polyamines. Physiologia Plantarum 54:189-193.ARIHARA, J., and CROSBIE, T.M. 1982. Relationshipsamong seedling and mature root system traits for maize.Crop Science 22:1197-1202.BARE, C.E., PAPPELIS, A.J., and SCHMID, W.E. 1971. Celldeath patterns in sugar cane stalk tissue following injuryand flowering. Sugar Journal 33:30-32.BeMILLER, J.N., and HOFFMANN, W.E. 1972. Relationshipof soluble carbohydrates to age of corn cob parenchymatissue. Phytochemistry 11:1321-1325.BeMILLER, J.N., HOFFMANN, W.E., and PAPPELIS, A.J.1972/1973. Relationship of protein metabolism to senescenceof corn (Zea mays L.) stalk parenchyma, cobparenchyma and first developed leaf tissue. Mechanismsof Ageing and Development 1:387-401.BeMILLER, J.N., HOFFMANN, W.E., and PAPPELIS, A.J.1973. Changes in tRNA methylase activity in senescingcob and stalk parenchyma tissue and the first developedleaf of corn (Zea mays L). Mechanisms of Ageing andDevelopment 2:363-369.BeMILLER, J.N., JOHNSON, D.C., and PAPPELIS, A.J.1969a. Relationship of nucleic acids to cell death in corncob parenchyma tissue. Phytopathology 59:989-991.BeMILLER, J.N., JOHNSON, D.C., and PAPPELIS, A.J.1970. Relationship of nitrogen, crude fiber, ether-solublesubstances and mineral nutrients to cell death in corn cobparenchyma tissue. Phytopathology 60:513-517.BeMILLER, J.N., LIU TU, Y.L., LIU, C.R., and PAPPELIS,A.J. 1976b. Relationship of nuclease activity and synthesisto senescence of corn (Zea mays L.) stalk pith, cobparenchyma and first developed leaf tissues. Mechanismsof Ageing and Development 527-436.BeMILLER, J.N., and PAPPELIS, A.J. 1965a. 2, 4-Dihydroxy-7-methoxy-1, 4-benzoxazin-3-one glucosidein corn: I. Relation of water-soluble, 1-butanol-solubleglycoside fraction content of pith cores and stalk rot resistance.Phytopathology 55:1237-1240.BeMILLER, J.N., and PAPPELIS, A.J. 1965b. 2, 4-Dihydroxy-7-methoxy-1, 4-benzoxazin-3-one glucosidein corn: II. Isolation of 6-methoxy-2(3)-benzoxazolinonefraction as a measure of glucoside content and tissuedifferences of glucoside content. Phytopathology55:1241-1243.166

BeMILLER, J.N., RIMSAY, R.L., and PAPPELIS, A.J. 1967.Extraction and purification of phenolic acids in corn. Transactionsof the Illinois State Academy of Science 60:68-71.BeMILLER, J.N., SPARKS, M.C.B., FONG, T.W., and PAPPELIS, A.J. 1976a. Relationship of senescence of corn(Zea mays L.) stalk pith, cob parenchyma and first developedleaf tissues to RNA content and synthesis. Mechanismsof Ageing and Development 5:419-426.BeMILLER, J.N., TEGTMEIER, D.O., and PAPPELIS, A.J.1969b. Constitutive cellulolytic enzymes of Diplodia zea.Pages 188-196 in Cellulases and their applications. Vol.95, Advances in Chemistry Series. Washington, D.C.,USA: American Chemical Society.BETTERTON, H.O. 1963. Seasonal trends in sugar contentand cell death in corn stalk tissue. M.Sc. thesis, SouthernIllinois University at Carbondale, Carbondale, Illinois,USA. 99 pp.BHATTACHARYA, P.K., and PAPPELIS, A.J. 1982. Cytofluorometricstudy of onion epidermal nuclei in responseto wounding and Botrytis allii infection. Physiological PlantPathology 21:217-226.BHATTACHARYA, P.K., and PAPPELIS, A.J. 1983.Nucleic acid, protein, and protein-bound lysine and argininepatterns in epidermal nuclei of the mature andsenescing onion bulb. Mechanisms of Ageing and Development21:27-36.BRITTON, M.P., and HOOKER, A.L. 1963. Failure to controlcorn stalk rots with above-ground applications ofprotectant fungicides. Plant Disease Reporter 47:470-471.BRUEHL, G.W. 1983. Nonspecific genetic resistance tosoilborne fungi. Phytopathology 73:948-951.CHRISTENSEN, J.J., and WILCOXSON, R.D. 1966. Stalkrot of corn. Monograph No. 3. St. Paul, Minnesota, USA:American Phytopathological Society. 59 pp.CLONINGER, F.O., ZUBER, M.S., CALVERT, O.H., andLOESCH, P.J., Jr. 1970. Methods of evaluating stalk qualityin corn. Phytopathology 60:295-300.COMMEAN, V.L. 1974. Changes in DNA, nuclear andnucleolar area and dry mass in aging corncob and stalkparenchyma tissue. M.Sc. thesis, Southern Illinois Universityat Carbondale, Carbondale, Illinois, USA. 40 pp.CRAIG, J., and HOOKER, A.L. 1961. Diplodia root andstalk rot of dent corn. Phytopathology 51:382-385.CURRAN, G. 1971. Relationship of polyamine content totissue senescence in corn. M.Sc. thesis, Southern IllinoisUniversity at Carbondale, Carbondale, Illinois, USA. 86pp.DABLER, J.M., PAPPELIS, A.J., and BeMILLER, J.N. 1969.Effect of phenolic acids and corn extracts upon sporegermination of Diplodia zeae. Phytopathology 59:1098-1101.DEACON, J.W., and HENRY, C.M. 1978a. Death of cerealroot cortex: Its relevance to biological control of take-all.Annals of Applied Biology 89:100.DEACON, J.W., and HENRY, C.M. 1978b. Studies on virulenceof the take-all fungus, Gaeumannomyces graminis,with reference to methodology. Annals of Applied Biology89:401 -409.DEACON, J.W., and HENRY, C.M. 1980. Age of wheat andbarley roots and infection by Gaeumannomyces graminisvar. tritici. Soil Biology and Biochemistry 12:113-118.DODD, J.L. 1980. Grain sink size and predisposition ofZea mays to stalk rot. Phytopathology 70:534-535.DONOVAN, L.S., JUI, P., KLOEK, M., and NICHOLLS, C.F.1982. An improved method of measuring root strength incorn (Zea mays L). Canadian Journal of Plant Science62:223-227.DORAN, J.W. 1982. Tilling changes soil. Crops and SoilsMagazine 34:10-12.DUNN, G.A. 1921. Note on the histology of grain roots.American Journal of Botany 8:207-211.DURLEY, R.C, KANNANGARA, T., SEETHARAMA, N.,and SIMPSON, G.M. 1983. Drought resistance ofSorghum bicolor. 5. Genotypic differences in the concentrationsof free and conjugated abscisic, phaseic andindole-3-acetic acids in leaves of field-grown droughtstressedplants. Canadian Journal of Plant Science63:131-145.DURRELL, L.W. 1923. Dry rot of corn. Iowa AgriculturalExperiment Station Research Bulletin No. 77.EZE, J.M.O., DUMBROFF, E.B., and THOMPSON, J.E.1983. Effects of temperature and moisture stress on theaccumulation of abscisic acid in bean. Physiologia Plantarum58:179-183.FONG, T.W. 1973. An investigation of protein synthesis,RNA synthesis, and ribonuclease activity in senescingcob and stalk parenchyma tissues and the first developedleaf of corn (Zea mays L). M.Sc. thesis, Southern IllinoisUniversity at Carbondale, Carbondale, Illinois, USA.GATES, L.F. 1970. Relationships between pith cell conditionsas assessed by tetrozolium chloride and incidenceof Gibberella stalk rot of corn. Canadian Journal of PlantScience 50:679-684.GIAQUINTA, R.T. 1983. Phloem loading of sucrose.Annual Review of Plant Physiology 34:347-387.GIFFORD, R.M., and EVANS, C.T. 1981. Photosynthesis,carbon partitioning and yield. Annual Review of PlantPhysiology 32:485-509.HOFFMANN, W.E. 1968. Relationship of lipids, solublecarbohydrates, and free amino acids to cell death in corn167

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QuestionsScheuring:Did you develop a scoring system for root cell pithdeath in conjunction with your stem pith scoringsystem? Wouldn't you think such a root and stemscoring system would be essential for adequatelyidentifying resistance to stalk rots?Pappelis:I did use a root parenchyma cell death system: 0,no dead cells; 1, less than half of the cortical cellsdead; and 2, more than half of the cortical cellsdead. For stalk rot, I recommend the pith conditionand discoloration rating systems I described in mymanuscript prepared for this meeting.171

Root and Stalk RotsCaused by Macrophomina phaseolinain Legumes and Other CropsJ.B. Sinclair*SummarySymptoms of charcoal rot and the isolation and identification of the causal fungus, Macrophominaphaseolina, are described. The disease cycle and factors that affect the epidemiologyof the disease are reviewed. Studies on various control practices are presented, A number ofstudies suggest resistance may be available in several crops. Since M. phaseolina causesdisease in stressed plants, maintaining vigorous plants through recommended cultural practices,particularly by providing adequate organic matter and moisture, should be followed.Systemic fungicides may be used when economically feasible.Macrophomina phaseolina (Tassi) Goid. (Rhizoctoniabataticola(Taub.) Butler) causes charcoal rotof root and stems, foliage blight, and fruit and tuberdecay. The fungus infects more than 300 plantspecies, including a wide range of cultivated crops,and although present in most cultivated soils of theworld, charcoal rot is prevalent in the warm temperateand tropical cropping areas when dry conditionsprevail or when plants are under water stress.The disease often appears on irrigated soybeanswhen water is withheld to promote maturity. Magalhaeset al. (1982) showed that the incidence ofcommon bean plant death caused by the fungusincreased from 8.6% under ideal soil moisture conditionsto 63.9% with 18 days of water deficit.Losses due to this disease are difficult to determinesince diagnostic symptoms usually appear wheninfected plants are in progressive senescence orunder low-moisture or other stress condition. However,infection may take place throughout thegrowing season, often causing continuous debilitationof the host. When severe, the pathogen canreduce stands, plant vigor, yields, and seed quality.Losses up to 77% have been estimated on soybeansdue to the disease. However, it is often difficultto determine yield losses due to the pathogenand those due to the stress factors that encouragethe disease.A report on the state of the knowledge of M.phaseolina was published as an annotated bibliography(Dhingra and Sinclair) in 1977 and a reviewof the literature (Dhingra and Sinclair) in 1978. Thispresent review uses in part the material from thesetwo references and that presented in the Compendiumof Soybean Diseases (Sinclair 1982).SymptomsSymptoms of the disease are usually confined tothe roots, crowns, and lower stalks, but infection ofthe above-ground parts of many crop plants hasbeen reported (Dhingra and Sinclair 1977,1978).Infected seedlings may show a reddish-browndiscoloration at the emerging portion of the hypocotyl,which may be confused with symptoms producedby infection by Rhizoctonia solani Kuehn.Infected melon seeds have given rise to infected*Professor of Plant Pathology, University of Illinois at Urbana-Champaign, 1102 S. Goodwin Ave., Urbana, IL 61801, USA.International Crops Research Institute for the Semi-Arid Tropics. 1984. Sorghum Root and Stalk Rots, a CriticalReview: Proceedings of the Consultative Group Discussion on Research Needs and Strategies for Control ofSorghum Root and Stalk Rot Diseases, 27 Nov - 2 Dec 1983, Bellagio, Italy. Patancheru, A.P. 502 324, India:ICRISAT.173

seedlings and increased the inoculum potential inthe soil (Reuveni et al. 1983). If infection occursthrough the roots, the discoloration appears at thesoil line and above. The discolored area turns darkbrown to black, and infected seedlings may dieunder hot, dry conditions. Symptom developmentmay be retarded under wet, cool conditions butcontinues once again with the return of hot, dryweather.In older plants, even though colonized earlier inthe season, symptoms appear when infectedplants are in progressive senescence or understress by low soil moisture and high temperature orother factor(s). After flowering, a light gray or silverydiscoloration develops in the epidermal and subepidermaltissues of the taproot and lower stem.When the epidermis is removed, small, blackmicrosclerotia may be so numerous as to give agrayish-black color to the tissue, resembling pow-dered charcoal (Fig. 1). Splitting of stems andtaproots reveals a reddish-brown discoloration ofthe vascular and pith tissues, with black streaks inthe woody portions. Sclerotia may be found in thepith and vascular elements (Fig. 2). Infected plantsproduce smaller leaves than normal, a subtle lossof vigor, and in a more advanced stage, leaves turnyellow and wilt, but remain attached (Sinclair 1982,pages 30-33).Fruit and vegetable decays have been describedfor many crops, including various cucurbits,papaya, and root crops (Dhingra and Sinclair1978). These are usually dry rots, unless accompaniedby other soft-rotting organisms, and showthe presence of the microsclerotia of the fungus.Foliage infection has been described for manycrops, including guava, jute, various Phaseolusspp, and tobacco (Dhingra and Sinclair 1978).Pod and seed infection is reported on a variety ofFigure 1. Symptoms of charcoal rot of soybeanscaused by Macrophomina phaseolina;when the epidermis of an infected plant isremoved, small black sclerotia are apparent(Courtesy: U.S. Department of Agriculture.)Figure 2. Charcoal rot of soybeans caused byMacrophomina phaseolina: microsclerotia inthe xylem vessels of a young plant. (Source:llyas and Sinclair 1974.)174

legumes, as well as other crops. The fungus isknown to be seedborne in common bean, subterraniumclover, cowpea, groundnut (peanut), jute,maize (corn), melon, foxtail millet, okra, sesame,and soybean (Dhingra and Sinclair 1978). Insesame, infection of the capsule was found in theinner wall, septum, placenta, and seeds, spreadingfrom base to apex (Singh and Singh 1982).Causal O r g a n i s mM. phaseolina is highly variable, differing amongisolates in cultural characteristics, sclerotial productionand size, presence or absence of pycnidia,and conidia size and shape. Isolates are ecologicallyand morphologically specific; one isolate recoveredfrom one part of the plant may not causedisease on another part (Dhingra and Sinclair1973). This characteristic of the fungus can causeproblems in selecting breeding lines for resistance.The fungus produces colonies in culture thatrange from white to brown to gray and becomedarker with age (Fig. 3a). Aerial mycelia, with completelyor partially appressed growth, may or maynot be produced. Some isolates form concentricgrowth rings. Hyphal branches generally arise atright angles to parent hyphae, but branching at anacute angle is common (Fig. 3b). Most branchesshow a characteristic constriction at the point ofunion, and a septum separates the lateral andmother hyphae, as in other Rhizoctonia spp. Theoptimum temperature for growth in culture rangesfrom 28° to 35°C.The jet black sclerotia of the fungus are smoothand round to oblong or irregular (Fig. 3c). Their sizeand shape vary within an isolate and on differentsubstrates. Sclerotia are uniformly reticulate andshow no special structural modification in internalform.Pycnidia, initially immersed in host tissues, areerumpent at maturity. They are more or less globose,membranous or subcarbonaceous, dark tograyish—becoming black with age, and generally100-200 µ m in diameter. The small truncate ostiolemay be inconspicuous or have a definiteopening.The conidia (pycnidiospores), which develop atthe tips of conidiogenous cells lining the inner wallof the pycnidium, are cut off by maturity and fill thepycnidial cavity. The conidia are single-celled;ovate, elongate or elliptical; sometimes curved orirregularly contoured; and hyaline and variable insize, with a 3:1 ratio of length to width. Pycnidia andconidia are produced under continuous light andunder intermittant light in some isolates, but not incomplete dark in culture (Machado 1980, Machadoand Kimati 1975). Michail et al. (1977) inducedpycnidia on soybean seeds in a water-agar-leafmedium at 20°C under 12-hour alternations of darkand ultraviolet light for 7-10 days. The role of conidiain spread of the disease is not understood.The fungus grows well on potato dextrose agarand produces sclerotia often 75-150 µ m in diameter,depending upon the nutritional level of the substrate(Fig. 3c).A number of selective media have been developedfor the isolation of M. phaseolina: two containingchloroneb, mercuric chloride, streptomycinsulfate, potassium penicillin G, and rose bengal(Meyer et al. 1973); two containing chlortetracydinehydrochloride, and streptomycin sulfate pluseither fenaminosulf, oxgall, and quintozene or fenaminosulf,oxgall, and rose bengal (Papavizas andKlag 1975); and one using chloroneb and streptomycinsulfate (Mihail and Alcorn 1982). A modifiedagar plate technique was described for detectingthe fungus in pea seeds (All et al. 1982).M. phaseolina and Botryodiplodia theobromaecan be confused in culture (Sinclair 1982, pages30-33).Disease Cycle and EpidemiologyActivity Before PenetrationThe activity of M. phaseolina in the soil beforepenetration and colonization of the host tissue wassummarized by Dhingra and Sinclair (1978). Mostcolonies of M. phaseolina from naturally-infestedsoils originate from free sclerotia in the soil (Papavizasand Klag 1975). The optimum conditions forthe germination of sclerotia in water agar was 24hours at 32°C, followed by 72 hours of dryingbetween germination flushes (Locke and Green1977). A number of compounds stimulate sclerotiagermination. Crude root exudates and sugar fractionsfrom okra roots stimulate sclerotial germinationand mycelial growth of M. phaseolina, andamino acids are inhibitory (Goel and Mehrotra1975). Germinating sesame seeds and seedlingshave stimulated sclerotia germination andattracted developing mycelia to the host roots(Abdou et al. 1979). In the spermosphere of soybean,sclerotia germinate within 2-3 mm of the175

Figure 3. Development of Macrophomina phaseolina on selective media: (a) a 7-day-old colony(arrow) showing sclerotia production from a soil sample naturally infested with the fungus andplated on chloroneb/Ceresan Wet medium; (b, c) plates of chloroneb/mercuric chloride/rosebengal medium, with (b) showing individual colonies 6 days after plating a soil sample artificiallyinfested with the test fungus; and (c) mycelial development from a single sclerotium 4 days afterplating. (Source: Meyer, Sinclair, and Khare 1973.)seed surface (Short and Wyllie 1978). Availablenutrients of the substrate affect sclerotia size: thericher the medium, the larger the sclerotia (Shortand Wyllie 1978).Gangopadhyay and Wyllie (1979) showed thatan excessive nutrient pool, i.e., high sugar andprotein, resulted in rapid germination, abundantgrowth, and saprophytism of M. phaseolina in culture,while a low nutrient pool resulted in increasedparasitism. However, Dhingra and Chagas (1981)found that the addition of nitrogen to soil completelyinhibited saprophytic colonization. Cerkauskas andSinclair (1982) reported that paraquat inhibitedgrowth of M. phaseolina incorporated into potatodextrose agar and in Fries medium, and inhibitedcolonization of soybean stem pieces in culture.Sclerotia may survive free in the soil orembedded in host residue in dry soils for long peri-176

ods. Short et al. (1980) showed that the severity ofcharcoal rot of soybean was directly related to thepopulation of germinable sclerotia in soils and thatyields were inversely related to the severity of thedisease. Moustafa and Wyllie (1974) found thatsoybean stubble was a major source of inoculumfor seedlings.Sclerotia of M. phaseolina are sensitive to soilf ungistasis (Short and Wyllie 1978) and cannot survivein wet soils for more than 7-8 weeks, andmycelia cannot survive in wet soils for more than 7days. Thus M. phaseolina is a poor competitor insoil. The nonpersistence of M. phaseolina in stemsin soil suggests that the saprophytic activity of thefungus does not effectively increase its inoculumdensity in soil (Cerkauskas et al. 1982).Growth of the fungus in a soil phase is limited bythe availability of nutrients. Populations of the fungusin soil increase when hosts are grown continuouslyin the same field, and the disease thusbecomes more severe in successive crops. Therole of conidia in the disease cycle is notunderstood.ColonizationThe penetration and colonization of host tissue byM. phaseolina was reviewed by Dhingra and Sinclair(1978). Sclerotia germinate on the surface ofroots and produce numerous germ tubes. Penetrationof the roots generally occurs from appressoriaformed over anticlinal walls of epidermal cells orthrough natural openings. The fungal hyphae firstgrow intercellulary, then intracellularly through thexylem, and form sclerotia that plug the vessels.Sclerotia can be formed in green or juvenile tissuesbut are usually formed as a result of moribundityand release of nutrients.Dhingra and Chagas (1981) studied the colonizationof bean and wheat stems by M. phaseolina intwo soils. Colonization was maximum at 15-20°Cand decreased with increasing soil temperature. At15°C more wheat than bean stems were colonized;at higher temperatures the reverse was true. Maximumcolonization occurred at 15-25% moistureholdingcapacity, and there was a decrease withincreasing soil moisture. In controlled experimentsit was found that infection of soybean seedlingstook place in a 15-37°C range of soil temperatures,with infection of seedling stems occurring only atthe higher temperatures; infection increased withincreased exposure time and temperature (Lockeand Green 1976).M. phaseolina probably causes disease via themechanical plugging of xylem by sclerotia (Fig. 2),and via toxin production, enzymatic action (pectolyticand cellulytic enzymes), and mechanical pressureexerted by penetration of the middle lamellae(Dhingra and Sinclair 1978, Sinclair 1982).Control StrategiesA disease management program designed to minimizeyield losses should include: (a) adapted resistantor tolerant cultivars, or cultivars with atendency to escape infection; (b) balanced fertility;(c) good water management; (d) crop rotation;(e) care in weed and insect control; (f) use of highqualityplanting seeds; (g) use of fungicides, eitheras seed, soil, or foliage treatments, if appropriate;and (h) use of antagonists and organic matter.Disease ResistanceThe use of disease-resistant or tolerant cultivars isthe most economical and efficient way to controlplant diseases. However, resistance to M. phaseolinais not widely reported. Resistance in safflowerwas reported by Qadri and Deshpande (1982); susceptibilityappeared to be associated with lowsugar content or a rapid drop in sugar followinginfection. In resistant and susceptible Indian mustardcultivars, there was a general increase inphosphatidase activity in inoculated susceptiblecultivars, and activity was considerably lower inresistant ones (Srivastava and Dhawan 1982).Soybean plants were reported to decrease in susceptibilitywith increased age (Chowdhuri and Karmakar1978). Short et al. (1978) suggested that thedifferences in the numbers of propagules in diseasedtissues were a measure of the degree ofcompatibility between soybean cultivars and M.phaseolina.Balanced FertilityAdequate, balanced fertility is important in reducingdisease losses since it appears that high nitrogentends to reduce the saprophytic ability of thefungus. Also, plants under stress from deficient ortoxic levels of nutrients are more susceptible to M.177

phaseolina than those grown in soil with wellbalancedfertility.Planting undamaged seeds as free as possiblefrom pathogens produces vigorous seedlings andplants that will tend to escape infection by M. phaseolinaand sustain fewer losses from otherpathogens.Water ManagementWater management practices influence charcoalrot development (Palti 1983). Flooding a field for3-4 weeks before planting will reduce the viability ofsoilborne sclerotia and mycelia. The onset of charcoalrot can be delayed by postponing the lastapplication of irrigation water, since the diseasedevelops rapidly under dry, hot conditions andwhen plants are under water and maturation stress.Crop RotationAlthough M. phaseolina has a wide host range,isolates tend to be somewhat host selective andare ecologically specific. Thus, crop rotation willtend to reduce disease. Bristow and Wyllie (1975)found that the inoculum density of M. phaseolina inthe soil at planting time from continuous soybeanplots was twice that of maize-soybean rotationplots, and that the extent of root colonization by thecharcoal rot fungus averaged 33% more ih continuoussoybean plots. They concluded that earlyplanting and rotation with maize reduced charcoalrot development. Tillage practices, the crops to usein a rotation, and the length of rotation have notbeen studied intensively for the control of charcoalrot. However, Bisht (1983) found that row spacings(25 and 76 cm) and six tillage practices in eithercontinuous soybeans or in a maize-soybean rotationdid not affect the occurrence of charcoal rot.Weed and Insect ControlPlants under stress from weed competition, insectinjury, or herbicide or insecticide damage will bemore susceptible to M. phaseolina. Therefore,carefully applied agricultural chemicals to controlweeds and insects will help prevent losses fromcharcoal rot, as well as from other plant diseases.Seed QualityUse of FungicidesA number of fungicides have been tested on avariety of crops for the control of M. phaseolina. Aselection of reports on some of these tests is summarizedin Table 1. Systemic as well as topicalfungicides have been used as seed and soil treatmentsand as foliage sprays.Systemic fungicides offer the most promise forchemical control of charcoal rot. Carbendazim as ajute seed treatment controlled the disease (Barmanand Prasad 1981), but not when used as a soiltreatment on bean (Satischandra et al. 1979).Benomyl, carbendazim, and mancozeb increasedfiber yield of jute when used as a seed treatment(Barman and Prasad 1981). Thiophanate controlledcharcoal root rot on sunflower (El-Dahab etal. 1980) and clover (El-Tobshy et al. 1981b), andthiophanate-methyl controlled the same diseaseon cowpea, sesame, and sunflower and controlledleaf blight on mungbean (Taneja and Grover 1982).Carboxin, thiabendazole, thiophanate, and ethridiazolecontrolled macrophomina root rot of Egyptianclover (El-Tobshy et al. 1981b),Topical fungicides, such as quintozene, controlledbean root rot (Satischandra et al. 1979); andthiram and mancozeb controlled postemergenceroot and collar rot of groundnut (Natarajan et aI.1983), but mancozeb did not control root rot of bean(Satischandra et al. 1979). Captan alone (Satischandraet al. 1979) or in combination with carboxin(El-Tobshy et al. 1981 b) controlled root rot ofbean and clover, respectively.Four isolates of M. phaseolina became temporarilyadapted to four fungicides in culture, and asreversion to the parental type occurred, morphologicalcharacters also changed (Pan and Sen1982).Use of Antagonists and Organic MatterTwo antagonists, Trichoderma viride and T. harzianum,were active in reducing M. phaseolina sclerotialviability in sterilized and nonsterilized soils(Sharma and Bhowmik 1983). Wheat straw and ricehulls used as soil additives controlled root rot ofbean caused by M. phaseolina, but not farmyardmanure or green grass (Satischandra et al. 1979).178

179Table 1. Fungicides reported to be effective against Macrophomina phaseolina either in vivo or in vitro or both.Fungicide Crop ReferenceBenomylCaptanCarbendazimJuteSoybeanIn cultureIn cultureSesame, mungbean,sunflowerSoybeanBeanJuteSunflowerSesame, mungbean,sunflowerBarman and Prasad 1981llyas et al. 1976Menten et al. 1976Singh and Chohan 1981Taneja and Grover 1982llyas et al.1976Satischandra et al. 1979Barman and Prasad 1981El-Dahab et al. 1980Taneja and Grover 1982Carboxin In culture Menten et al. 1976Carboxin + captan Clover EI~Tobshy et al.1981a,1981bCopper 8-quinolinolate Clover El-Tobshy et al.1981a,1981bEtridiazole Clover EI-Tobshy et al. 1981bMancozeb Jute Barman and Prasad 1981Groundnut Natarajan et al. 1983Metham Soybean Gray 1979Methyl 4-[2(2-dimethylamino acetamide)phenyl]-3-thioallophanateSesame, mungbean,sunflower Taneja and Grover 1982Methoxy ethylmercury chloride+thiram Cotton Raju et al. 1982QuintozeneThiabendazoleThiophanate-methylThiramIn cultureSunflowerCottonBeanCloverSoybeanSunflowerCloverSoybeanSesame, mungbean,sunflowerSoybeanGroundnutMenten et al. 1976Narasimhan and Prakasam1983Raju et al. 1982Satischandra et al. 1979EI-Tobshy et al. 1981a, 1981bllyas et al.1976El-Dahab et al. 1980El-Tobshy et al. 1981allyas et al. 1976Taneja and Grover 1982llyas et al.1976Natarajan et al. 1983Triforine Soybean llyas et al. 1976Zineb In culture Kaur and Deshpande 1981Future Research Priorities1. Yield losses. Field studies need to be conductedto accurately determine yield lossesdue to M. phaseolina and those due to thestress conditions that favor development ofcharcoal rot. Ideally, genetically related "resistant"and "susceptible" cultivars should be

compared under stress conditions favorableto disease development. However, it must beknown that the cultivars do not react differentlyto the stress situation.2. Nonchemical control. Field studies areneeded to compare certain cultural practices,including the addition of potential antagonists,for control of charcoal rot. The control of soilmoisture levels and the use of organic amendmentsshould be studied in relation to diseasedevelopment. Results from published studiesare contradictory as to the importance of rotation,tillages, spacing, and other cultural practices.Field studies on the effect of these factorson charcoal rot development in sorghumshould be studied.3. Chemical control. Published data suggestthat further studies need to be conducted onwhether soil or plant application of systemicfungicides provides the most efficient andeconomical means of controlling charcoal rot.4. Integrated control. To provide the most efficientmeans of controlling charcoal rot, thebest combination of nonchemical and chemicalcontrol methods should be determined.ReferencesABDOU, Y.A., AL-HASSAN, S.A., and ABBAS, H.K. 1979.Effects of exudation from sesame seeds and seedlings onsclerotial germination and mycelium behaviour of Macrophominaphaseoiina, the cause of sclerotial wilt in the soil.Agricultural Research Review (Cairo) 57:167-174.ALI, S.M., PATERSON, J., and CROSBY, J. 1982. A standardtechnique for the detecting seed-borne pathogens inpeas, chemical control, and testing commercial seed inSouth Australia. Australian Journal of Experimental Agricultureand Animal Husbandry 22:348-352.BARMAN, B., and PRASAD, Y. 1981. Seed treatment ofjute against stem and root-rot incited by Macrophominaphaseoiina, Journal of Research, Assam Agricultural University(Assam, India) 22:48-249.BISHT, V.S. 1983. Effect of Cercospora sojina and Phomopsisspp. on soybean seed quality and yield, and ofproduction systems on diseases and yield of soybean.PhD. thesis, University of Illinois at Urbana-Champaign,USA. 303 pp.BRISTOW, P.R., and WYLLIE, T.D. 1975. The effect ofcrop rotation and date of planting on charcoal rot ofsoybean. Proceedings of the American PhytopathologicalSociety 2:83 (abstract).CERKAUSKAS, R.F., DHINGRA,O.D.,and SINCLAIR, J.B.1982. Effect of herbicides on competitive saprophyticcolonization by Macrophomina phaseolina of soybeanstems. Transactions of the British Mycological Society79:201-205.CERKAUSKAS, R.F., and SINCLAIR, J.B. 1982. Effect ofparaquat on soybean pathogens and tissues. Transactionsof the British Mycological Society 78:495-502.CHOWDHURI, A.K., and KARMAKAR, S.K. 1978. Theinfluence of plant age on the susceptibility of soybean(Glycine max L. Merrill) to Macrophomina phaseoiina(Tassi) Goid. Indian Agriculturalist 22:181-183.DHINGRA, O.D., and CHAGAS, D. 1981. Effect of soiltemperature, moisture, and nitrogen on competitivesaprophytic ability of Macrophomina phaseoiina. Transactionsof the British Mycological Society 77:15-20.DHINGRA, O.D., and SINCLAIR, J.B. 1973. Location ofMacrophomina phaseoli on soybean plants related toculture characteristics and virulence. Phytopathology63:934-936.DHINGRA, O.D., and SINCLAIR, J.B. 1977. An annotatedbibliography of Macrophomina phaseoiina 1905-1975.Vicosa, Brazil: Imprensia Universitaria, Universidade Federalde Vicosa. 244 pp.DHINGRA, O.D., and SINCLAIR, J.B. 1978. Biology andpathology of Macrophomina phaseoiina. Vicosa, Brazil:Imprensia Universitaria, Universidade Federal de Vicosa.166 pp.EL-DAHAB, M.K.A, TARABETH, A.M., and MOHAMED,S.E. 1980. Studies on sunflower diseases in Egypt: 1.Studies on charcoal rot and its control. Egyptian Journalof Phytopathology 12:113-122.EL-TOBSHY, Z.M., EL-SAYED, E.I., RAMMAH, A., andABD EL-SATTAR, M.A. 1981a. Pathogenicity and controlof three fungi associated with damping-off and root-rot ofthe Egyptian clover Trifolium alexandrinum L Faculty ofAgriculture, Ain Shams University, Research Bulletin No.1674.14 pp.EL-TOBSHY, Z.M., EL-SAYED, E.I., ABD EL-SATTAR,M.A., and RAMMAH, A. 1981b. Studies on the control ofdamping-off and root-rot diseases of the Egyptian clover,Faculty of Agriculture, Ain Shams University, ResearchBulletin No. 1718. 11 pp.GANGOPADHYAY, S., and WYLLIE, T.D. 1979. The effectof carbon:nitrogen ratios on sclerotial germination andpathogenicity of Macrophomina phaseoiina. Phytopathology67:1028 (abstract).GOEL, S.K., and MEHROTRA, R.S. 1975. Biochemicalnature of root exudates of Abelmoschus esculentus inrelation to pathogenesis of root and collar rot caused byRhizoctonia bataticola. Acta Phytopathologica AcademiaeScientiarum Hungaricae 10:41-49.180

GRAY, L.E. 1979. Effect of soil fumigation on survival ofMacrophomina phaseolina in soybean stem residue. Phytopathology69:540 (abstract).ILYAS, M.B., ELLIS, MA, and SINCLAIR, J.B. 1976.Effectof soil fungicides on Macrophomina phaseolina sclerotiumviability in soil and in soybean stem pieces. Phytopathology66:355-359.ILYAS, M.B., and SINCLAIR, J.B. 1974. Effects of plantage upon development of necrosis and occurrence ofintraxylem sclerotia in soybean infected with Macrophominaphaseolina. Phytopathology 64:156-157.KAUR, M., and DESHPANDE, K.B. 1981. In vitro evaluationof fungicides and antibiotics against Macrophominaphaseolina (Tassi) Goid., the incitant of leaf spot of soybean(Glycine max). Hindustan Antibiotics Bulletin 23:41 -44.LOCKE, J.C., and GREEN, R.J., Jr. 1976. The effect of soiltemperature on infection of soybean seedlings by Macrophominaphaseolina. Proceedings of the American PhytopathologicalSociety 3:276 (abstract).LOCKE, J.C., and GREEN, R.J., Jr. 1977. The effect ofvarious factors on germination of sclerotia of the charcoalrot fungus, Macrophomina phaseolina. Proceedings ofthe American Phytopathological Society 4:97 (abstract).MACHADO, C.C. 1980. [Sporulation of Macrophominaphaseolina (Tassi) Goid. and feasibility of a spore inoculationmethod in screening germplasm for resistance.]M.Sc. dissertation, University of Sao Paulo, Piracicaba,Brazil. 66 pp. (In Portuguese, English summary).MACHADO, C.C., and KIMATI, H. 1975. [Effect of light onformation of pycnidia of Macrophomina phaseolina inculture.] Summa Phytopathologica 1:65-66 (inPortuguese).MAGALHAES, A.A. de, CHOUDHURY, M.M., MILLAR,A.A., and ALBUQUERQUE, M.M. de. 1982. [Effect of soilwater deficit on Macrophomina phaseolina infection onbean.] Pesquisa Agropecuaria Brasileira 17:407-411 (inPortuguese).MENTEN, J.O.M., MACHADO, C.C., MINUSSI, E., CASTRO, C., and KIMATI, H. 1976. [Effect of some fungicideson the growth of Macrophomina phaseolina (Tassi) Goid.in vitro.] Fitopatologia Brasileira 1:57-66 (in Portuguese,English summary).MEYER, W.A., SINCLAIR, J.B., and KHARE, M.N. 1973.Biology of Macrophomina phaseoli in soil studied withselective media. Phytopathology 63:613-620.MICHAIL, S.H., ABD EL-REHIM, M.A., and ABU ELGA-SIM, E.A. 1977. Pycnidial induction in Macrophominaphaseolina in seed samples of four soybean cultivars.Acta Phytopathologica 12:311-313.MIHAIL, J.D., and ALCORN, S.M. 1982. Quantitative recoveryof Macrophomina phaseolina sclerotia from soil.Plant Disease 66:662-663.MOUSTAFA, A.M., and WYLLIE, T.D. 1974. Preliminarystudies on overwintering and survival of Macrophominaphaseolina. Proceedings of the American PhytopathologicalSociety 1:127 (abstract).NARASIMHAN, V., and PRAKASAM, N. 1983. Efficacy ofcertain fungicides in the control of root rot of sunflower.Pages 87-88 in Proceedings of the National Seminar onManagement of Diseases of Oilseed Crops. Madurai,India: Tamil Nadu Agricultural University.NATARAJAN, S., NARAYANASAMY, P., and KANDAS-WAMY, T.K. 1983. Control of post-emergence root rot andcollar rot diseases of groundnut. Pages 29-30 in Proceedingsof the National Seminar on Management of Diseasesof Oilseed Crops. Madurai, India: Tamil Nadu AgriculturalUniversity.PALTI, J. 1983. Coordination of disease control options inirrigated crops. Page 69 in Abstracts of papers presentedat the Fourth International Congress of Plant Pathology,University of Melbourne, Queensland, Australia.PAN, S., and SEN, C. 1982. Persistence of tolerance andcross resistance among fungicide-adapted isolates ofMacrophomina phaseolina. Zeitschrift fur Pflanzenkrankheitenund Pflanzenschutz 89:399-405.PAPAVIZAS, G.C., and KLAG, N.G. 1975. Isolation andquantitative determination of Macrophomina phaseolinafrom soil. Phytopathology 65:182-187.QADRI, S.M.H., and DESHPANDE, K.S. 1982. Studies onroot/collar rot of safflower caused by Rhizoctonia bataticola.Indian Botanical Reporter 1:141-142.RAJU, K.S., PANDU, S.R., and ADISESHAIAH, J. 1982.Varietal reaction and evaluation of fungicides against rootrot of cotton. Indian Journal of Mycology and Plant Pathology11:294-295.REUVENI, R., NACHMIAS, A., and KRIKUN, J. 1983. Therole of seedborne inoculum on the development ofMacrophomina phaseolina on melon. Plant Disease67:280-281.SATISCHANDRA, K.M., HIREMATH, R.V., and HEGDE,R.K. 1979. Effect of organic amendments and fungicideson the saprophytic activity of Rhizoctonia bataticolacausing root rot of beans. Indian Phytopathology 32:543-546.SHARMA, R.C., and BHOWMIK, T.P. 1983. Sclerotial populationof Macrophomina phaseolina in field soil undertropical climate and the effects of inorganic amendmentsand soil antagonists on their viability. Page 254 inAbstracts of papers presented at the Fourth InternationalCongress of Plant Pathology, University of Melbourne,Queensland, Australia.SHORT, G.E., and WYLLIE, T.D. 1978. Inoculum potential181

of Macrophomina phaseolina. Phytopathology 68:742-746.SHORT, G.E., WYLLIE, T.D., and AMMON, V.D. 1978.Quantitative enumeration of Macrophomina phaseolinain soybean tissues. Phytopathology 68:736-741,SHORT, G.E., WYLLIE, T.D., and BRISTOW, P.R. 1980.Survival of Macrophomina phaseolina in soil and inresidue of soybean. Phytopathology 70:13-17.SINCLAIR, J.B. 1982. Compendium of soybean diseases.St. Paul, Minnesota, USA: American PhytopathologicalSociety. 104 pp.SINGH, R.A., and CHOHAN, J.S. 1981. Effect of Benlateon growth and spore germination of Macrophomina phaseolina.Pesticides 15(7):8.SINGH, T., and SINGH, D. 1982. Transmission of seedborneinoculum of Macrophomina phaseolina from seedto plant. Proceedings of the Indian Academy of Sciences91:357-370.SRIVASTAVA, S.K., and DHAWAN, S. 1982. Phosphatidaseactivity in Brassica juncea plants infected with isolatesof Macrophomina phaseolina and its role inpathogenesis. Bulletin of the Torrey Botanical Club109:508-512.TANEJA, M., and GROVER, R.K. 1982. Efficacy of benzimidazoleand related fungicides against Rhizoctoniasolani and R. bataticola. Annals of Applied Biology100:425-432.QuestionsOdvody:Were all of the variant isolates of M. phaseolinafrom the same plant still virulent pathogens onsoybean?Sinclair:Yes.Odvody:Could you speculate on the importance of pycnidiain the disease cycle of M. phaseolina where it doesoccur on the host plant?Sinclair:Nothing has been published on the importance ofpycnidia in the life cycle. Pycnidia production canoccur on any portion of the soybean plant.Williams:You said that the pathogen has over 400 hosts.Then you said it specialized between maize andsorghum. What is your message?Sinclair:The pathogen isolated from various crops likemaize, soybean, squash, etc., can be crossinoculated.However, the isolates from the samecrop in continuous maize or soybean are morevirulent than if coming from a different crop (rotation).This has been shown from 5 years' data oncontinuous maize or continuous soybeans.Eastin:If charcoal rot is taking its toll from nearly the beginningin soybeans as you suspect, how do you measurethe toll?Sinclair:It would require studies under controlledconditions.Pappelis:When you pass the organism through a crop severaltimes, does the organism become morevirulent?Sinclair:I don't believe in the bridge-post theory. It's only atheory. The isolate adapts to the crop by passingthrough the same crop many years.Omer:Did you state that the fungus can attack activecells?Sinclair:Yes, it's in 2-week-old seedlings.Omer:Is it not the case that the fungus attacks only deador senescing cells?Sinclair:This is the challenge I am posing. Sorghum scientistsshould look for the fungal attack early in thecrop growth stage, since in other crops this pathogenis becoming virulent much earlier.Williams:How does the seed infection occur?Sinclair:It is through the pod and not systemic.182

Experience with Root and Stem Rots ofCrops Other than SorghumSummary and SynthesisJ.E. Partridge*It is difficult, if not impossible, to find another cropplant to compare with sorghum, considering thatsorghum is primarily grown as a nonsenescingplant that produces a "dry" seed as the agriculturalproduct of interest. After considering some of thepossibilities, we find that the woody perennials arethe closest "crop," but the biochemical, physiological,and phenotypical differences are sufficient todissuade us in that comparison.Other crops that may be useful for comparisonare the oil seed crops, including sunflower, safflower,and castor bean. In these crops, a Fusariumcomplex such as we find in sorghum (as reviewedby Dr. Zummo in these proceedings) or maize (asreviewed by Dr. Pappelis in these Proceedings) hasnot been characterized. The Fusarium species thatare pathogenic to these crops typically cause aroot rot and/or wilt, and not the stalk deteriorationtypical in sorghum. Conversely Macrophominaphaseolina does occur in sunflower.Macrophomina Stalk RotsM. phaseolina has a wide host range, causing diseasein over 293 plant species. Known in SouthAmerica as Pesta Negra, it is the most destructivestalk rot of sunflower under high temperature anddrought conditions. Its occurrence is unpredictableand, while frequent in southern areas where hightemperature and drought are common, it is rare innorthern areas.According to Cobia and Zimmer (1979, pp 27-28):Usually, symptoms are not apparent untilafter flowering, when poorly filled heads areevident and premature ripening and drying ofthe stalks occur. The diseased stalks normallyare discolored at the base, the pith isdisintegrated, and the vascular fibers have ashredded appearance. After a period of hotand dry weather, the fibers become coveredwith small black sclerotia.This description of the disease and its etiologyleads one to wonder if the internal shredding is acomponent of the disease contributed by the pathogenirrespective of the host, while the lodgingcomponent is contributed by the particular host.This is not to say that lodging does not occur innongramineous hosts.Fusarium Stalk Rot of Maizeand Natural SenescenceThe following is a discussion of research conductedby Partridge et al. (1984) and presentlyawaiting publication, It is presented here because Itwas not available for review by Dr. Pappelis and inhopes that its presentation might aid in our understandingof the disease:Although different methods have been used toevaluate hybrids for stalk rot reaction, there is at*Assistant Professor, Department of Plant Pathology, University of Nebraska, Lincoln, NE 68583-0722, USA.International Crops Research Institute for the Semi-Arid Tropics. 1984. Sorghum Root and Stalk Rots, a CriticalReview: Proceedings of the Consultative Group Discussion on Research Needs and Strategies for Control ofSorghum Root and Stalk Rot Diseases, 27 Nov - 2 Dec 1983, Bellagio, Italy. Patancheru, A.P. 502 324, India:ICRISAT.183

184least one common factor present in most evaluations.Because of the size of most experiments,investigators have found it necessary to collectdata as a single event. We reasoned that sincestalk rot is of pathogenic origin, the disease shoulddevelop progressively over time. Since not allmaize hybrids reach maturity on the same day, wefelt that useful information on disease developmentcould be obtained by planting hybrids of similarmaturity and monitoring stalk manual-crushabilityby taking data at weekly intervals.At the beginning of data acquisition, isolationswere made and it was determined that all plants ofall hybrids were infected by Fusarium moniliformeand/or Fusarium graminearum and/or Fusariumequiseti. Neither Diplodia maydisnor Macrophominaphaseolina was present. Beginning when stalksof all hybrids were still green and continuing until 5days after killing frost, we took weekly data onmanual crushability of the second internode abovethe brace roots.Briefly, the data (Fig. 1) indicate that stalk rotsymptom expression progresses as a simple interestdisease. In terms of Van der Plank (1963, pp40-51), the r value (infection rate) is constant for allhybrids because the infection was 100% at the timedata collection was begun. The rate of symptomexpression appears to be characteristic of the individualhybrid.Any discussion of a disease that occurs insenescing, senescent, or moribund tissue is inherentlyfraught with the difficulty of separating thenatural loss of integrity due to the senescenceprocess from the pathological decomposition thatis occurring at the same time. We prefer to use theterm "crushability" where loss of integrity is dueprimarily to the natural senescence process andthe role of internal parasites has not actually beendetermined. The term "stalk rot" we reserve forpathological decomposition that occurs frompathogenic origin. In our experiments, stalk rot isheld to be a condition resulting from the activity ofpathogens or parasites and clearly apparent onlyafter physiological maturity or killing frost.Our data indicate that even when the role ofmicroorganisms in the destruction of stalk tissuehas been amply demonstrated, it is erroneous notto consider the role of natural stalk senescence inthe disease. Accordingly, we interpret the linearincrease of stalk crushability prior to physiologicalmaturity as primarily a measure of the rate ofsenescence peculiar to each hybrid. In theabsence of other data, one cannot ignore the pos-80604020020020020020020020020020A = N7a x Mo17B = B59 x N152C = H99 x A632D = W64a x B73E = N159 x N160F = Mo17 x B73G = H99 x B73H = Mo17 x H99I = W64a x W117J = N139 x B7319791981ABCDEFGHI020J012 18 23 2 9 14 1923 28SeptemberOctoberMonth801008010080100801008010080100801008010080100Figure 1. Percent crushable stalks versus age.sible role of organisms in modifying the rate ofsenescence; however, it is equally true that onecannot disregard the fact that senescence in maizeoccurs with or without the involvement ofmicroorganisms.806040200

Once physiological maturity of the stalk hasbeen reached or senescence is complete, the roleof microorganisms becomes apparent and theircontribution to stalk rot is pronounced.In the absence of true physiological resistance,the parasites infect early in the life of the plant, butbecome pathogens only as the plant senesces.The key to disease management of this type ofstalk rot of maize (and possibly sorghum) lies in thepotential to develop hybrids that have a rate of ear(head) senescence (dry down) sufficiently morerapid than the rate of senescence of the lower stalkto provide a time interval for harvest.In summary, it is apparent that the stalk rot diseasephenomenon that involves the pathogenicdecomposition of the stem or stalk is not restrictedto sorghum, grasses, or even annual plants. Additionally,those organisms responsible for stalk rot(i.e., Fusarium spp and Macrophominaphaseolina)have similar environmental requisites for diseasedevelopment in a large and varied number of hosts.And finally, the host is not an inert member in theinteraction leading to the disease. Its physiologicalcondition as affected by age, stage, maturity, andenvironment plays a very key role in determiningthe time of onset of pathogenesis and the severityof the disease.ReferencesCOBIA, D.W., and ZIMMER, D.E. 1979. Sunflower productionand marketing. North Dakota Agricultural ExperimentStation Bulletin 25.PARTRIDGE, J.E., WYSONG, D.S., and DOUPNIK, B.L.[1984.] Natural senescence and stalk rot expression incorn. Plant Disease (in press).VAN DER PLANK, J.E. 1963. Plant diseases: epidemicsand control. New York, New York, USA: Academic Press.DiscussionRelation of Nutrient Deficienciesto Root and Stalk Diseases of MaizeSchneider:Potassium affects cell death in maize.Pappelis:We have gotten K deficiency even at normal levelsof K, especially when N is low. When we addedincrements of K, it could be overcome; but we couldalso reduce K deficiency by adding N.Schneider:Is there a mechanism for this?Pappelis:No. We used complete nutrients in our studies(Hoagland solution).Schneider:Is there a role of K in carbon translocation?Induced senescence can occur with low K.Clark:As for cell death, I have no comment. Potassium isinvolved in cycling or translocation of carbon. Potassiumalso interacts with N; NH 4 inhibits K uptakeand NO 3 enhances K uptake.Doupnik:There are no low K soils in Nebraska, and we foundno influence of K on stalk rot.Maranville:Nebraska soils are high in K, and we have neverfound a K deficiency by lowering N.Pappelis:By altering N and K, we got what we think was a Kdeficiency in our greenhouse studies.Clark:From mineral deficiency studies, it is sometimesdifficult to separate K deficiency from some otherdeficiencies.Schneider:From my studies on mineral nutrition and Fusariumon celery, K affected the disease, California soilsare high in K also, but when I added K with CI the185

disease was controlled, in contrast to K 2 SO 4 andKNO 3 . The source of N also affected the disease.Earlier studies indicated similar types of effects ofstalk rot on maize [Younts, S.E., and Musgrave, R.B.1958. Chemical composition, nutrient absorption,and stalk rot incidence of corn as affected by chloridein potassium fertilizer. Agronomy Journal50:426-429].Claflin:Does temperature (especially cooler temperature)affect K uptake?Clark:Theoretically yes, but this may not be of muchpractical importance since cooler temperaturesalso decrease plant growth.Maranville:In soils, NH + 4 is converted to NO 3 - , and NO 3 - is thepredominant form of N taken up by plants.Clark:Is the K deficiency really an Mg deficiency? Theylook very much alike in many cases.Charcoal Rot (Macrophomina phaseolina)Vidyabhushanam:Dr. Sinclair, in your presentation, you mentionedthat resistance to charcoal rot is complicated. Hasany work been done in this regard on soybean? Ifso, what are the findings?Sinclair:No, the problem of charcoal rot on soybean is notconsidered significant enough in the U.S. to breedfor resistance. The disease occurs in some years,but the losses are never of such a level that breedingfor resistance is economical.Partridge:Soybean plants tend to compensate for losses ofplants in the row. Could this be the reason onewould not detect certain amounts of seedlinglosses due to Macrophomina?Sinclair:Yes, in part. It's always difficult to measure yieldlosses in soybean due to seedling disease,because soybean plants tend to branch and thuscompensate for reduced stands.Williams:You recorded seed transmission of Macrophominain soybean. How does it get into the seed?Sinclair:We have not done any histopathology on this pathogen.But we have evidence of the presence of thepathogen in the tissues from the base to the top ofthe plant. I'm sure the pathogen penetrates theseed—if not systemically, then through the pods.Claflin:Are you saying that this is a passive transmission inthe seed for this organism?Sinclair:The seeds were surface sterilized with 70%ethanol, Chlorox, then washed with distilled water,before being placed on filter paper. The transmissionwas internal.Pappelis:Our experience was that we could never get charcoalrot on immature seedlings from soybeanseeds collected from the lower part of the plant. Wedid not know where the organism on mature plantscame from, but it did not come from the seed.Where the organism came from is an open question.We have never seen immature plants withcharcoal rot. We have seen many other organismssuch as Fusarium and Alternaria on immatureplants.Sinclair:Did you find Macrophomina on immature seed?Mature seed?Pappelis:Not on immature seed. We sterilized pods, but wenever got the organism. For 5 years, we gotextremely low levels or no charcoal rot in ourexperiments.Odvody:Are pycnidia involved?Sinclair:The role of pycnidia in the life cycle of this organismhas not been studied. I now have students workingon this.Odvody:On sesame, I've found a lot of pycnidia. On186

187sorghum and maize, I didn't find any natural occurrence.Isolates from these plants produce pycnidiain specific culture media under long-wave ultravioletlight, but not as readily as sesame isolates.Sinclair.I would like to see sorghum scientists try a techniquewe use. We treat soybean stems, pods, petioles,and leaves with paraquat or glyphosate andcan detect latent infection of Macrophomina, Colletotrichum,Phomopsis, Circospora kikuchii, andC. sojina. Green stem tissues without diseasesymptoms are dipped in the herbicide (glyphosateis safer to use) and plated on filter paper. In 5 to 7days, fruiting structures of the fungi appear. We candetect the fungi 2 to 3 weeks in advance of thatnoted in the field. It's a good technique to detectdisease. Other scientists are also using it. I don'tknow whether it will work for a monocot likesorghum.Odvody:We were readily able to isolate Macrophomina fromsymptomless infected roots by incubating them inlaboratory humidity chambers after roots were surfacesterilized.Pande:We have had two kinds of experiences: In one wecould not get any Macrophomina from symptomlessroots. But in the sorghum plant there are primaryroots that die early and hang from the crown ofthe plant. Macrophomina can be obtained fromthese roots, but not from the healthy roots of thesame plant. We have successfully isolated thepathogen from the seedling stage to maturity. Thesecond situation occurred when we artificiallyinoculated the young seedlings that were grown insterilized Hoagland culture. On the 12th day, irrespectiveof the variety, we got a kind of discolorationwhen the Macrophomina was put aseptically intothe medium. When infected seedlings were plantedin sterilized soil, they stayed alive for a while beforedying. However, this requires more detailed investigations,which we are presently engaged in.Omer:Does infection start at the cotyledon or crown?Sinclair:Macrophomina is in the soil all the time and penetratessoybean directly. It does not require woundsor natural openings. The sclerotia will germinatenear host roots and penetrate them directly. Theorganism doesn't need to penetrate the cotyledonsor leaves or other plant parts.Rosenow:Because sorghum intemodes aren't of equal lengthlike those in maize, and the lower part of thesorghum stem has many nodes, this might causedifficulties in looking at specific internodes, as hasbeen suggested in maize. Dr. Pappelis, do you haveany suggestions based on your experience inmaize?Pappelis:The way we do it is published, and we also have alot of unpublished data. This can be determinedeasily. We have looked at numerous maize linesfrom many stalks.Jordan:As temperature increases, the optimum water orosmotic potential for growth is low. Often growth isreduced to a point where optimum growth shiftsfrom -5 to -20 or -30 bars. Has anyone anexplanation?Schneider:We note this for Verticillium and various Fusariumspecies. J. Levitt gave an explanation for this,although I don't remember what it was, in his bookon stress physiology [1972. Responses of plants toenvironmental stresses. New York, N.Y, USA: AcademicPress].Pappelis:It may be a pH phenomenon. For pathogens takenfrom maize, if the pH changed from 3 to 8, no growthoccurred at 3, but growth did occur at 5. If the tissuewas ground and added to media of a resistantvariety, the growth of the fungus was inhibited. ThepH effects are different for Gibberella zeae. Aninhibitor may not be present; it may be a matter of apH change. The pH of an onion cell may be 5.5, butright next to it the pH of a fungus cell may be 3 to3.5. Other organisms show different results, and Idon't know what these mean.Rosenow:We have a hard time sticking a toothpick into thesame internode all the time, especially when 90%of the stem is peduncle. With nodes so closetogether, how do we determine which internode to

use? Should we count down from the top of theplant?Pappelis:If I can't feel the node, I drill (I don't use a toothpick)to the center. If I don't hit the center, I don't rate thatplant. I usually inoculate at least 15 plants, knowingI won't hit the center on all, and take ratings only ofplants that have been inoculated in the center.Sometimes I slice the stem to make sure that theinoculum is in the appropriate place. Plants in therow are evenly spaced to reduce other variables.The job isn't easy, and a lot of variability can arise.Is anyone aware of recent studies on ethylenebiosynthesis and how those data might be relatedto methylase activity in senescing cells? [Editor:See Adams, D.D., and Yang, S.F. 1979. Ethylenebiosynthesis: Identification of 1-aminocyclopropane-1-carboxylic acid as an intermediatein the conversion of methionine to ethylene.Proceedings, National Academy of Science (USA)76:170-174.]188

Control of SorghumRoot and Stalk Rots

The Role of Fungicides in the Control ofSorghum Root and Stalk DiseasesR.J. Williams and O. Nickel*SummaryThe present knowledge and research activity on the use of fungicides to control sorghum rootand stalk diseases are reviewed. Seedling diseases caused by seed- and soilbome fungi arereadily controlled by treating seed with small quantities of appropriate fungicides, with combinationsof systemic and nonsystemic compounds finding increasing use. Virtually nothing isknown about the potential role of fungicides for the control of root and stalk rots of adultsorghum plants, though fungicides are available with activity against the causal organisms.More information is needed on the biology and epidemiology of these diseases in order to betterassess the practical possibilities for their control by fungicides. The below-ground infection andearly colonization sites are difficult targets for fungicide application, but systemic products,particularly the new generation with high activity at low rates, could offer useful possibilities forintegration with host-plant resistance and crop-management control practices.The importance of sorghum as a food crop in thetropics, the need to rapidly increase sorghum productionin many less-developed countries where itis a staple food, and the importance of pest anddisease control for the achievement of increasedproduction have been strongly emphasized inrecent conferences and publications (ICRISAT1980, ICRISAT 1982, Williams et al. 1983).During the past 15 years a major internationalplant breeding effort has been underway to develophigh-yielding cultivars of sorghum. It has not beendifficult to develop new sorghum genotypes withhigh yield potential, but it has been difficult toachieve these potentials on farms in the tropics dueto the adverse effects of a wide range of environmentaland biotic stresses (ICRISAT 1982), someof which are considerably more severe on the newhigh-yield-potential cultivars than on traditionallandrace cultivars, e.g., grain molds (Williams andRao 1981) and stalk rots (Dodd 1980).It is now well accepted that for sorghum cultivarswith high-yield potential to be useful in the tropicsand subtropics they need protection against a widerange of pests and pathogens. There is a strongresearch effort in several countries to find and usehost-plant resistance to many of the biotic enemiesof sorghum, and given time and adequate resources,this approach can be successful for manyof them. However, the development of cultivarswith resistance to a wide range of pests and pathogenswill take time, the resistant cultivars could bevulnerable to "breakdown" through adaptivechanges by their genetically variable enemies, andadequate resistance to the full range of pests andpathogens attacking the crop may not be availableor may not be feasible to incorporate. There is,therefore, a need to consider the role that otherdisease control measures can play in the urgentand important endeavor of rapidly increasing onfarmproduction of sorghum in the less-developedworld.The future of successful, stable disease controlmust involve the careful integration of all appropriatedisease control methods, to maintain diseaselevels below those that cause significant losses inproduction and to minimize the opportunities for*Phytopathologists, Ciba-Geigy AG, Agricultural Division, CH-4002, Basel, Switzerland.International Crops Research Institute for the Semi-Arid Tropics. 1984. Sorghum Root and Stalk Rots, a CriticalReview: Proceedings of the Consultative Group Discussion on Research Needs and Strategies for Control ofSorghum Root and Stalk Rot Diseases, 27 Nov - 2 Dec 1983, Bellagio, Italy. Patancheru, AP. 502 324, India:ICRISAT.191

pathogens to adapt to and overcome the diseasecontrol measure(s). There is a need for pragmatism,innovation, and above all open-mindedness inconsidering the possible measures that could beused to control the sorghum pest and disease complex.An impressive array of fungicides is availablewith strong protective and curative activity againsta wide range of plant pathogenic fungi, and moreare likely to become available in the near future.While it is recognized that a large proportion ofsorghum farmers in the tropics and subtropics areresource poor and cultivate small farms and thattherefore they cannot be expected to use fungicideson a large scale as the sole means of controlof the sorghum disease complex, we believe itwould be a mistake to dismiss the possibilities forthe judicious and integrated use of appropriate fungicidesin sorghum disease managementprograms.In this paper, at the invitation of the InternationalCrops Research Institute for the Semi-Arid Tropics(ICRISAT), we have reviewed the role of fungicidesin the control of sorghum root and stalk diseases.The basic objectives, as specified in the ICRISATinvitation, are to:a. assess present knowledge and researchactivity,b. determine gaps of knowledge and research,c. determine future research and strategies forcontrol and management.Key Questions for ConsiderationThe key biological questions that need to be consideredare:a. which are the important organisms that inciteroot and stalk diseases?b. do fungicides exist that are biologically effectiveagainst these organisms?c. can the fungicides be brought to the criticalinfection/colonization sites at the criticalstages of crop growth to effectively control theorganisms before they incite damaging levelsof disease?The key technical, economic, and social considerationsconcern:a. the technical skills and complexity of applicationequipment required to deliver the fungicidesto the target sites at the appropriatedosages and crop growth stages;b. the costs of the fungicides, application equipment,and the actual application relative to theincreased value of the treated crop;c. the safe use of the fungicide on the farm, withregard to crop tolerance, human safety, andenvironmental compatability.We believe it to be important to first thoroughlyexplore the biological questions, to establish whatis biologically possible, and not to preclude the useof fungicides at the outset because of apparenttechnical and/or economic constraints. These latterparameters can change rapidly and dramaticallywith changes in such factors as governmentpricing policies and crop production levels.The Target Organismsand DiseasesThe important stalk and root disease problemsdefined by ICRISAT in the invitation to prepare thisreview are:a. fusarium root and stalk disease complexb. charcoal rot (Macrophomina phaseolina/Rhizoctoniabataticola)c. pythium root and seedling rotsd.. anthracnose stalk rot (Colletotrichumgraminicola)e. periconia root and stalk rotsf. acremonium wiltg. cephalosporium wilth. other root and stalk rotsIt is interesting, and correct, that seedling diseaseshave been included among the root andstalk diseases, for, as will be discussed, the attackon the primary roots and shoots of the germinatingseeds and the pre- and postemergent seedlings byseed- and soilborne fungi represents an importantarea for disease control.Seed and Seedling DiseasesThe ProblemThe germinating seeds and young seedlings ofsorghum are vulnerable to invasion and infectionby a large number of seed- and soilborne fungi that192

cause seed rot, seedling death, and stunted seedlinggrowth, resulting in reduced plant populationsand nonuniform crop growth (Tarr 1962). Adverseenvironmental factors that reduce the rate of germinationand seedling development, such as lowsoil temperature, waterlogging, and drought,increase the problems of seed rot and seedlingdisease, while the seedling pathogens, throughtheir damaging effects on young roots and stems,reduce the ability of seedlings to withstand andrecover from pre- and postemergence stress problemssuch as shootfly attack and drought.Many diverse seed- and soilborne fungi arereported to be associated with seed rot and seedlingdisease in sorghum (Table 1), including Oomycetes(e.g., Pythium spp), Basidiomycetes (e.g.,Rhizoctonia solani), and Ascomycetes (e.g., Gibberellaspp, Glomerella spp, Dreschlera spp). Fungalpathogens that incite diseases of aerial organsof adult plants, such as Helminthosporium turcicum,Gloeocercospora sorghi, and Phoma insidiosa,and more saprophytic fungi such asAspergillus spp and Penicillium spp, can, undersuitable conditions, also cause sorghum seed rotand seedling disease (Tarr 1962, Dhanraj 1979).In addition to the fungi that cause seed rot andseedling disease, sorghum seedlings are vulnerableto infection by highly specialized fungi, such asPeronosclerospora sorghi and Sphacelotheca spp,that develop systemically within the growing plantto cause disease in the adult plant (Sphacelothecaspp) and seedling and adult plant (P. sorghi). Thereare also indications that the fungi involved in stalkrots of the maturing plants may first infect at a muchearlier stage of plant development, but more evidenceis needed on how early the infection occurs.Control MeasuresAlthough there are differences among sorghumcultivars in vulnerability to seed rots based ondegree of seed hardness (Tarr 1962), several factorsact against the successful development ofsorghum cultivars resistant to seedling diseases,including:a. the wide range of organisms involved,b. the unspecialized facultative pathogenicity ofsome of the most important causal fungi, andc. the high degree of vulnerability of seedlingtissues to colonization by soil- and seedbornefungi.Table 1. Sorghum seed and seedling pathogens.(Source: Tarr 1962.)DiseaseSeed rotDamping-offSeedling blightRoot rotDowny mildewCovered smut cLoose smut cHead smut cCausal fungusAlternaria spp aAspergillus spp aHelminthosporium turcicumPenicillium sppPhoma insidiosaPyrenochaeta terrestrisPythium spp bRhizopus spp aCorticium rolfsiiFusarium culmorum bFusarium moniliforme bPenicillium oxalicumPythium graminicola bPythium spp bRhizoctonia solani bColtetotrichum graminicolaFusarium graminearumHelminthosporium turcicumMacrophomina phaseolinaPhenicillium oxalicumPyrenochaeta terrestrisPeronosclerospora sorghiSphacelotheca sorghiSphacelotheca cruentaSphacelotheca reilianaa. Primarily saprophytic.b. Main fungi causing poor emergence of sorghum.c. Infection at seedling stage, but symptoms not expressed untilflowering.Cultural measures that can be used to reducethese disease problems include the selection ofclean undamaged seed for planting, and, in someregions, avoiding planting in cold wet soils.The most widely applicable and consistentlyeffective method to control seed rot, seedling disease,and seedling infection by systemic pathogensof adult plants is the treatment of seed orplanting furrows with fungicidal chemicals. Thesystemic fungicides, which protect against a widespectrum of plant pathogenic fungi, are particularlyvaluable, as they enter the seedling tissues andprotect the entire seedling for relatively longperiods.In the first half of this century inorganic compoundssuch as copper carbonate, copper sul-193

194phate, and sulphur, and mercury-based productswere used to treat sorghum seed in various soaking,steeping, sprinkling, and dusting treatments(Tarr 1962). In cold soils, sulphur caused emergencereduction that was not apparent in tropicalcountries, and the mercurials also had problems ofphytotoxicity above certain critical applicationrates. The spectra of activity of the organomercurialfungicides were broader than those of the inorganiccopper and sulphur fungicides, and theywere somewhat less phytotoxic at the relative dosagesrequired for effective control of seed- andsoilborne fungi. Until the end of the 1970s the organomercurialfungicides were widely used throughoutthe world in seed treatments against a diverserange of plant pathogenic fungi. However, becauseof their high mammalian toxicity and persistence,and the growing realization of the hazards of suchproducts, the use of the organomercurial fungicideshas by today been severely restricted or evencompletely banned (as in Australia, Algeria, Canada,Morocco, New Zealand, South Africa, and theUSA). Their withdrawal from several other countriescan be expected in the near future (Bowling1978).From the late 1940s well-tolerated nonmercurialorganic compounds, which were relatively low intoxicity compared with the organomercurials, suchas thiram (tetramethylthiuram disulphide) and captan[N-(trichloromethylthio)-cyclohex-4-ene-1, 2-dicarboximide] began to be widely used in dust andslurry treatments, often combined with an insecticidesuch as gamma-BHC, for the protection ofsorghum seed and seedlings (Tarr 1962), Thesefungicides have a strong protective/eradicantactivity against a wide range of plant pathogenicfungi, and sorghum seed treatment with them, oftenin combination with insecticides/is still practicedtoday, with farmers in some countries able to buyinexpensive sachets of premixed products at thelocal village store.The development of systemic fungicides in the1960s and 1970s has provided a powerful newgroup of weapons to use in the war on seed andseedling diseases, e.g., (a) the benzimidazole fungicides,which show considerable activity againstmany diverse pathogens, some of which (e.g., Colletotrichumspp, Fusarium spp, Rhizoctonia spp,Penicillium spp) are involved in the seed-rot/seedling-disease complex; (b) the oxathiin derivatives,carboxin and oxycarboxin, which are highlyeffective against Basidiomycete fungi, thus providingopportunities for the control of R. solani and thesmut fungi; and (c) the acylalanine fungicides, firstTable 2. Recent literature on the control of sorghum seed mycoflora and on the effectiveness of fungicides inincreasing sorghum plant establishment in India through seed treatment.SourceMunghate and Raut1982Raut and Wangikar1982Bhale and Khare1980Bidari et al. 1978Sharma et al. 1976Patil-Kulkarni et al.1972Type of testBlotter test of seedmycoflora controlBlotter test of seedmycoflora controlPot test of plantestablishmentPot test of plantestablishmentField test of plantestablishmentField test of plantestablishmentFungal generainvolvedAlternana, Cladosporium,Curvularia,Drechslera, Fusarium,PhomaAlternaria, Cladosporium,Curvularia,Drechslera, FusariumCurvulariaFusarium, Curvularia,HelminthosporiumCurvularia, Fusarium,Alternaria, VerticilliumRhizoctonia (inoculumintroduced)Most effectivefungicides(in rank order)Dosage(% W/W)thiram, captan 0.25thiram 0.23thiram (and) 2-methoxyethylmercurychlorideferbam, benomyl,thiram0.250.2thiram, captan 0.4carboxin, benomyl 0.6

epresented by the highly active metalaxyl (Urechet al. 1977), with specific activity against Oomycetes,of which Pythium spp play a major role inseedling damping-off, particularly when seed isplanted in cold wet soil. Metalaxyl has also beenshown to provide excellent protection in sorghum,and other cereals, against the systemic downy mildews(Anahosur 1980, Frederiksen and Odvody1979,Schwinn 1980).In Tables 2 and 3 we have summarized resultsfrom publications from India and the USA in whichreports were made on control of seed- and soilbornefungal pathogens of sorghum seedlings. Thecurrent trend in the USA appears to be the combinationof the broad-spectrum nonsystemic fungicidessuch as thiram or captan with one of themodern fungicides, whereas in India the singlecompounds are still mainly used.It is quite apparent from the above that thereexists today a wide range of fungicides effectiveagainst virtually the whole range of fungi that rotseeds and cause death and disease in seedlings. Iflocal researchers can determine what are theimportant local seed and seedling pathogens ofsorghum, suitable pesticide mixes can probably bedeveloped for use in seed treatments for effectivecontrol.Seed treatment with fungicides at the farm levelis a simple operation that requires little technicalskill and no expensive or complicated equipment.The quantities of fungicide products needed foreffective seedling disease control are small (generallyin the 0.3-1 g a.i./kg range), making seedtreatment more economically feasible for a largernumber of farmers than any other means of fungicidetreatment of the sorghum crop.Table 3. Recent literature on the effectiveness of fungicides used as seed treatments in increasing sorghumplant establishment in field tests in the USA.SourceHansing 1974Philley andFrederiksen1975Hansing 1975Hansing 1976Hansing 1978Fungal generainvolvedFusarium, Pythium,RhizoctoniaNot specifiedFusarium, Pythium,RhizoctoniaFusarium, Pythium,RhizoctoniaFusarium, Pythium,Rhizoctonia et al.Most effectivefungicidesthiram+carboxinthiram+carboxinPPG-152 50 WOlin OAC 5-478750 WU.S. Units1.9 oz/bu+1.7 oz/bu4.0 oz a.i./cwt+4.0 oz a.i./cwt5.0 oz/buDosageMetricequivalents a2.1 g/kg+1.9 g/kg2.5 g a.i./kg+2.5 g a.i./kg5.5 g/kg4.0 oz/bu 4.4 g/kgPCNB 23.2%+2.0 oz/bu 2.2 g/kgetridiazole 5.8%+OAC 5-1563 48 F 2.1 oz/bu 2.3 g/kgcaptan-60%+dieldrin-15%Anzalone 1980 Pythium, Fusarium captan 4carbendazim 7%+maneb 70%Anzalone 1982Fusarium, Pythium,Rhizoctoniaa. Approximate values, converted from U.S. Units.thiram 17%+carboxin 17%1.67 oz/bu 1.8 g/kg3.4 fl. oz/bu4.0 oz/bu3.9 ml/kg4.4 g/kg4.0 oz/bu 4.4 g/kg195

Stalk and Root Rots of Adult PlantsThere are very few reports in the literature ofresearch on the fungicidal control of stalk and rootrots of sorghum after the crop has passed theseedling stage (Tables 4 and 5). For maize, suchreports are somewhat more numerous, but they arefew compared with the numbers on the fungicidalcontrol of seedling diseases and smuts of sorghumand of chemical control of nematodes in maize(Table 5). This dearth of 'available literature couldindicate that:a. these diseases are not regarded as sufficientlyimportant to warrant much research effort,b. they are difficult to work with,c. they are difficult to control with fungicides, andthus positive results have been few,d. these are more easily used, more effective, ormore economically viable means of control.Table 4. The relative frequency of entries on variouscategories of sorghum pathology in Reviewof Plant Pathology 1973-1982.CategoryAll diseasesSeed fungi/germination/establishmentFungicide seed treatmentsRoot and stalk rotsChemical control of root and stalk rotsa. Total number was 434 entries.% of entries100 a103.570.7Table 5. The relative frequency of reports ofresearch on the use of fungicides/nematicidesfor the control of various diseases andnematodes in sorghum and maize in Fungicideand Nematicide Tests from 1974 to1983. aThe numbers (%) ofreports forDiseasegroup Sorghum MaizeAll diseases & nematodesSeedling diseasesRoot rotsStalk rotsSmutsNematodesa. i.e., results of 1973-1982.26(100) 67(100)11 (42.3) 3(4.5)0(0) 1 (1.5)0(0) 5(7.5)10(38.5) 0(0)3(11.5) 33(49.3)Experience gained in attempts to increasesorghum production over the past 20 years showsclearly that stalk rots are a major constraint to theachievements of high grain yield, and that as yet noeasily used economically viable, effective meansof control is available (ICRISAT 1980, ICRISAT1982). The root and stalk rots are difficult to workwith, because of (a) their physical location, belowground level and within the stalk tissue; (b) theseveral pathogens that can be involved; and (c)their interactions with environmental stress andcrop productivity levels.The Causal OrganismsThe three fungi of greatest importance in stalk rotetiology in sorghum appear to be M. phaseolina (R.bataticola), Fusarium moniliforme, and C. graminicola.A fourth, Cephalosporium acremonium(=Acremonium strictum ?) can also cause seriousstalk rot, but appears to be more local in occurrence.The relative importance of these in the tropicshas not been systematically determined, but it isbelieved that charcoal rot, caused by R. bataticola(the sclerotial stage of M. phaseolina), and fusariumstalk rot are the most widespread on sorghum.Apart from the milo disease caused by Periconiacircinata, which has been well studied and controlledwith host plant resistance on a sustainedbasis for many years, little is known of root rot ofsorghum, and the only major studies of sorghumroot problems appear to be those on the root parasitesbelonging to the Striga spp (Ramaiah andParker 1982).Control with FungicidesCurrent Knowledge.We have not been able to find any reports of conclusiveresearch results on the fungicidal control ofsorghum stalk and root rots. Clinton (1960)observed a slight but nonsignificant reduction inlodging in a crop in which thiram was used as adrench (173 g/ha) applied shortly after flowering.Reports of control of R. bataticola incited root andstalk rots in other crops are summarized in Table 6.In the most recent report found, that of Taneja andGrover 1982, complete control of sunflower andsesame root rot was achieved by seed treatmentwith benomyl or thiophanate-methyt at 2 g productper kg seed.196

Table 6. Summary of reports on control of Rhizoctonia bataticola induced diseases in several crops.Source Type of test Crop Disease Effective control compoundsTaneja andGrover 1982Goel andMehrotra1973Clinton 1960Seymour andCordell 1979Vir et al. 1972Field testswith seedapplicationPot testwith seedapplicationField testwith thefungicidewatered intothe soilshortly afterfloweringField testwith soilfumigationField testwith foliarsprays/plant drench(~1100 litres/ha)a. Lodging reduced only slightly.SunflowerSesameOkraRoot rotRoot rotSeedlingdampingoffbenomyl, thiophanate methylcarbendazim-60, benomyl,thiophanate methylCeresan, thiram, PCNBApplicationrates0.2% W/W02% W/W0.3% W/WSorghum Lodging (thiram) a 173g/haPineSoybeanSeedlingmortality+charcoalroot rotCharcoalrotmethyl bromide (67%) +chloropicrin (33%)thiophanate, furcarbanil390 kg/ha1000 ppm(1.1 kg/ha)In contrast to field studies, there are numerousreports of the in vitro effectiveness of fungicides toinhibit the growth of the major stalk rot pathogens.However, activity in vitro is not necessarily relatedto utility for disease control in the growing crop, andthus we do not believe it appropriate to present adetailed review of these in vitro studies.It appears that the only field crops that are regularlytreated with fungicides for control of a basalstalk disease of the adult plants are barley andwheat in Europe, where 70-80% of the croppedarea is treated with foliar sprays of, until veryrecently, mainly benzirnidazole fungicides, for thecontrol of eyespot (Pseudocercosporella herpotrochoides).The degree of control achieved dependsupon the disease pressure, which is primarilyrelated to the weather, but reductions in the diseaseindex from 80% to 20% is an acceptable andachieveable target. In the past 2 years, problems ofpathogen resistance to benzirnidazole fungicideshave arisen, and different fungicide groups arebeing examined to cope with this problem (Trow-Smith 1983).The major difficulty, in the absence of an effectivebasipetally translocated fungicide is to get sufficientproduct to the critical infection and earlycolonization sites. However, the trend is towardsystemic fungicides with high activity at low rates,such as the sterol-inhibiting triazole compounds,and these new products need to be evaluated fortheir activity.Gaps in Knowledge and ResearchThe major areas in which gaps in our knowledgewill need to be filled if we are to objectively assessthe potential role of fungicides in contributing to thepractical control of root and stalk rots in the adultsorghum crop are:197

a. the biology and epidemiology of the diseases,b. relationships with other diseases and stressfactors.c. the relationship between disease levels andcrop loss,d. the availability of and ease of handling hostplantresistance.The more complete the state of knowledge onthe biology and epidemiology of the diseases, thegreater will be the opportunity to identify criticalpoints in the disease life cycles when the pathogenswould be most vulnerable to fungicidal action.The key parameters are:a. the "overwintering'' mechanismsb. the sources of primary inoculumc. the stages of growth when primary infectionoccursd. the physical location of the primary infectionsitese. the colonization and disease developmentdynamics from the primary infection sitesf. the role of secondary infectionFungicides can be used as a valuable researchtool to help obtain the information to fill these gaps(e.g., the role of seedbome inoculum, or whetherinfection of seedlings is important, can be evalu-ated through the use of appropriate fungicide seeddressings), and thus it would be wrong to wait untilwe fully understand the biology and epidemiologyof the diseases before we bring fungicides into theresearch action. However, once the targets aremore clearly known, more accurate experimentationon the biological potentials for fungicide usewill be possible. Once biological efficacy is demonstrated,the questions of economic and technicalfeasibility will need to be examined.There are many gaps, and the way to fill them isthrough research. The objectives of this meetingare to identify the gaps and define the research,with priorities, to fill them.Suggestions for Future ResearchWe cannot give precise suggestions for experimentationbecause of our lack of knowledge ofsome of the key elements of the target diseases.However, we can describe some possible scenariosand the approaches that would appear to beappropriate, e.g.:a. pathogen entirely seedborne - chooseappropriate fungicides based on the fungalspecies (Table 7) and examine the effects ofTable 7. Information on fungicide groups a that are appropriate for use in research trials for the control ofsorghum root and stalk diseases (including seedling disease).Fungicide group Activity Transport character Target pathogensAcylalanines Systemic Primarily acropetal,though some basipetalmovement reportedOomycetes: Pythium, Phytophthora,Peronosclerospora, Sclerospora,SclerophthoraBenzimidazoles Systemic Acropetal Many, excluding Oomycetes anddark-spored Ascomycetes; particularlyeffective on Fusarium spp andColletotrichum sppOxathiinderivativesPhthalimidesThiocarbamatesSystemicNonsystemic protectantProtective/eradicantnonsystemicAcropetalBasidiomycetes: Rhizoctonia spp;smut fungi; Helminthosporium: CurvulariaMany diverse pathogensMany diverse fungiTriazoles Systemic Acropetal Typhula, smut fungi, and many cerealfoliar pathogensa. Omission of any fungicide group does not necessarily indicate that certain fungicides belonging to those groups could not be potentiallyuseful for the control of sorghum root and stalk diseases.198

seed treatments using from 0.2 to 1 g a.i./kgseed;b. pathogen soilbome but initiates infectionat the seedling stage - choose appropriatefungicide mixtures (Table 7) (a protectant/eradicant plus a systemic) and examine theeffects of seed treatments using from 0.2 to 1 ga.i./kg seed;c. pathogen soilborne and infection occurson roots near the stem base some unknowntime after the seedling stage is completed -choose appropriate fungicides based on pathogenidentity (Table 7) and make applicationsaround the stem bases at fixed growth stages,accompanied by some destructive samplingand attempted isolation of the pathogen fromstem base tissues.Concluding RemarksThe use of fungicides in seed treatments is effectivein sorghum for the control of seed - and soilbornepathogenic fungi that cause seed rots andseedling disease. It remains to be determined whateffect seed treatment can have on the root andstalk rots of the adult plants. The time of occurrenceand location of infection and colonizationsites are key factors that will determine the type ofexperimentation required to test the potential effectivenessof fungicides to control the later occurringroot and stalk rots. Fungicides can be a usefulresearch tool in investigations of the biology andepidemiology of these diseases. Given the spectrumof activity of the systemic fungicides, and thepotential availability of products with high activity atlow application rates, it may be feasible to devisebiologically effective control treatments. Only whenthis has been done will it be possible to determine(a) whether practical economically viable on-farmuse of such control is possible, and (b) the possibilitiesfor the development of integrated control systems,with fungicides combined with host-plantresistance and other crop management controlprocedures.ReferencesANAHOSUR K.H. 1980. Chemical control of sorghumdowny mildew in India.Plant Disease 64:1004-1006.ANZALONE, L. 1980. Fungicide and Nematicide Tests(American Phytopathological Society, St. Paul, Minnesota)35:190.ANZALONE, L. 1982. Fungicide and Nematicide Tests(American Phytopathological Society, St. Paul, Minnesota)37:170.BHALE, M.S., and KHARE, M.N. 1980. Significance ofCurvularia lunata associated with Sorghum vulgareseeds. Phytopathologische Zeitschrift 99:357-361.BIDARI, V.B., SATYANARAYAN, H.V., HEGDE, R.K., andPONNAPPA, K.M. 1978. Effect of fungicides against theseed rot and seedling blight of hybrid sorghum CSH-5.Mysore Journal of Agricultural Sciences 12:587-593,BOWLING, C.C. 1978. Rice seed treatments. Pages 74-78 in Seed treatments, Collaborative International PesticidesAnalytical Council (CiPAC) Monograph 2 (ed. K.A.Jeffs).CLINTON, P.K.S. 1960. Some pests and diseases ofsorghum and their control in the central rainlands of theSudan. Empire Journal of Experimental Agriculture28:294-304.DHANRAJ, K.S. 1979. Seedling blight of sorghum, CurrentScience 48:588-589.DODD, J.L. 1980. The photosynthetic stresstranslocationbalance concept of sorghum stalk rots.Pages 300-305 in Sorghum Diseases, a World Review:Proceedings of the International Workshop on SorghumDiseases, sponsored jointly by Texas A&M University(USA) and ICRISAT. Patancheru, A.P. 502 324, India:ICRISAT.FREDERIKSEN. R.A.,and ODVODY, G. 1979. Chemicalcontrol of sorghum downy mildew. Sorghum Newsletter22:129.GOEL, S.K., and MEHROTRA, R.S. 1973. Rhizoctonia rootrot and damping-off of okra and its control. Acta BotanicaIndica 1:45-48.HANSING, E.D., 1974. Fungicide and Nematicide Tests(American Phytopathological Society, St. Paul, Minnesota,USA) 29:144-146.HANSING, E.D. 1975. Fungicide and Nematicide Tests(American Phytopathological Society, St. Paul, Minnesota,USA) 30:147-148.HANSING, E.D. 1976. Fungicide and Nematicide Tests(American Phytopathological Society, St, Paul, Minnesota,USA) 31:187-188.HANSING, E.D. 1978. Fungicide and Nematicide Tests(American Phytopathological Society, St. Paul Minnesota,USA) 33:172-173.ICRISAT. 1980. Sorghum Diseases, a World Review: Proceedingsof the International Workshop on Sorghum Diseases,sponsored jointly by Texas A&M University (USA)199

and ICRISAT. Patancheru. A.P. 502 324, India: ICRISAT.469 pp.ICRISAT. 1982. Sorghum in the Eighties: Proceedings ofthe International Symposium on Sorghum, 2 Vols. Sponsoredby INTSORMIL, ICAR, and ICRISAT. Patancheru,A.P. 502 324, India: ICRISAT.MUNGHATE, A.G., and RAUT, J.G. 1982. Efficacy of ninedifferent fungicides against fungi frequently associatedwith sorghum seed. Pesticides 16(8):10-18.PATIL-KULKARNI, B.G., PATIL, N.K., and MALEBEN-NUR, N.S. 1972. Studies with oxathiin derivatives andother chemicals for the control of seed rot, damping-offand downy mildew of sorghum. Mysore Journal of AgriculturalSciences 6:1 -4.PHILLEY, G.L.,and FREDERIKSEN, R.A.1975. Fungicideand Nematicide Tests (American PhytopathologicalSociety, St. Paul, Minnesota, USA) 30:148.RAMAIAH, K.V., and PARKER, C. 1982. Striga and otherweeds on sorghum. Pages 291 -302 in Sorghum in theEighties: Proceedings of the International Symposium onSorghum, sponsored by INTSORMIL, ICAR, and ICRISAT.Patancheru, A.P, 502 324, India: ICRISAT.RAUT, J.G., and WANGIKAR, P.D. 1982. Efficacy of elementalsulphur fungicides in the control of seed-bornefungi of sorghum other than smuts. Pesticides 16:23-24.SCHWINN, F.J. 1980. Prospects for chemical control ofthe cereal downy mildews. Pages 220-222 in SorghumDiseases, a World Review: Proceedings of the InternationalWorkshop on Sorghum Diseases, sponsored jointlyby Texas A&M University (USA) and ICRISAT. Patancheru,AP. 502 324, India: ICRISAT.SEYMOUR, C.P., and CORDELL, C.E. 1979. Control ofcharcoal root rot with methyl bromide in forest nurseries.Southern Journal of Applied Forestry 3(3):104-108.SHARMA, H.C., JAIN, N.K., and AGARWAL, R.K. 1976.Effect of seed treatment with fungicides alone and incombination with carbofuran on stand and yield ofSorghum bicolor (L.) Moench. JNKVV Research Journal10(1 )(Suppl): 83-84,TANEJA, M., and GROVER, R.K. 1982. Efficacy of benzimidazoleand related fungicides against Rhizoctoniasolani and R. bataticola. Annals of Applied Biology100:425-432.TARR, S.A.J. 1962. Diseases of sorghum, sudan grassand broom corn. Kew, Surrey, U.K.: CommonwealthMycological Institute. 380 pp.623-631 in Proceedings of the 1977 British Crop ProtectionConference. Croydon, Surrey, U.K.: British Crop ProtectionCouncil.VIR, D., GANGOPADHYAY, S., and GAUR, A. 1972. Evaluationof some systemic fungicides and antibioticsagainst Macrophomina phaseoli. Pesticides 6:25.WILLIAMS, R.J., DAVIES, J.G. and MUGHOGHO, LK.1983. Prospects for successful integrated control of bioticyield-reducing agents of sorghum and pearl millet in thetropics. Pages 904-912 in Vol. 3, Proceedings of the 10thInternational Congress of Plant Protection. Croydon, Surrey,U.K.: British Crop Protection Council.WILLIAMS, R.J., and RAO, K.N. 1981. A review of sorghumgrain molds. Tropical Pest Management 27:200-211.QuestionsVidyabhushanam:Considering the soilborne nature of charcoal rotand the expression of the disease at the later stageof plant growth, do you think that seed dressing withsystemic fungicides would be effective?Williams:We don't know and we need to find out. If, asseveral persons here have indicated, infectionoccurs early in the life of the plant, there will certainlybe possibilities for the control of this infectionwith fungicide seed treatment.Odvody:Do you see any continuing problem with theacropetal translocation of most systemic fungicideswhen trying to control root and stalk problems,and do you feel that soil treatments forlong-term and seed treatments for short-term controlswill overcome these problems?Williams:It is certainly a problem. The use of soil-appliedgranules, particularly with a slow release component,could provide the answer. We need to testthese in the field.TROW-SMITH, R. 1983. Resistant eyespot is hitting wintercereal crops. Farmers Weekly (U.K.) 99(14):52.URECH, P.A., SCHWINN, F., and STAUB, T. 1977. CGA48988, a novel fungicide for the control of late blight,downy mildews, and related soil-borne diseases. Pages200

Cultural and Biological Controlof Root and Stalk Rot Diseases of SorghumB. Doupnik, Jr.*SummaryRecommendations for the control of root and stalk rot diseases of sorghum have basicallyremained unchanged over the past 50 years. These recommendations integrate severalcultural practice decisions and host resistance into a crop production management systemthat reduces stress to the crop during the critical periods of anthesis and grain filling. Some ofthe more important cultural practice decisions are discussed. These include: (1) varietyselection, (2) seed quality and seed treatment, (3) plant population, (4) nutrition, (5) croprotation, (6) conservation tillage, (7) control of other diseases and insects, (8) planting date, (9)irrigation, and (10) early harvestThe state of the art in utilization of biological control as an aid to reduce root and stalk rotdiseases of sorghum is briefly discussed. There is no precedent for the successful biocontrol ofsoilborne pathogens at this time except under highly artificial conditions. The potentialintegration of new developments in genetic engineering and rhizosphere technology, however,offer promise for the future development of biological control.Areas of research needed to improve cultural and biological control of root and stalk rotdiseases of sorghum are listed.Recommendations for the control of stalk rot diseasesof sorghum (Sorghum bicolor (L) Moench)and maize (Zea mays L) have basically remainedunchanged over the past 50 years. The followingreferences from private seed companies, landgrant colleges, and the USDA are just a few of themany examples that could be cited to illustrate thispoint: Anonymous (1974), Berry (1979), Christensenand Wilcoxson (1966), Doupnik et al.(1983), Edmunds and Zummo (1975), Home andBerry (1980), Jacobsen et al. (1979), Koehler(1960), Koehler and Holbert (1938), Livingston(1945), Shurtleff (1980), Ullstrup (1978), andWrather and Palm (1983). These recommendationsintegrate host resistance (standability?) witha number of cultural or crop management practices.Most of this integration is aimed towardsreducing stress and/or delaying senescence ofthe host plant.Compared to that in maize, relatively littleresearch has been carried out with sorghum on theintegration of cultural practices with host resistanceto control stalk rot. Many researchers haveextrapolated information derived from studies onmaize to sorghum because of the similarity of thetwo species. In many cases these extrapolationsdo appear to be valid. Since there are someobvious differences between the two species, however,these interpretations should be confirmed. Inaddition to the genetic differences, many sorghumvarieties differ from maize in their ability to: (1) tiller,(2) remain nonsenescent, and (3) become semidormantduring periods of extreme stress.Sorghum is also quite often grown under drastically*Professor of Plant Pathology, University of Nebraska, South Central Station, Box 66, Clay Center, NE 68933, USA.EDITOR'S NOTE: This paper arrived as the conference proceedings were going to press and is printed as received,International Crops Research Institute for the Semi-Arid Tropics. 1984. Sorghum Root and Stalk Rots, a CriticalReview: Proceedings of the Consultative Group Discussion on Research Needs and Strategies for Control ofSorghum Root and Stalk Rot Diseases, 27 Nov - 2 Dec 1983, Bellagio, Italy. Patancheru, A.P. 502 324, India:ICRISAT.201

different environments and cultural practices thanmaize. The current status of cultural control of rootand stalk rot diseases of sorghum is discussedbelow.Another potential method to reduce plant diseasesis the utilization of biological control. Interestin the use of biological agents to control plant diseaseshas increased dramatically during the pastdecade (Linderman et al. 1983). Extensive reviewsof the literature on biological control by Baker(1968), Baker and Cook (1974), Cook and Baker(1983), and Papavizas and Lumsden (1980) indicate,however, that at the present time there are nosuccessful reports of controlling soilborne diseasesexcept under highly artificial conditions. Thefuture feasibility of integrating biological controlwith cultural practices and host resistance to controlroot and stalk rot diseases of sorghum isdiscussed below.Cultural ControlCultural control of plant diseases is obviously not anew concept. Crop rotation, for example, has longbeen recognized as an effective means of reducinglosses from certain diseases, even when a susceptiblehost is planted. In the following discussion,I will attempt to briefly summarize our presentknowledge on the cultural control of root and stalkrot diseases of sorghum. As mentioned above,much of our information relative to cultural practicesthat can help reduce sorghum root and stalk rotdiseases has been extrapolated to sorghum fromresearch on maize.Cultural control of stalk rot diseases primarilyinvolves the integration of several crop productionmanagement practices and host resistance. Oneof the main objectives of cultural control is toreduce stress to the crop at critical times (anthesisand grain filling) during the growing season. Sincestress is such an important factor in predisposingthe sorghum plant to the development of stalk rotdiseases, the following publications are cited asresource references: Colhoun (1973), Cook(1973), Cook and Papendick (1972), Dodd (1980a,b, c), Doupnik and Frederiksen (1983), Edmunds(1964), Odvody and Dunkle (1979), Schneider andPendery (1983), Schoeneweiss (1975), andSumner (1968).A general review on cultural control of infectiouscrop diseases has been published by Palti (1981).Excellent reviews on the cultural control of stalk rotdiseases of maize have also been published byChristensen and Wilcoxson (1966), Shurtleff(1980), and Pappelis and BeMiller (these proceedings).In addition, nearly every author in these proceedingshas made reference to the role thatcertain cultural practices play in the integration oftheir assigned subject matter areas to the generalproblem of root and stalk rot diseases of sorghum. Itis for this reason, then, that an in-depth discussionof each cultural practice covered in this paper willnot be made if it has been covered in other papersin these proceedings.Variety SelectionOne of the first and most critical crop productionmanagement decisions a grower will make is whichsorghum variety to plant. Since there are differinglevels of host resistance available to most growers,this decision is very important since the more stalkrot-susceptiblevarieties may even develop stalkrot in the absence of any obvious predisposingstress conditions. Past performance under similarenvironmental and geographic conditions offers avery good basis for selection. Satisfactory performanceshould include such factors as lodging resistance(standability), yield, maturity, resistance tostress (especially water deficits), resistance toother diseases, and resistance to insects.A generalization with regard to maturity is thatshorter season varieties are more susceptible tostalk-rotting diseases than are longer season varieties.This puts many growers in a "Catch 22"situation, especially in the underdeveloped, semiarid,tropical production areas since most of theimproved high-yielding sorghum varieties are actuallyshorter-season than the lower yielding varietiesthat they replaced. Since this relates to a moresenescent type of sorghum that is more sensitive tostress at anthesis and grain filling than a morenonsenescent type, you end up with a potentiallyhigh-yielding sorghum that is supersusceptible tostalk rot diseases.Whether the resulting lodging problem has beenstress-and/or pathogen(s)-induced is probablyunimportant since the end result is the same. Thegoal of the sorghum breeder and the hope of thegrower is to eventually have available highyielding,nonsenescent sorghum varieties that arewell adapted for their particular environmental andgeographic conditions. Additional information onthe importance of host resistance and variety202

selection can be obtained from the articles by Buddenhagen(1983), Christensen and Wilcoxson(1966), Shurtleff (1980), and Henzell et al.,Maunder, and Rosenow (these proceedings).Seed Quality and Seed TreatmentMost researchers feel that the primary infectionsite for the sorghum stalk rot pathogens is the rootsystem (Frederiksen, Mughogho and Panda,Odvody and Forbes, Partridge et al., Pappelis andBeMiller, and Zummo, these proceedings). Theplanting of sound, disease-free seed that has beentreated with a broad-spectrum fungicide shouldthen give some protection against these pathogensby either reducing or delaying infection. Thus, theplanting of sound, fungicide-treated seed is a culturalpractice that should be integrated into the cropproduction management system (Christensen andWilcoxson 1966, Shurtleff 1980).Williams and Nickel (these proceedings) havethoroughly reviewed the effectiveness of fungicidesto control stalk rot diseases. At the presenttime, however, fungicides do not offer much forcontrol other than as a seed treatment to delayearly infection. The complex etiology and epidemiologyof the many seed- and soilborne root pathogensthat may be encountered make it anextremely difficult problem to control (Bowen andRovira 1976, Curl 1982, Park 1963). The developmentof new-generation, systemic fungicides thatwill be effective in controlling stalk rot diseasesoffers future possibilities (Williams and Nickel,these proceedings).Plant PopulationThe association of high plant populations withincreased incidences of stalk rot has been knownfor a long time. In fact, many sorghum breederstake advantage of this very predictable response toimprove their screening programs for stalk rot resistance(Henzell et al., Maunder, and Rosenow,these proceedings). This association is thought tobe primarily related to water-deficit-induced stressdue to increased competition for the available soilmoisture (Duncan, Eastin et al., Maranville andClegg, and McBee, these proceedings). Unfortunately,many growers do not give enough attentionto their plant population decisions; yet it is a culturalpractice that they have a lot of control over.NutritionThe influence of nutrition on the incidence andseverity of stalk rot of sorghum and maize has beenreviewed by Huber and Watson (1974), Murphy(1975), and Jordan et al. (these proceedings).Unfortunately, much of the information on theeffects of nutrition on stalk rot has been extrapolatedto sorghum from research on maize and othercrops (Abney 1971, Otto and Everett 1956, Tayloret al. 1983, Warren et al. 1975, and Younts andMusgarave 1958). To summarize the influence ofnutrition upon stalk rot: high rates of nitrogen/potassiumdeficiency, and/or unbalanced ratios ofnitrogen and potassium will increase stalk rot disease.Fertilizer application should be based on soiltests and realistic yield goals. As with plant populations,decisions on fertility are often not givenenough attention; yet these are cultural practicesover which many growers have considerablecontrolPlanting DateDepending on the length of the growing season andthe geographic location, this is a cultural practicedecision that can be used to reduce stalk rot. Thegoal here is to avoid environmental stress duringthe critical periods of anthesis and grain filling(Dodd 1980a; Duncan, McBee, these proceedings).This would have more impact in the tropicand semitropic zones than in the temperate zones.Crop RotationFor many diseases crop rotation, as opposed tomonoculture, is an effective cultural practice tohelp control plant diseases (Curl 1963, Shipton1977). Such is not the case, however, for the stalkrot diseases of sorghum This is due to the diversityand wide host range of the stalk rot pathogens(Dhingra and Sinclair 1978; Reed et al. 1983;Frederiksen, Mughogho and Pande, Odvody andForbes, and Zummo, these proceedings) and theirability to survive saprophytically on crop residuesand/or as specialized structures in the soil for longperiods of time (Cook et al. 1973; Katsanos andPappelis 1969; Nyvall and Kommedahl 1968,1970;and Vizvary and Warren 1982). However, as discussedbelow, crop rotation in conjunction withconservation tillage may offer some control of stalkrot.203

Conservation TillageConservation tillage offers a useful tool to conservesoil moisture as well as to reduce wind and watererosion In addition, the residue maintained on thesurface will reduce soil temperature and temperaturefluctuation. The plant disease consequencesof conservation tillage have been thoroughlyreviewed (Boosalis et al. 1969, Boosalis and Doupnik1976, Boosalis et al. 1981, Cook et al. 1978, andSumner et al. 1981).In many cases conservation tillage has resultedin an increase in disease problems. This is especiallytrue when crops are monocultured. However,a unique 3-year conservation tillage rotation system(wheat-sorghum-fallow) known as ecofallowthat has been developed for the semi-arid CentralGreat Plains area of the United States has actuallyreduced the incidence and severity of sorghumstalk rot while increasing yields (Doupnik et al.1975, Doupnik and Boosalis 1980). In this case it isbelieved that the increased soil moisture storageand the lower, more constant soil temperatures arethe major factors accounting for the reduced stalkrot problems. The sorghum rotation with wheatallows one to plant directly into the residue ofanother crop, which has very few common pathogens,rather than into the residue of the same crop.The growing of two different crops appears to be auseful mechanism, then, to avoid the disease consequencesencountered when monoculturing ispracticed under conservation tillage.Control of Other Diseases and InsectsAs with many of the other cultural practices discussedabove, the control of other diseases and ofinsects is part of an overall crop production systemobjective to reduce stress to the sorghum plants(Christensen and Wilcoxson 1966, Gates and Mortimore1972, Pappelis and Katsanos 1966, andShurtleff 1980). The "other disease" categoryshould also include nematodes (Claflin, theseproceedings).Host resistance should be utilized when available;and, where feasible, chemicals should beemployed to help control these other diseases andinsects.IrrigationWhen available and where applicable, timely irrigationcan be used to reduce early-season stress(Schneider and Pendery 1983), as well as stress atanthesis and grain filling (Dodd 1980a, b, c; Eastinet al., and McBee, these proceedings).Timely HarvestIf field symptoms and visible signs suggest thatstalk rot disease is developing in a given field afterphysiological maturity of the grain is reached, plansshould be made to harvest early. This will helpprevent excessive field losses due to lodging andunharvestable heads (Doupnik et al. 1983).Biological ControlThe concept of biological control as a mechanismto reduce plant disease is not new. The literature onbiocontrol is very extensive and has been recentlyreviewed by Cook and Baker (1983), Linderman etal. (1983), and Papavizas and Lumsden (1980).The current "state-of-the-art" of biocontrol suggests,however, that there is no precedent for thesuccessful control of any soilborne disease exceptunder highly artificial conditions. Most of the successfulexamples of biocontrol involve "singlepathogen:single host" systems under containergrowngreenhouse conditions. Attempts to demonstratethese same biocontrol systems under fieldconditions, however, have generally failed. Most ofthe reported field successes of biocontrol involvediseases of woody plants, propagated plant pieces,and seedlings. This should not be interpreted as anindictment of the feasibility of developing biologicalcontrol measures for root and stalk rot diseases ofsorghum; however, it should be pointed out that inorder for successful biological control systems tobe developed, the etiology and epidemiology of thedisease(s) must be thoroughly known. The basicgaps in our knowledge concerning the etiology andepidemiology of sorghum root and stalk diseaseshave been repeatedly emphasized throughoutthese proceedings.Even with the thorough understanding of the etiologyand epidemiology of the root and stalk rotdisease complex of sorghum, biological control willundoubtedly be very difficult to obtain. This is due tothe fact that there are several different pathogensinvolved (i.e., Fusarium moniliforme Sheldon,Macrophomina phaseolina (Tassi) Gold, and Colletotrichumgraminicola (Cesati) Wilson), In addition,these pathogens have a wide host range and204

the ability to survive saprophytically as well as toact as weak parasites in sorghum if the opportunityarises (i.e., host cell death).The general concept of biological controlencompasses a wide array of potential mechanisms.These include, among others, antagonism(i.e., hyperparasitism—Boosalis 1964 and De LaCruz and Hubbell 1975) and suppressive soils(Hornby 1983, Scher and Baker 1980, Schneider1982, Weller 1983). Another area of much interestand activity at this time is the role of mycorrhizae inthe development of root diseases (Gerdemann1968, Marx 1972, Marx and Schenck 1983,Schenck 1981, Zak 1964). Sorghum roots appearto be good hosts of mycorrhizal fungi. The potentialfor exploiting these sorghum mycorrhizae as biologicalbuffers against a variety of biotic and abioticstresses is of great interest. This is especially truein view of the extensive research developmentsoccurring in biotechnology. Genetic engineeringmay offer very powerful tools in the near future forthe designing of specific biological control agents.Areas of Research N e e d e dThe complex etiology and epidemiology of the rootand stalk rot diseases of sorghum have been majorstumbling blocks for improved disease control.Changing attitudes in disease management andfuture developments in the integration of culturaland biological controls with improved hostresistance, however, offer promise for the future(Andrews 1983, Baker 1983, and Delp 1983).Based on previous discussions (Anonymous1980) and information presented during theseproceedings on cultural and biological control, thefollowing research needs are identified:1. Conservation tillage—Determine long-termeffects of conservation tillage on stalk rot diseases,including multilocational evaluations for diseasesuppression similar to the suppression achieved inthe Central Great Plains areas of the USA.2. Plant population and nutrition—Determine ifnonsenescent/nontillering sorghums react thesame as senescent/tillering sorghums to changesin population and nutrition with regard to diseaseincidence.3. Mycorrhizae—Identify mycorrhizae associatedwith sorghum roots and explore the role they mightplay in the development of root and stalk rotdiseases.4 Fungicides and plant growth regulators-Explore the possibilities of using new-generationsystemic fungicides and/or plant growthregulators (such as antitranspirants) as additionaltools to reduce stalk rot.5. Integration of cultural practices and hostresistance—Make multilocational evaluations ofcrop production management systems (integrationof cultural practices and host resistance) that havebeen shown to suppress root and stalk rotdiseases.ReferencesABNEY, T.S., and FOLEY, D.C. 1971. Influence of nutritionon stalk rot development in Zea mays. Phytopathology61:1125-1129.ANDREWS, J.H. 1983. Future strategies for integratedcontrol. Pages 431 -440 in Challenging problems in planthealth. St. Paul, Minnesota, USA: American PhytopathologicalSociety.ANONYMOUS. 1974. How to prevent and identify troublesomegrain sorghum diseases. A management manual.Des Moines, Iowa, USA: Asgrow Seed Co. 15 pp.ANONYMOUS. 1980. Recommendations of the workshopon sorghum diseases: Head blight and stalk rots.Pages 463-464 in Sorghum Diseases, a World Review:Proceedings of the International Workshop on SorghumDiseases, Sponsored jointly by Texas A&M University(USA) and ICRISAT. Patancheru, A.P. 502 324, India:ICRISAT.BAKER, K.F. 1983. The future of biological and culturalcontrol of plant diseases. Pages 422-430 in Challengingproblems in plant health. St. Paul, Minnesota, USA: AmericanPhytopathological Society.BAKER, K.F., and COOK, R.J. 1974. Biological control ofplant pathogens. San Francisco, California, USA: W.H.Freeman and Co. 433 pp.BAKER, R. 1968. Mechanisms of biological control ofsoilborne pathogens. Annual Review of Phytopathology6:263-294.BERRY, C. 1979. Sorghum lodging is a manageable problem.Crops Quarterly (PAG inhouse publication) 1(1 ):14-15.BOOSALIS, M.G. 1964. Hyperparasitism. Annual Reviewof Phytopathology 2:363-376.BOOSALIS, M.G., COLVILLE, W.L., and SUMNER, D.R.1969. Effect of intensive cultural practices on soil-borneand related corn diseases. Pages 12-20 in Disease consequencesof intensive and extensive culture of fieldcrops (ed., JA Browning) Jowa State University Depart-205

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atlas. Texas A&M University Cooperative Extension ServicePublication B-1323, College Station, Texas. 16 pp.HUBER D.M., and WATSON, R.D. 1974. Nitrogen formand plant disease. Annual Review of Phytopathology12:139-165.JACOBSEN, B.J., WHITE, D.G., HOOKER, A.L, SHUR-TLEFF, M.C., and NOWLIN, B.E. 1979. Corn stalk rots.University of Illinois Department of Plant Pathology Reporton Plant Diseases No. 200, Urbana, Illinois. 6 pp.KATSANOS, R.A., and PAPPELIS, A.J. 1969. Relationshipof living and dead cells to spread of Colletotrichum graminicolain sorghum stalk tissue. Phytopathology 59:132-134.KOEHLER, B. 1960. Corn stalk rots in Illinois. University ofIllinois Agricultural Experiment Station Bulletin 658,Urbana, Illinois. 90 pp.KOEHLER, B., and HOLBERT, J.R. 1938. Combating corn.diseases. University of Illinois Agricultural ExperimentStation and Extension Service Circular 484, Urbana, Illinois.35 pp.LINDERMAN, R.G., MOORE, L.W., BAKER, K.F., andCOOKSEY, D.A. 1983. Strategies for detecting and characterizingsystems for biological control of soilborne plantpathogens. Plant Disease 67:1058-1064.LIVINGSTON, J.E. 1945. Charcoal rot of corn andsorghum. University of Nebraska Agricultural ExperimentStation Research Bulletin 136, Lincoln, Nebraska. 32 pp.MARX, D.H. 1972. Ectomycorrhizae as biological deterrentsto pathogenic root infections. Annual Review ofPhytopathology 10:429-454.MARX, D.H,, and SCHENCK, N.C. 1983. Potential ofmycorrhizal symbiosis in agricultural and forest productivity.Pages 334-347 in Challenging problems in planthealth, St. Paul, Minnesota, USA: American PhytopathologicalSociety.MURPHY, L.S. 1975. Fertilizer efficiency for corn andgrain sorghum. Pages 49-72 in Proceedings of the 30thAnnual Corn and Sorghum Research Conference.Washington, D.C., USA: American Seed TradeAssociation.NYVALL, R.F., and KOMMEDAHL, T. 1968. Individualthickened hyphae as survival structures of Fusariummoniliforme in corn. Phytopathology 58:1704-1707.NYVALL, R.F., and KOMMEDAHL, T. 1970. Saprophytismand survival of Fusarium moniliforme in corn stalks. Phytopathology60:1233-1235.ODVODY, G.N., and DUNKLE, L.D. 1979. Charcoal stalkrot of sorghum: Effect of environment on host-parasiterelations. Phytopathology 69:250-254.OTTO, H J., and EVERETT, H.L. 1956. Influence of nitrogenand potassium fertilization on the incidence of stalkrot in corn, Agronomy Journal 48:301 -305.PALTI, J. 1981. Cultural practices and infectious cropdiseases. Berlin, Heidelburg, New York: Springer-Verlag.243 pp.PAPAVIZAS, G.C., and LUMSDEN, R.D. 1980. Biologicalcontrol of soilborne fungal propagules. Annual Review ofPhytopathology 18:389-413.PAPPELIS, A.J., and KATSANOS. R.A. 1966. Effect ofplant injury on senescence of sorghum stalk tissue. Phytopathology56:295-297.PARK, D. 1963. The ecology of soil-borne fungal diseases.Annual Review of Phytopathology 1:241-258.PUTNAM, A.R., and DUKE, W.B. 1978. Allelopathy inagroecosystems. Annual Review of Phytopathology16:431-451.REED, J.E., PARTRIDGE, J.E., and NORDQUIST, P.T.1983. Fungal colonization of stalks and roots of grainsorghum during the growing season. Plant Disease67:417-420.SCHENCK, N.C. 1981. Can mycorrhizae control root disease?Plant Disease 65:230-234.SCHER, F.W., and BAKER, R. 1980. Mechanism of biologicalcontrol in a Fusarium-suppressive soil. Phytopathology70:412-417.SCHNEIDER, R.W. (ed). 1982. Suppressive soils and plantdisease. St. Paul, Minnesota, USA: American PhytopathologicalSociety. 88 pp.SCHNEIDER, R.W., and PENDERY, W.E. 1983. Stalk rot ofcorn: Mechanism of predisposition by an early-seasonwater stress. Phytopathology 73:863-871.SCHOENEWEISS, D.F. 1975. Predisposition, stress, andplant disease. Annual Review of Phytopathology 13:193-211.SHIPTON, P.J. 1977. Monoculture and soilborne plantpathogens. Annual Review of Phytopathology 15:387-407.SHURTLEFF, M.C. 1980. Compendium of corn diseases(2nd ed.). St. Paul, Minnesota, USA: American PhytopathologicalSociety. 105 pp.SUMNER, D.R. 1968. The effect of soil moisture on comstalk rot. Phytopathology 58:761-765.SUMNER, D.R., DOUPNIK. B., and BOOSALIS, M.G. 1981.Effects of reduced tillage and multiple cropping on plantdiseases. Annual Review of Phytopathology 19:167-187.TAYLOR, R.G., JACKSON, T.L., POWELSON, R.L., andCHRISTENSEN, N.W. 1983. Chloride, nitrogen form, lime,and planting date effects on take-all rot of winter wheat.Plant Disease 67:1116-1120.ULLSTRUP, A.J. 1978. Corn diseases in the United States207

and their control (Revised). U.S. Department of AgricultureHandbook Number 199. Washington, D.C..55 pp.VIZVARY, M.A., and WARREN, H.L. 1982. Survival of Colletotrichumgraminicola in soil. Phytopathology 72:522-525.WARREN, H.L., HUBER, D M , NELSON, D.W., and MANN,O.W. 1975. Stalk rot incidence and yield of corn asaffected by inhibiting nitrification of fall-applied ammonium.Agronomy Journal 67:655-660.WELLER, D.M. 1983. Colonization of wheat roots by afluorescent Pseudomonad suppressive to take-all. Phytopathology73:1548-1553.WRATHER, J.A., and PALM, E.W. 1983. Controlling diseasesof grain sorghum. University of Missouri ExtensionDivision Agricultural Guide No. 4354, Columbia, Missouri.6 pp.YOUNTS, S.E., and MUSGRAVE, R.B. 1958. Chemicalcomposition, nutrient absorption, and stalk rot incidenceof corn as affected by chloride in potassium fertilizer.Agronomy Journal 50:426-429.ZAK, B. 1964. Role of mycorrhizae in root disease. AnnualReview of Phytopathology 2:377-392.QuestionsMaranville:Measurements of soil temperature at 5-centimeterdepth may reflect meaningful differences in germinationand early growth. Do you feel, however,those graphs you showed were valid for meaningfuldifferences later in the season when any root activityis much deeper?Doupnik:We suspect (but don't have the data) that soiltemperatures were affected at deeper depths. Certainlymoisture loss through evaporation is greatlyreduced under the reduced tillage system, andheat reflection would be greatly reduced. Whateffect this has is not known, but probably a coolerplant environment in general would be less stressful.Temperature is just one component of stress,but an important component along with moisture inpredisposition to stalk rot development.hybrid CSH 6 grown under rainfed condition in Indiaat the three plant population densities of 66675,133350,266 700 plants/ha did not show any significantdifferences in lodging and charcoal rot, andas such all three populations behaved equally susceptible.However, under irrigated conditions withirrigation stopped at 50% flowering or earlier, lowerplant populations showed less lodging and charcoalrot than higher plant populations.Doupnik:In the rainfed situation, the threshold level of stressprobably wasn't reached. In other words, you maystill have opportunity to increase plant populationsand yield potential without increasing problemswith stalk rot. In regard to irrigation, early-seasonenvironments favorable for higher yields followedby drought stress at grain filling stage would resultin less stress effect under the lower populations,hence, less stalk rot.Schneider:At what depth were soil temperatures measured?Doupnik:At 2.5 to 5 centimeters.Odvody:Allen and Boosalis showed that endomycorrhizalincidence in wheat was greater following crestedwheat grass than in wheat monoculture. Have youconsidered a mutual or single endomycorrhizalbenefit from sorghum because of the crop rotationsinvolved in the ecofallow system?Doupnik:Boosalis et al. have initiated a study to look at thisaspect. The question is that, since sorghum andmaize are much better hosts for mycorrhizal fungi,will a rotation of these crops with wheat increasethe mycorrhizal population of wheat roots versusmonoculturing of wheat?Pande:Would you like to comment on the behavior of plantpopulations under the following two cultural practices,with respect to available moisture: sorghum208

Breeding for Resistance to Rootand Stalk Rots in TexasD.T. Rosenow*SummaryThe moisture stress/charcoal rot/lodging complex is the most important type of stalk rot inTexas, and much breeding work has been directed toward this problem. Selection is doneunder field conditions in large nurseries where irrigation is withheld to allow moisture stress todevelop during the grain-filling stage. In the past, charcoal-rot-infested toothpicks wereinserted into the stalks, and the spread of infection, stalk rot, and lodging were used asindicators in selection. At present, charcoal rot resistance is considered primarily a postfloweringdrought response trait—generally referred to as "stay-green" or nonsenescence. Theresponse we select is the ability of plants to remain alive and fill the grain normally, with stalksthat remain alive and resist lodging and charcoal rot when under severe moisture stress duringthe late stages of grain development. The presence of the stay-green trait correlates well withresistance to charcoal rot and lodging. Significant progress has been made in the incorporationof the stay-green trait into high-yielding, agronomically desirable lines. Sources of resistanceand the breeding and selection techniques are discussed.Stalk and root rots are serious problems insorghum. Plants weakened by stalk and root rotslodge easily, with loss in harvestable grain. Also,stalk rots cause premature plant death before grainis physiologically mature, curtailing grain yields.Stalk rots are often associated with environmentaland pest stresses, such as those caused bydrought, greenbugs, and mites. These stressescommonly occur in the sorghum-producing areasof Texas.Lodging in sorghum is often associated with stalkrots. Considerable research is reported on the causalfactors and the relationship between moisturestress, stalk rots, and lodging—especially withrespect to charcoal rot (Edmunds and Zummo1975, Hoffmaster and Tullis 1944, Hsi 1961, Malmand Hsi 1965, Voigt and Edmunds 1970). The majorstalk rots of the Great Plains are charcoal rot(Macrophomina phaseolina (Tassi) Goid.) and fusariumstalk rot (Fusarium moniliforme Sheld.). In thehumid southern areas, the red rot phase of anthracnose(Colletotrichum graminicola (Cesati) Wilson)is important, although fusarium stalk rot can also besevere. Charcoal rot develops only in plants thathave been predisposed by moisture stress duringthe late stage of grain development and is especiallysevere when moisture stress is accompaniedby high temperatures (Edmunds et al. 1965,Edmunds 1964a, Odvody and Dunkle 1979). Techniquesto screen for charcoal rot were developedby Hsi (1961), Malm and Hsi (1965), Edmunds(1964a, 1964b), and Edmunds et al. (1965). Thetechniques involve either artificial or natural (dryclimate)moisture stress during the graindevelopmentstage, combined with inoculation ofthe stalk by an infested toothpick. Conditions favor-*Professor, Sorghum Breeder, Texas A&M University, Texas Agricultural Experiment Station, Rt. 3. Lubbock, TX 79401,USA.International Crops Research Institute for the Semi-Arid Tropics. 1984. Sorghum Root and Stalk Rots, a CriticalReview: Proceedings of the Consultative Group Discussion on Research Needs and Strategies for Control ofSorghum Root and Stalk Rot Diseases, 27 Nov - 2 Dec 1963, Bellagio, Italy. Patancheru, A.P. 502 324, India:ICRISAT.209

ing fusarium stalk rot are less well understood. It isusually most severe when cool wet weather followshot dry weather (Edmunds and Zummo 1975).Root rots are also important and are sometimesinvolved in the stalk rot problem (Edmunds et al.1973, Johnson et al. 1966). Phythium spp appearedto cause extensive lodging and serious grain loss innorthwestern Texas in 1971 (Edmunds et al. 1973),and in specific genotypes in more recent years(Odvody, personal communication). Weak neck isgenerally considered to be a nonparasitic diseaseassociated with a weakness at the base of thepeduncle (Edmunds and Zummo 1975). However,Frederiksen et al. (1973, 1982) and Zummo andFrederiksen (1973) reported that when fusariumhead blight is severe and the rot progresses downthe stalk, it can result in weak neck and stalklodging.Insects, such as the greenbug, are important inpredisposing sorghum plants to stalk rots, but littleresearch has been done on this aspect. Teetes etal. (1973) showed that charcoal rot was moresevere following toothpick inoculation ofgreenbug-infested plots. In 1978, J.W. Johnson(Texas Agricultural Experiment Station, Lubbock,Texas; personal communication) found that undernatural conditions more charcoal rot developed ingreenbug-susceptible hybrids than in resistanthybrids when moisture stress and large numbers ofgreenbugs were present. The Banks grass miteand the sugarcane root stalk weevil are alsobelieved to accelerate stalk rot.Since lodged plants are often the end result ofrotted stalks, research on selection for lodging resistancewill be discussed. In maize, Zuber (1973)improved stalk strength through the use of variousselection techniques. Al-Tayar (1974) and Schertzet al. (1978) tried various stalk-strength measurementson sorghum, and found that bending dryplants and green stalk penetration were the mostpromising. Mechanical properties associated withlodging-resistant genotypes were reported byBashford et al. (1976) and Esechie et al. (1977).These included shorter, stockier plants with extensiveleaf sheath coverage, shorter peduncles, anda thicker rind. Resistant lines matured later, weremore perennial in habit, and contained higher totalnonstructural carbohydrates.Anatomical variation in sorghum stalk intemodeswas studied by Schertz and Rosenow (1977). Largedifferences were found in the number of cells withlignifted walls and in the degree of lignification inthe epidermis, subepidermis, and vascular bundles.Lodging-resistant lines generally had themost lignification.Several earlier reports describe differencesamong sorghums in resistance to stalk rots(Edmunds et al. 1965, Frederiksen and Rosenow1971, Malm and Hsi 1965, Tarr 1962, Voigt andEdmunds 1970). However, none of the lines possesseda sufficiently high level of resistance tocontribute substantially to improved stalk-rotresistanttypes. New Mexico-31 was the firstsorghum line developed and released primarily forits charcoal rot resistance.In 1972, Rosenow reported on a promisingprocedure for selecting for lodging and charcoal rotresistance. Five years later, Rosenow (1977) andRosenow et al. (1977) indicated excellent progressin developing sorghums with resistance to charcoalrot and lodging in Texas. In recent years,sorghums with a high degree of resistance to charcoalrot and lodging have been reported in Texasby Frederiksen and Rosenow (1980), Rosenow(1980), and Rosenow and Frederiksen (1982); atICRISAT by Rao et al. (1980); and in West Africa byFrowd(1980).The use of leaf and plant death ratings (degree ofpremature plant senescence) to predict subsequentstalk rot (primarily charcoal rot) was firstdiscussed by Rosenow et al. (1977) and Rosenow(1977). Ratings were made when plants wereunder moisture stress during the late grain developmentstage. They found significant correlationsbetween nonsenescence, charcoal rot resistance,and lodging resistance. Duncan (1977) and McBeeet al. (1983) described some characteristics ofnonsenescing sorghums, including carbohydratelevels in their stalks. Katsanos and Pappelis (1965)reported a direct relationship between senescingtissue and susceptibility to stalk rots. Dodd (1977,1980) described a "photosynthetic stresstranslocationbalance" concept of predisposition tostalk rot in maize and sorghum. The concept proposedagrees well with observations I have madeon sorghum. Dodd's theory is that root and stalk rotpredisposition begins with the senescence of roottissue because of an insufficient supply of carbohydrate.The senescing cells are invaded bymicroorganisms that may be only weakly pathogenicor nonpathogenic to vigorous cells, reducingthe ability of the plant to obtain water. Eventuallytranspiration rates exceed water uptake and permanentwilting occurs, followed by the death ofleaves and stalk. At this stage several differentorganisms may invade the stalk, resulting in visible210

stalk rot and lodging. The predisposition is thereforeaffected by the rate of photosynthesis and therate of translocation of carbohydrates to the roots.Stresses that reduce the rate of photosynthesisinclude water deficit, leaf destruction, light reduction,and mineral deficiency. The size of the carbohydratesink in developing grain is very importantin determining the level of stress necessary toinduce stalk rot predisposition.The relationship of drought stress to charcoal rotin sorghum was discussed by Rosenow et al.(1983). They identified two distinct stressresponses. The "preflowering" response occurswhen plants are under significant moisture stressprior to flowering. The "postflowering" responseoccurs when plants are under severe water stressduring the grain-filling stage. Symptoms of postfloweringdrought-stress susceptibility include prematureplant (leaf and stem) death or prematureplant senescence, stalk rot (charcoal rot), stalkdisintegration and lodging, and reduced seed size.Rosenow et al. proposed that selecting for tolerrance to postflowering drought stress by selectingagainst premature plant death and lodging is anefficient and effective method of developingcharcoal-rot-resistant sorghums.Screening andEvaluation TechniquesThe relationship between moisture stress duringthe late grain development stage (postflowering)and charcoal rot is the basis for our breeding program.We believe that most charcoal rot resistancecan be explained by tolerance to postfloweringdrought stress, as explained by Rosenow et al.(1983). We commonly use the term "stay-green" todescribe plants or lines that possess postfloweringdrought tolerance. Other terms sometimes usedsynonymously with stay-green are nonsenescenceand late-season drought tolerance.The screening and evaluation techniques weuse at the Texas Agricultural Experiment Stationhave proven effective in improving resistance toseveral types of stalk rot. The major features of theprogram are: (a) initial identification of lodging resistanceor nonsenescence by any worker in anynursery, (b) initial screening in single-row observationor in individual pedigree breeding plots in alarge field nursery allowed to stand for a long periodafter maturity, and (c) screening for the stay-greentrait, as well as for other types of lodging resistance,in replicated trials at several locations.The initial screening phase is primarily for resistanceto after-freeze stalk breakage and weak neckresulting from strong winds (often exceeding 80kmph) during the winter months. Lines or hybridswith good resistance to this type of lodging are thenentered in replicated trials throughout Texas,where they are exposed to lodging pressure, moisturestress, stalk or root rots, and any other naturaldiseases or insect pests. In West Texas they areplanted in postflowering drought-tolerance screeningnurseries. In these nurseries, ideal growingconditions are maintained during early plantgrowth, especially regarding moisture availability.As plants near flowering, irrigation is withheld in anattempt to induce moisture stress during the lategrain-development stage. Stress during this periodpredisposes plants to charcoal rot.In the past we inoculated plants by insertingtoothpicks infested with the causal organism, M.phaseolina, into an internode of the stalk, usually2.5 to 5 cm above the soil surface. Inoculation wasgenerally done 2 weeks after flowering, but timingdid not appear to be critical as long as it was afterflowering, but before physiological maturity. Normallyfive plants were inoculated in each of two orthree replications. After 3 to 4 weeks or later, inoculatedstalks were split and the stalk disintegrationand charcoal rot invasion were rated on a 1 to 5scale, where < 1 = less than one intemode affected;1 = one internode invaded but rot did not passthrough any nodal area; 2 = two internodesinvaded; 3 = more than two invaded; 4 = more thanthree invaded, sometimes with sclerotia; and 5 =extensive invasion, shredding, death, and sclerotiapresent. We sometimes also rated for stalk disintegration,other than charcoal rot, as an indication ofpossible resistance to other stalk rots.The breeding and screening techniques wepresently use to develop resistance to moisturestress-relatedstalk rot and how it relates to ourdrought resistance breeding program were presentedby Rosenow and Clark (1982, 1983),Rosenow et al. (1981,1982,1983), and Woodfin etal. (1979). In nurseries where screening is for postfloweringdrought tolerance and lodging, staygreenis evaluated at the late grain-developmentstage or shortly after maturity. Each entry or plot issubjectively rated for the amount of premature leafand stem death on a scale of 1 to 5, where 1 =completely green and 5 = dead, Leaf and stemratings can be made together or separately. Thenursery is often altowed to stand for an extended211

period following maturity to allow stalk lodging tooccur This facilitates the identification of entrieswith weakened but not severely rotted stalks.Entries can also be rated for yield and other traitsand selections made. Maturity is critical becauseplants in the vegetative stage are very resistant tosenescence. Also there is a period just prior tophysiological maturity when sorghum is very susceptibleto plant senescence and stalk rot. Plants afew days earlier or later in maturity may show littlesenescence. Therefore, flowering notes are takenon all plots and comparisons of charcoal rot,senescence, and lodging are made only amongplants at similar stages of maturity.Additional data taken on the replicated testsinclude plant height/head exsertion, desirability (anestimate of yield), and in some cases, grain yield.Lodging notes, recorded as the percentage oflodged plants, are taken periodically throughout theseason whenever significant lodging occurs.Results and DiscussionExcellent progress has been made in breedingsorghum lines for improved charcoal rot and lodgingresistance (Table 1). Note the vast improvementin lodging and charcoal rot resistance of theresearch breeding lines compared to the standardcheck lines. The average flowering dates are notsufficiently different to account for the differencesin lodging and charcoal rot.Charcoal rot and lodging ratings for 12 of the bestsource lines, along with five check varieties, arepresented in Table 2. All 12 lines had lower charcoalrot ratings and lodging percentages than NewMexico-31. All but one of the 12 entries werederived from lines developed in the sorghum conversionprogram (Stephens et al. 1967). The staygreentrait of these lines has proven very stableacross environments, both in Texas and internationally(e.g., Sudan).Although lines such as those described abovehave a high degree of stay-green or postfloweringdrought tolerance, most perform poorly whensevere drought stress occurs prior to flowering.Conversely, most sorghum lines with excellent prefloweringmoisture stress tolerance are susceptibleto postflowering stress. However, some genotypeswith moderate levels of stay-green also performwell under preflowering stress. Crosses have beenmade between and among pre- and postfloweringstress tolerant source lines and elite, high-yieldinglines in an attempt to develop high-yielding sorghumswith good levels of stay-green, combined witha high level of preflowering drought tolerance. Thebreeding materials are planted for drought evaluationat five locations in West Texas:Halfway - limited irrigation (postflowering stress)Lubbock - limited irrigation (postflowering stress)Lubbock - dryland (season-long stress)Big Spring - dryland (preflowering stress)Chillicothe - dryland (preflowering stress)In these nurseries, selection is based on the staygreentrait and lodging resistance, with emphasison entries that also perform well under prefloweringstress. In 1983, F 6 s from the initial crosses wereevaluated. Good progress appears to have beenmade in combining good levels of stay-green withpreflowering drought tolerance into lines withimproved yield potential. Comparison of somepromising new B-line breeding materials withcheck varieties are presented in Table 3.Data presented in Table 4 show that hybridsinvolving charcoal- and lodging-resistant parentallines have superior charcoal rot ratings, leaf-plant-Table 1. Summary of agronomic, lodging, and charcoal rot data from the Texas Agricultural Experiment StationStatewide Sorghum Lodging Test.EntriesDate of 50%flowerResearch lines (20) Aug 14Standard (5) Aug 131975 1976Lodging (%)Lodging aCharcoalLPD(%) rating a rating a 2/10 3/89.3 1.364.6 3.32.83.40.5 13.868.1 90.7a Flowering data, charcoal rot, and leaf-plant death (LPD) ratings from Halfway, Texas. Lodging rating taken from Lubbock, Texas (datataken in late winter or on date indicated).212

Table 2. Charcoal rot and lodging of selected sorghum lines, Lubbock and Halfway, Texas, USA; 4-yearaverages.Charcoal rot Lodging bDesignation Type or pedigree rating a (%)SC35-6 IS12555 der. (Durra) 1.5 2.8SC56-6 IS12568 der. (Caud/Niger) 1.4 5.6SC56-14 IS12568C (Caud/Niger) 0.6 2.8R9188 IS17459 der. (SC599-6 sel.) 1.2 34.6R9247 IS17459 der. (SC599-6 sel.) 0.8 11.0NSA440 Kafir der. 1.0 3.01790E (SC56 x SC33) der. 1.6 19.31790L (SC56 x SC33) der. 1.2 3.61778 (SC56 x SC33) der. 0.6 10.2R1584 (SC56 x SC170)der. 0.8 2.0B4R (BTx406 x Rio) der. 1.0 3.8SC170-6-17 IS12661 der. (Zerazera) 1.1 39.4New Mexico-31(check) 1.7 54.0BTx378(check) Redlan 2.2 89.8Tx7000 (check) Caprock 2.7 90.3BTx399 (check) Wheatland 1.7 65.2TAM428(check) IS12610 der. (Zerazera) 2.6 86.4a. Rated on 1-5 scale: l three internodes, 5 = death.b. Taken late in winter following exposure to strong winds.Table 3. Comparison of breeding and parental sorghum lines for charcoal rot and other characteristics, Lubbock,Texas, USA, 1983.StemGrainLodging a Charcoal LPD base Peduncle yieldDesignation (%) rating b rating c rating d rating d (kg/ha)(BTx625xB35-6)-HL19 0 0.70 2.9 1.2 1.8 3030(BTx625 x B35-6)-LDE73 0 0.45 3.5 1.2 2.1 3215(BTx625 x B35-6)-LEC 0 0.83 2.8 1.1 1.5 3080B35-6 0 0.48 2.7 1.1 1.7 2010BTx625 38 3.40 4.6 4.3 3.5 3500BTx623 40 2.00 4.7 2.8 3.5 3140Tx7000 13 3.40 4.6 4.1 .3.9 3740a. Moisture-stress-type lodging (November 7).b. Charcoal rot rating of toothpick-Inoculated plants: 0 = no infection, 1 = one internode infected, 5 = death, sclerotia, shredded.c. Leaf-plant-death rating (emphasis on premature leaf death): 1 = no leaf death, 5 = all dead (November 7).d. Base of stalk and peduncle "stay-green" rating: 1 = completely green and alive, 5 = all dead (November 21).death ratings, and lodging resistance, especially ifboth parents are resistant. Also, some hybridsmade with one highly stay-green parent and onehighly senescing parent show excellent pre- andpostflowering drought tolerance (stay-green). Wehave not conducted inheritance studies on charcoalrot or lodging resistance, but F 1 and F 2 dataindicate that in many lines resistance is recessive,while in a few lines it appears to be quite dominant.Hybrids involving such lines as R9188 and A599213

(Table 4) perform like the susceptible parent. Insome lines, especially those involving SC35-6(A35), resistance appears to be dominant(Rosenow 1980). Lodging and charcoal rot resistanceis quite heritable, but not by a single gene asreported by Coleman and Stokes (1958) in sorgo.The stay-green trait we have selected appears tobe very stable over a wide environmental range. Ithas been screened in Arizona, throughout Texas,Mexico, and in Sudan.Grain yield should be carefully considered whenbreeding and selecting for the stay-green trait andcharcoal rot resistance. In general, as grain yield isincreased and lower grain-to-stover ratiosachieved, stalk rot susceptibility is increased. Also,hybrids are more susceptible than varieties. Untilrecently, few U.S. commercial hybrids have exhibiteda high degree of stay-green or charcoal rotresistance; however, some new commercialhybrids are now appearing that possess good staygreen.In a study of lodging resistance, the green-stalkpuncture-pressure screening technique was used(Rosenow 1977) on previously selected lodgingand charcoal-rot-resistant lines that had highpuncture pressures. However, a selection studywithin a random-mated population, TP9, showedthat selection based on individual plant puncturepressure was ineffective in increasing lodging resistancefrom that of the base population. Selectionbased on lack of lodging of individual plantswithin the population or on lodging percentagesof S 1 rows resulted in a significant increase inlodging resistance (unpublished data).In another study of a possible selection technique,aerial infrared photography as described byBlum et al. (1978) was used on nurseries undermoisture stress. However, differences in canopycolor showed no association with plant senescence,lodging, or drought ratings (Rosenow 1977).It appeared that color (and therefore canopytemperature) differed considerably among genotypes,but appeared to be a trait of the genotypeand not associated with response to moisturestress.Another study evaluated charcoal rot resistancein isogenic genetically juicy-stem and dry-stemmedsorghum lines. There was no difference in theircharcoal rot reaction (unpublished data).Selection for the stay-green trait in sorghum hasindirectly resulted in high levels of resistance tofusarium head and peduncle blight and possibly tof usarium stalk rot. The Rio (SC599) derivative lines,which are among the most stay-green and resistantto charcoal rot, are very resistant to fusariumhead blight (Frederiksen et al. 1973) and Banksgrass mite (Foster et al. 1977). Although no specificbreeding work has been done on pythium root rot,and it only occurs occasionally, highly susceptiblelines can be identified by premature plant deathTable 4. Senescence, lodging, charcoal rot, and grain yield of selected sorghum hybrids at Lubbock and Halfway,Texas, USA.LPD Charcoal Lodging c YieldDesignation rating a rating b (%) (kg/ha)A35 x SC56-14 R x R d 1.9 1.1 2 5910A35xR9188 RxR 2.1 1.0 13 6050A599 x SG56-14 R x R 1.8 1.0 73 6940A1778 x R9247 RxR 1.9 1.0 15 5940A599 x NSA440 RxR 2.2 1.1 22 5910ATx399 x SC56-14 S x R 1.9 1.6 65 5010ATAM618 x R9188 S x R 3.6 1.9 88 5500ATAM618 x NSA440 S x R 2.2 1.5 72 5500ATx399 x 1790E S x R 2.0 1.1 42 6600A599 x TAM428 R x S 3.0 2.8 100 6190ATx399 x Tx2536 S x S 2.7 1.7 99 5220ATx378 x Tx2536 S x S 2.7 2.7 100 5360a. Leaf-plant death rated on 1 -5 scale: 1 = none, 5 = dead.b. Rated on 1 -5 scale: < 1 = < one Internode, 1 = one internode, 4 = > three internodes, 5 = death.c. Lodging data taken in February.d. Parental line rating on charcoal and lodging: R = resistant, S = susceptible.214

and lodging, so resistance has likely been selectedin some of our materials.The identification and extensive use ofanthracnose-resistant sorghums from convertedmaterials in the past 10 years has essentially eliminatedanthracnose stalk and peduncle rot fromSouth Texas. Screening for anthracnose is doneprimarily in Georgia, with some in Puerto Rico. Periconiaroot rot resistance is an outstanding exampleof breeding success. Resistant lines were selectedin the late 1930s, and resistance (single geneinheritance) has remained stable for over 40 years.ConclusionsAlthough stalk rot resistance is a complex phenomenon,much progress has been made in developmentof efficient screening techniques and inbreeding for higher levels of resistance. We havemade progress in two areas: genotypes have beenselected with (a) anatomically stronger stalks and(b) a different physiological response to moisturestress. These latter types do not become predisposedto stalk rot by moisture stress as easily ascommon sorghum. By selecting within earlygenerationbreeding material in multiple nurserieswith variable stress and yield potential, progresshas been made in combining good levels of staygreenwith wide adaptation and good yield potential.Use of the visual leaf-plant death or stay-greenrating is recommended as a very efficient selectionmethod. Breeding and selection for stalk and rootrot resistance should be done in a totalperformanceprogram, with strong emphasis onyield potential, adaptation, maturity, and other traitssuch as insect and disease resistance.Future Research N e e d s1. Research on the physiological and/or biochemicalbasis of the stay-green trait.2. Determination of the physiological basis forpreflowering drought tolerance, and how itdiffers from postflowering tolerance (staygreen).Such information is needed whenbreeding for charcoal rot resistance as a partof total performance.3. More widespread use of currently availableknowledge of screening and selection proceduresand techniques by breeders and pathologiststo breed for improved charcoal rotresistance. Emphasis should be on field performance,utilizing the best possible controlsover timing of stress and uniformity of soilmoisture. The stay-green trait should be usedas an efficient breeding tool to select for charcoalrot resistance.AcknowledgmentsThis research was supported in part by grant AID/DSAN/XII/G-0149 from the Agency for InternationalDevelopment, Washington, D.C. 20523, USA.ReferencesAL-TAYAR, F.A. 1974. Stalk strength measurements topredict field lodging in Sorghum bicolor (L) Moench.Ph.D. thesis, Texas A&M University, College Station,Texas, USA. I26 pp.BASHFORD, L.L., MARANVILLE, J.W., WEEKS, S.A., andCAMPBELL, R. 1976. Mechanical properties affectinglodging of sorghum. Transactions of the AmericanSociety of Agricultural Engineers 19:962-966,BLUM, A, SCHERTZ, K.F., TOLER, R.W., WELCH, R.I.,ROSENOW, D.T., JOHNSON, J.W., and CLARK, L.E. 1978.Selection for drought avoidance in sorghum using aerialinfrared photography. Agronomy Journal 70:472-477.COLEMAN, O.H., and STOKES, I.E. 1958. The inheritanceof weak stalk in sorgo. Agronomy Journal 50:119-120.DODD, J.L 1977. A photosynthentic stress-translocationbalance concept of com stalk rot. Pages 122-130 in Proceedingsof the 32nd Annual Corn and SorghumResearch Conference (eds. H.D. Loden and D. Wilkinson).Washington, D.C., USA: American Seed TradeAssociation.DODD, J.L. 1980. The photosynthetic stresstranslocationbalance concept of sorghum stalk rots.Pages 300-305 In Sorghum Diseases, a World Review:Proceedings of the International Workshop on SorghumDiseases, sponsored jointly by Texas A&M University(USA) and ICRISAT. Patancheru, A.P. 502 324, India:ICRISAT.DUNCAN, R.R., 1977. Characteristics and inheritance ofnonsenescence in Sorghum bicolor (L.) Moench. Ph.D.thesis, Texas A&M University, College Station, Texas,USA. 70 pp.EDMUNDS, L.K. 1964a. Combined relation of plant maturity,temperature, and soil moisture to charcoal stalk rotdevelopment in grain sorghum. Phytopathology 54:514-517.215

EDMUNDS, L.K. 1964b. Use of Arizona climate to inducecharcoal rot in grain sorghum. Plant Disease Reporter48:300-302.EDMUNDS, L.K., VOIGT, R.L., and CARASSO, F.M. 1965.Charcoal rot induction and development in the field inArizona. Pages 47-50 in Proceedings of the Fourth BiennialGrain Sorghum Research and Utilization Conference,sponsored by the Grain Sorghum Producers' Association(GSPA) and the Sorghum Improvement Conference ofNorth America, Lubbock, Texas. Available from GSPA,Abemathy, Texas, USA.EDMUNDS, L.K., VOIGT, R.L., FREDERIKSEN. RA, andDUNKLE, L.D. 1973. Root and stalk rot problems in theGreat Plains, Pages 88-92 in Proceedings of the EighthBiennial Grain Sorghum Research and Utilization Conference,sponsored by the Grain Sorghum Producers' Association(GSPA) and the Sorghum ImprovementConference of North America, Lubbock, Texas. Availablefrom GSPA, Abemathy, Texas, USA.EDMUNDS, L.K., and ZUMMO, N. 1975. Sorghum diseasesin the United States and their control. U.S. Departmentof Agriculture Handbook No. 468. Washington, D.C.,USA: U.S. Government Printing Office. 47 pp.ESECHIE, H.A., MARANVILLE, J.W., and ROSS, W.M.1977. Relationship of stalk morphology and chemicalcomposition to lodging resistance in sorghum. CropScience 17:609-612.FOSTER, D.G., TEETES, G.L, JOHNSON, J.W.,ROSENOW, D.T., and WARD, C.R. 1977. Field evaluationof resistance in sorghums to Banks grass mite. CropScience 17:821-823.FREDERIKSEN, R.A., CASTOR, L.L., and ROSENOW, D.T.1982. Grain mold, small seed and head blight: the Fusariumconnection. Pages 26-36 in Proceedings of the 37thAnnual Corn and Sorghum Research Conference.Washington, D.C., USA: American Seed TradeAssociation.FREDERIKSEN, R.A., and ROSENOW, D.T. 1971. Diseaseresistance in sorghum. Pages 71 -82 in Proceedings of the26th Annual Corn and Sorghum Research Conference,Washington, D.C., USA: American Seed TradeAssociation.FREDERIKSEN, R.A., and ROSENOW, D.T.1980. Breedingfor disease resistance in sorghum. Pages 137-167 inBiology and breeding for resistance to arthropods andpathogens in agricultural plants (ed. M.K. Harris). Proceedingsof the International Short Course in Host PlantResistance, 22 July-4 Aug 1979, Texas A&M University,College Station, Texas, USA. Texas Agricultural ExperimentStation MP-1451.605 pp.FREDERIKSEN, R.A., ROSENOW, D.T., and WILSON, J.M.1973. Fusarium head blight of sorghum in Texas. Pages33-36 in Proceedings of the Eighth Grain SorghumResearch and Utilization Conference, Lubbock, Texas.Available from GSPA, Abemathy, Texas, USA.FROWD, J.A. 1980. Sorghum stalk rots in West Africa.Pages 322-324 in Sorghum Diseases, a World Review:Proceedings of the International Workshop on SorghumDiseases, sponsored jointly by Texas A&M University(USA) and ICRISAT. Patancheru, A.P. 502 324, India:ICRISAT. 469 pp.HOFFMASTER, D.E., and TULLIS, E.C. 1944. Susceptibilityof sorghum varieties to Macrophomina dry rot (charcoalrot). Plant Disease Reporter 28:1175-1184.HSI, D.C.H. 1961. An effective technique for screeningsorghum for resistance to charcoal rot. Phytopathology51:340-341.JOHNSON, D.L, DAVIDSON, A.D., and HEATHMAN, E.S.1966. Fusarium root rot of Sorghum vulgare. Phytopathology56:148 (abstract).KATSANOS, R.A., and PAPPELIS, A.J. 1965. Seasonaltrends in density and cell death in sorghum stalk tissue.Phytopathology 55:97-99.MALM, N.R., and HSI, D.C.H. 1965. Charcoal rot studies inNew Mexico. Pages 51 -53 in Proceedings of the FourthBiennial Grain Sorghum Research and Utilization Conference,sponsored by the Grain Sorghum Producers' Association(GSPA) and the Sorghum ImprovementConference of North America, Lubbock, Texas. Availablefrom GSPA, Abernathy, Texas, USA.McBEE, G.G., WASKOM, R.M., III, MILLER, F.R., andCREELMAN, R.A. 1983. Effect of senescence and nonsenescenceon carbohydrates in sorghum during late kernelmaturity states. Crop Science 23: 372-376.ODVODY, G.N., and DUNKLE, L.D. 1979. Charcoal stalkrot of sorghum: effect of environment on host-parasiterelations. Phytopathology 69:250-254.RAO, K.N., REDDY, V.S., WILLIAMS, R.J., and HOUSE,L.R. 1980. The ICRISAT charcoal rot resistance program.Pages 315-321 in Sorghum Diseases, a World Review:Proceedings of the International Workshop on SorghumDiseases, sponsored by INTSORMIL, ICAR, and ICRISAT. Patancheru, A.P. 502 324, India: ICRISAT.ROSENOW, D.T. 1972. Selection for lodging resistance ingrain sorghum. Page 18 in Agronomy Abstracts. Madison,Wisconsin, USA: American Society of Agronomy.ROSENOW, D.T. 1977. Breeding for lodging resistance insorghum. Pages 171-185 in Proceedings of the 32ndAnnual Corn and Sorghum Research Conference.Washington, D.C., USA: American Seed TradeAssociation.ROSENOW, D.T. 1980. Stalk rot resistance breeding inTexas. Pages 306-314 in Sorghum Diseases, a WorldReview: Proceedings of the International Workshop onSorghum Diseases, sponsored jointly by Texas A&M Uni-216

versity (USA) and ICRISAT. Patancheru, A.P. 502 324,India: ICRISAT.ROSENOW, D.T., and CLARK, L.E. 1982. Drought tolerancein sorghum. Pages 18-30 in Proceedings of the 36thAnnual Corn and Sorghum Research Conference.Washington, D.C., USA: American Seed TradeAssociation.ROSENOW, D.T., and CLARK, L.E. 1983. Use of postflowering drought tolerance in a sorghum breeding program.Page 119 in Proceedings of the 13th Biennial GrainSorghum Research and Utilization Conference, sponsoredby the Grain Sorghum Producers' Association(GSPA) and the Sorghum Improvement Conference ofNorth America. Available from GSPA, Abernathy, Texas,USA.ROSENOW, D.T., CLARK, L.E., and WOODFIN, C.A. 1981.Breeding for drought resistance in sorghum. Page 11 inProceedings of the 12th Biennial Grain SorghumResearch and Utilization Conference, sponsored by theGrain Sorghum Producers' Association (GSPA) and theSorghum Improvement Conference of North America.Available from GSPA, Abernathy, Texas, USA.ROSENOW, D.T., CLARK, L.E., and WOODFIN, C.A. 1982.Screening for drought tolerance in sorghum using fieldnurseries. Pages 81 -82 in Agronomy Abstracts. Madison,Wisconsin, USA: American Society of Agronomy.ROSENOW, D.T., and FREDERIKSEN, R.A. 1982. Breedingfor disease resistance in sorghum. Pages 447-455 inSorghum in the Eighties: Proceedings of the InternationalSymposium on Sorghum, sponsored by INTSORMIL,ICAR, and ICRISAT. Patancheru, A.P. 502 324, India:ICRISAT.ROSENOW, D.T., JOHNSON, J.W., FREDERIKSEN, R.A.,and MILLER, F.R. 1977. Relationship of nonsenescenceto lodging and charcoal rot in sorghum. Page 69 in AgronomyAbstracts. Madison, Wisconsin, USA: AmericanSociety of Agronomy.ROSENOW, D.T.. QUISENBERRY, J.E., WENDT, C.W.,and CLARK, L.E. 1983. Drought tolerant sorghum andcotton germplasm. Agricultural Water Management7:207-222.SCHERTZ, K.F., AL-TAYAR, F.A., and ROSENOW, D.T.1978. Comparison of methods for evaluating stalkstrength in sorghum. Crop Science 18:453-456.SCHERTZ, K.F., and ROSENOW, D.T. 1977. Anatomicalvariation in stalk internodes of sorghum. Crop Science17:628-631.STEPHENS, J.C., MILLER, F.R., and ROSENOW, D.T.1967. Conversion of alien sorghums to early combinegenotypes. Crop Science 7:396.TARR, S.A.J. 1962. Diseases of sorghum, sudan grassand broom corn. Kew, Surrey, U.K.: CommonwealthMycological Institute. 380 pp.TEETES, G.L., ROSENOW, D.T., FREDERIKSEN, R.A., andJOHNSON, J.W. 1973. The predisposing influence ofgreenbugs on charcoal rot of sorghum. Texas AgriculturalExperiment Station, College Station, Texas, USA (PR-3173). 6 pp.VOIGT, R.L., and EDMUNDS, L.K. 1970. Tolerance tocharcoal rot in hybrid grain sorghum. Page 22 in AgronomyAbstracts. Madison, Wisconsin, USA: AmericanSociety of Agronomy.WOODFIN, C.A., ROSENOW, D.T., CLARK, L.E., andJOHNSON, J.W. 1979. Differential response of sorghumcultivars to drought stress. Page 82 in AgronomyAbstracts. Madison, Wisconsin, USA: American Societyof Agronomy.ZUBER, M.S. 1973. Evaluation for progress in selection forstalk quality. Pages 110-122 in Proceedings of the 28thAnnual Corn and Sorghum Research Conference (ed, D.Wilkinson). Washington, D.C., USA: American Seed TradeAssociation.ZUMMO, N., and FREDERIKSEN, R.A. 1973. Head blightof sorghum in Mississippi. Page 37 in Proceedings of theEigth Grain Sorghum Research and Utilization Conference,sponsored by the Grain Sorghum Producers' Association(GSPA) and Sorghum Improvement Conferenceof North America/Lubbock, Texas. Available from GSPA,Abernathy, Texas, USA.QuestionsMughogho:I was impressed by your presentation slide taken inthe Sudan showing one of your nonsenescent lineslooking green in a field where other lines hadsenesced and lodged. It would be useful to know ifall the lines were of the same maturity group, sinceplant growth stage has an important bearing onplant water use and hence drought resistance andpredisposition to stalk rots and lodging.Rosenow:There was a wide range in maturity in this breedingnursery, and the stay-green expression in this casewas not related to maturity. We recognize theextreme importance of maturity in this expression,so we make comparisons only among genotypes ofsimilar maturity.Partridge:Have any isolations been made previous to theearly plant death expression to determine if there217

are other organisms present in the stalk tissue thatmight potentially be involved?Rosenow:Dr. Frederiksen did some isolation work severalyears ago and consistently found organisms inroots at an early stage, but no work was done onisolation from stalks at this later stage.Seetharama:Is there any study where someone has comparedthe water use pattern of stay-green and other typesof genotypes? Or has anybody compared their rootcharacteristics? Is such a study useful?Rosenow:Yes, Dr. Charles Wendt has used the soil neutronprobe technique to evaluate stay-green versussenescing types under both rainout shelters andfield conditions. He found little or no difference intotal water extracted or in the depth from whichwater was extracted. He found slight differences inrate of moisture extraction, with senescing typesusing water slower in early stages of growth, butcontinuing to use more water later in the season,relative to senescing genotypes. Also Dr. W.R. Jordanhas studied the rooting and wafer use patternof one stay-green line, SC56, and found that it had adeeper root system and utilized more water fromdeeper soil depths late in the season. Althoughthese studies showed some differences, it seemsthat the visual evaluation is much easier with biggerdifferences. However, I believe studies on roots areessential to basic studies of drought tolerance, but Iquestion if roots can be used efficiently in a screeningtechnique at this time.Pande:Under what cultural practices did you test staygreenmaterial? If under irrigated, at what plantgrowth stage did you stop the irrigation? If rainfed,what was the total rainfall before planting and afterplanting, with respect to plant growth stage?Rosenow:We screen the plants primarily in nurseries in WestTexas, where we fertilize well and irrigate well duringearly stages of growth. Irrigation is then withheldprior to flowering to allow moisture stress todevelop during the grain-filling stage. We also dosome evaluation under rainfed conditions in Southand Central Texas, where rainfall is higher. In theseareas, there is a rather deep, heavy clay soil, whichis essentially full of water prior to flowering. Theplants normally receive sufficient rainfall during theearly season, with decreasing rainfall and highertemperatures as they approach maturity.Pande:Have you tested this material under different soiltypes with differences in water-holding capacity?Rosenow:Yes, from sandy to clay soils in West Texas tosandy and clay soils in Sudan, and the stay-greentrait behaves consistently. A problem with thehighly stay-green types in sandy soil is that stressoften develops prior to flowering and greatly retardshead development, which then does not allow sufficientsink development to produce stress duringgrain fill.Seetharama:What percentage of genotypes considered resistantto drought at terminal stage of growth are alsostalk rot resistant?Rosenow:For charcoal rot resistance and the way we definepostflowering drought tolerance, the relationship isessentially 100%.Frederiksen:Is the stay-green trait stable across locations?Rosenow:Yes— from Arizona, all over Texas, Sudan, andIndia.218

Breeding for Stalk Rot Resistanceas a Component of AcceptableAgronomic PerformanceA.B. Maunder*Stalk Rots of the Arid AmericasAt the time of sorghum hybrid introduction in theUnited States in 1956, the most serious diseasewas thought to be charcoal rot (causal agent,Macrophomina phaseolina). Although head smut(causal agent, Sphacelotheca reiliana) produced aserious yield loss in the Coastal Bend area ofTexas, the stalk rots common to more arid and hotconditions (caused by M. phaseolina, Fusariummoniliforme, and other lesser organisms) wereestimated to account for 4.5% of sorghum yieldlosses in the United States (USDA 1965). Also, F.moniliforme is by far the most serious causal agentof stalk rot on sorghums in Argentina. With thesestalk rots responsible for half of the U.S. total diseaseloss (9%) during this period and with the earlyhybrids all known to be susceptible to charcoal rot,a breeding effort towards charcoal rot resistanceseemed natural for a commercial research programaffecting all U.S. sorghum acreage, themajority of which was being grown from the aridsouthwest (Arizona, New Mexico, Texas) northeastthrough the Great Plains to South Dakota,In this paper I would like to specifically report onthe Dekalb AgResearch, Inc., approach to stalkrots, with primary emphasis on charcoal rot.Anthracnose, although considered significant andallocated research funding, will not be consideredbecause of its quite different environmentalrequirements.Breeding ApproachThree steps are required to develop a diseaseresistanthybrid: (1) finding a source of resistancewith a useable level of heritability, (2) combiningthis resistance with other required crop traits, and(3) isolating parental lines that in hybrid combinationmaintain an acceptable level of resistancewithout sacrificing yield. The disproportionatenumber of resistance genes to yield genes, thelatter sometimes estimated at nearly 5000, suggestsan applied breeding approach quite differentfrom a basic attempt to isolate a genetic source ofresistance.Since both charcoal rot and fusarium stalk rot aremost likely to develop under heat- and moisturestressedgrowing conditions and multiple locationsare expensive, a dependable field screen is difficultto simulate. At one time the University of Arizonaprovided a screen where supplemental irrigationwas the only water normally available during thegrowing season. However, temperatures theregenerally exceeded the 38°C said to be optimumfor charcoal rot.Charcoal Rot ResistanceEarly GenerationsWe grew two nurseries in 1960, one at Lubbock, theother in eastern New Mexico, in an attempt to*Vice President, Dekalb-Pfizer Genetics, Route 2, Lubbock, TX 79415, USA.NOTE: This paper is based on the author's 28 years of experience in the commercial sorghum industry. Furtherinformation can be obtained directly from him.International Crops Research Institute for the Semi-Arid Tropics. 1984. S o r g h u m Root and Stalk Rots, a CriticalReview: Proceedings of the Consultative G r o u p Discussion on Research Needs and Strategies for C o n t r o l ofS o r g h u m R o o t and Stalk Rot Diseases, 27 Nov - 2 Dec 1983, Bellagio, Italy. Patancheru, A.P. 502 324, I n d i a :ICRISAT.219

improve the odds for adequate infection on 820entries of inbreds and hybrids. The New Mexiconursery was on soil known to have a high naturalbuildup of M. phaseolina. At the time of booting,supplemental moisture was withheld on the Lubbockentries, which were grown at relatively highpopulations and high nitrogen levels.Dr. D.C.H. Hsi of New Mexico State Universitymade significant initial suggestions for thesescreenings and provided the pathogen isolates foruse in 1960. The fungus was cultured on toothpickscoated with potato dextrose agar. Three distinctisolates were used, and their identity was maintainedduring the early generations. Sources ofisolates varied, with our main objective being toutilize those with the most virulence. Toothpickinoculation of stalks was made at approximately 5cm above the soil level 3-4 weeks after flowering.Eighteen readings for each of the 700 test entriesaveraged from 1.3 cm to 27.2 cm infection from thepoint of inoculation.As seen in Table 1, conditions favored charcoalrot development at Lubbock compared to the NewMexico location. At Lubbock the homozygousmaterial averaged 7.8 cm infection, compared to11.9 cm for the hybrids. Generally the hybrids weremore severely infected than the mean of the parents,and frequently more than the most susceptibleparent, suggesting that susceptibility wasdominant. Lines showing resistance were rescreenedto eliminate escapes. Some entries wereobviously resistant; others mechanically excludedthe fungus through internal structural barriers (e.g.,compressed nodes); and finally tolerance throughTable 1. Frequency distribution of Macrophominaphaseolina growth from point of inoculationin the stalks of 700 sorghum genotypes in1960 screenings at Lubbock, Texas, andTexico, New Mexico, USA.No. of entriesGrowth of fungus(cm) Lubbock Texico0.0- 2.9 22 1493.0- 5.9 123 2186.0- 8.9 169 1779.0-11.9 153 8212.0-14.9 132 4115.0-17.9 64 2018.0-20.9 19 721.0-23.9 5 124.0-26.9 1 027.0-29.9 1 0the lodging resistance provided by a stiff stalk wasanother possible source of improvement.The better lines were not only crossed in diallelesbut also used as source material for pedigree-typebreeding. New lines suggested that progresswould be possible, but slow, because of escapesand the complexity of the inheritance. Three yellowendosperm derivatives were the basis for segregatingpopulations with elite but susceptibleinbreds until 1964, when New Mexico 31 wasreleased by Malm and Hsi (1964).Hybrid ApplicationMale or restorer lines resistant to charcoal rot weredeveloped ahead of male-steriles, both because ofthe loss of generations in going from B to A linesand also because the initial pedigrees with resistancewere of an R or male type. Resistant malesteriles,while agronomically acceptable, alwaystraces back to some R or male germplasm as thesource of their resistance. The recurrent or predominantparentage of these new resistant femaleswas of a kafir, milo-kafir, or U.S. x plant introductionderivative.By 1970, or 11 summer generations into thisprogram, an experimental hybrid, X-1486 (later tobe designated C-42c), was recommended for production.This pedigree was our first charcoal-rot-"resistanf hybrid, with the male parent comingdirectly from cycle 1 of the resistant x susceptiblepopulations. The sterile, a stiff-stalk line, traces tokafir-milo x a Nigerian yellow plant introduction.Charcoal rot readings showed a significantimprovement compared to checks, and yield wasacceptable (see Table 2). Both parents exhibitedthe stiff stalk trait, considerable drought resistance,and a degree of nonsenescence. Seed yield of thefemale, plant height, and more than normal uppernodebreakage late in the season limited theTable 2. Percent growth of Macrophomina phaseolinain the stalk and yield of sorghum hybridC-42c compared to two check hybrids(1969-70) at Lubbock, Texas, USA.HybridDEKALB C-42aDEKALB E-57RS-610Fungus growth Yield(% of check) (% of check)61 10532 10310 115220

acceptance of this dryland hybrid. A pedigree usingthis female, however, was used quite extensively inAustralia as C-42t.Several hybrids with resistance in both parentsdemonstrated good resistance in natural and inoculatedfield tests, but failed to be competitive. X-635for example, yielded 91.5%, 95.4%, and 96.5% ofthe checks over 3 years, with a quite acceptablecharcoal rot level. DEKALB C-46, however, whichhad a charcoal-rot-resistant male and a droughttolerant,stiff-stalked female, gave an equally lowcharcoal rot reading, but more importantly, understress, it stood and yielded well. The droughtaspects of this hybrid appeared to be due to (a)nontillering, (b) reduced transpiration, (c) osmoregulation,and/or (d) nonsenescence.C-46 became available in 1982 as DK-46. thishybrid has resistance to greenbug biotypes C, D,and E and apparently has even better stalk qualityand yield potential. The pollinator of DK-46 is atropical x charcoal-rot-resistant derivative, with thehybrid showing outstanding stalk quality. Unfortunately,the male tends to be a specific combiner. In1983, a year of record heat and drought, DK-46saw its first year of sizeable commercial plantingsand gave excellent performance. A big questionremains, of course, as to whether it was selectedfor nonsenescence or charcoal rot resistance, butthe critical measurement for stalk rot remains positiveand includes resistance to fusarium stalk rot.Other useful lines have come from the program,but after 16 years line development was reduced in1975. The significance of nonsenescenceemphasized the need for continual field testingunder limited water levels. Also, milo types in hybridcombination showed the obvious advantages ofthe introduction of yellow endosperm germplasminto commercial hybrids. R.E. Karper and O.J. Websterprobably accomplished as much or more withtheir initial yellow endosperm introductions andbreeding as was gained at the time of hybridizationin 1956.Another commercial hybrid, DK-57, uses a malefrom this program converted to greenbug biotype Cresistance. Finally, an additional charcoal-rotresistantline is in advanced testing in hybrid combination,with especially good stress results.Relationship to Drought ResistanceThe quantitative nature of drought resistancesuperimposed on the complex physiologicalrequirements of charcoal rot resistance suggeststhat more might be accomplished by breeding fordrought resistance. Here at least yield would be anintegral objective if drought resistance were relatedto dry matter production per unit of water. As thecharcoal rot program, discussed previously,matured in line development, so in turn did a parallelprogram that screened germplasm for thesedrought traits: (a) diffusive resistance, (b) heat tolerance,(c) dormancy, and (d) root development.Dormancy refers to the plant remaining healthy butwith limited or no growth.The above screening suggested good heritabilityfor all these traits, but no one alone gave enoughdrought resistance, and the yield level was notacceptable. Therefore the quantitative task of combiningyield with drought resistance and stalk rotresistance suggested a population approach.These populations must contain known germplasmfor the three objectives. In addition, a screeningsystem that adequately evaluated yield, drought,and stalk rot was essential.Our approach was based on recurrent selection,with germplasm containing lines known to havedesirable components of drought resistance, linesfrom our charcoal rot program, stiff-stalk lines, andgermplasm of known good combining ability.Initially we confined our program to the male orrestorer side but used testers of known heat anddrought tolerance on the female side, except for alater, stiff-stalked sterile which has now beendropped for reasons of hybrid maturity. This materialwas tested under both drought stress and irrigation,and initial testcrosses were evaluated in asimilar fashion.Evaluation in advanced replicated trials wasconducted in the following environments: Lubbockdryland, Lubbock limited irrigation (20-25 cm),Southwest Kansas dryland, and South CentralNebraska favorable dryland. Most hybrids tendedto have high location interaction, with either gooddrought or good optimum performance related tothe check means. The second year of testing, however,emphasized those performing well across allmoisture levels,Stress in 1983 was more severe than in 1982,giving an excellent evaluation. In addition, plants inthe third replication at Lubbock were inoculatedwith charcoal rot. Yield data from 1982 and 1983will be regressed against test means to determineB-values. It is hoped that we can avoid extremesbeyond B < 0.90 or > 1.10 when selecting newreleases by this approach. An improvement in stalk221

quality is also anticipated, both from the germplasminvolved and from the natural field screeningacross environments, as well as from toothpickinoculations.Relationship to Insect ResistanceInfestations of greenbug or mites are frequentlyassociated with a heavy degree of lodging, besidescausing reduced yield. Since these insects predisposethe plant to various fungal organisms, theavailability of hybrids resistant to sorghum greenbugsin 1976 significantly reduced lodging in theU.S. crop, just as the widespread use of yellowgermplasm did in the 1960s, Additionally, insectresistance might:a. allow "dormancy" to be a trait in drought resistanceby keeping plants healthy duringstress,b. produce better control of stomatal response inreducing transpiration,c. produce more photosynthetic activity by theresistant form, as with nonsenescentsorghum.Unfortunately, although mites are obviously closelyrelated to lodging problems, progress with resistanceto Banks grass mite (Oligonychus pratensis)has been slow, A breeding program concernedwith stalk rots must include insect resistance as anadditional component of recombination andscreening.Fusarium Stalk RotAt the time we began the charcoal rot program wereviewed an ongoing fusarium stalk rot program. Alimited attempt at inoculation and subsequentreadings suggested that we confine our effort tocharcoal rot. We relied somewhat on previousresearch suggesting that varieties resistant to M.phaseolina often are resistant to F. moniliforme.Also, there was the suggestion that in our materialthe degree of resistance to charcoal rot wasgreater than to fusarium stalk rot.The 1983 season gave us plenty of opportunity tosee field differences in the level of resistance to F.moniliforme from Lubbock, Texas, to Nebraska.Often the two pathogens were found together, andwe verified the existence of resistance to both inthe same material.Argentina, the second largest sorghum producerin the Western Hemisphere, experiences muchmore loss from F. moniliforme than from other stalkrottingorganisms. In Argentina the breeding programattempts to screen over nine environments adiverse group of hybrids (5000 in 1982-83). Themost severe incidence of fusarium stalk rot inArgentina occurred in 1982-83 to the west andsouthwest of the sorghum belt, approximating 32-36° S, with much less effect in the warmer but morehumid north.An approach to be tested in 1983-84 in Argentinawill allow us to choose a set of 35 hybrids known tobe outstanding in performance but whose level ofresistance to F. moniliforme is unknown. These willbe grown at three hot-spot locations at both normal(200000 plants/ha) and heavy populations(400000 plants/ha) in replication. The high populationshould stress the plants enough to allow stalkquality in the presence of the organism to bescored. Also, we will be able to observe testcrosseswith new material having a nonrecurrent parentwith F. moniliforme resistance. Whereas susceptibilityto F. moniliforme also appears to be dominant,we note considerable variation between hybrids,suggesting the potential for improvement througheffective screenings of a range of hybrid genotypes,as well as through line development.Genetic Variabilityand Charcoal RotLevel and Type of ResistanceThe range of inbred reaction to charcoal rot pointsout very clearly that genetic gain can be achievedthrough selection. For example, using three isolatesof M, phaseolina we obtained the meanvalues shown in Table 3. Unfortunately hybridsTable 3. Mycelial growth of three isolates of Macrophominaphaseolina in the stalks of threecultivars at Lubbock, Texas, USA.PedigreeRedbjne 60New Mexico 31Superior inbredMycelial growth in stalk(cm)31.71.32.0222

223often do not reflect even partial dominance forresistance. With susceptibility dominant, perhaps itis not surprising to see overdominance beingexpressed. Certainly a hybrid with more water-useefficiency and a greater sink will be under morestress later in the season.The first released hybrids with a heavy componentof milo or kafir-milo derivatives for pollinators,and frequently with kafir-milo females, wereextremely susceptible. With a recessive type resistance,breeding becomes twice as difficult sinceboth parents must be resistant and also combinewell for hybrid yield. The introduction of improvedyellow endosperm germplasm during the 1960s notonly added improved yield, drought resistance, anddisease resistance, but also had a major impact onstalk quality. The healthier plants resulting from redx yellow and yellow x yellow crosses were muchmore resistant to charcoal rot.Although not a charcoal-rot-resistant hybrid inthe strict sense, DK-46 has generally stood betterthan other commercials when stressed at a similarphysiological growth stage, as was clearly demonstratedthrough the stress of 1983. No doubt thenonsenescence and osmo-regulating ability of thehybrid is a big factor if we accept the premise thatthe health of the plant is all-important in its ability toresist the organism.The breeder need only to add the stiff stalk trait toa hybrid to greatly improve the odds for a standingplant at harvest. This use of tolerance to stalk rotwas first shown with E-57, a hybrid released in 1964and still grown rather extensively, especially inAustralia. Additional favorable traits of E-57 are"dormancy" and an improved level of nonsenescence.Since the nodal tissue appears to temporarilyslow down the upward movement of the organism,a hybrid based on short plant stature can beexpected to have less relative internode damage.Efforts to incorporate a 4-dwarf parent, whichshortens a hybrid and generally pleases the producer,have also been responsible for reducingstalk rot loss.Advances In Drought ToleranceEven if a "true" charcoal-rot-resistant hybrid failedto result from this extensive program, numeroussuccessful inbreds that added a new dimension todrought resistance were developed. Aiming for luxuriousearly growth followed by stress during andafter pollination has given us every opportunity toisolate nonsenescent germplasm. The secondphase of this program will allow recurrent selectionto increase the heterotic potential of the lines developedby this method. However, caution must begiven to any assumption that inbreds selected fordrought or stalk rot resistance can be expected toproduce hybrids with more than averagestandability.Basic ResultsAlthough extremely sensitive to the environmentthe toothpick screening system is a useful tool tothe breeder. Replication and screening over severalyears may be required to verify classification.During the early years we used no less than threeisolates of M. phaseolina at all times. No correlationexisted between virulence in culture and structuraldamage or growth within the plant. Actually, ourweakest culture was the most virulent in the plant.As pointed out previously, the shorter internodesof 4x3-dwarf hybrids can add a level of mechanicalresistance. In 1967 some six inbreds isogenic forthe Dw2 height gene were grown in the charcoal rotnursery with three sources of inoculum. The 3-dwarfs had 40% more measured charcoal rotdevelopment than the 4-dwarfs of a similar geneticbackground. Also, the 3-dwarfs had a higher percentageof lodging, as might be expected.To gain some insight into the importance ofdrought resistance and, in part, to verify the importanceof the waxy bloom found on most sorghum,we evaluated isogenic forms of three sorghum varietiesin the 1971 charcoal rot nursery. Two replicationswith a combined total of 12 measurements offungus growth favored the normal plants (Table 4).Table 4. Macrophomina phaseolina growth in inoculatedstalks of bloom and bloomless varietiesof sorghum in 1971 charcoal rotnursery.VarietyMartin BlMartin blCombine Kafir 60 BlCombine Kafir 60 blRedbine BlRedbine blBloompresentabsentpresentabsentpresentabsentMycelial growthin stalk(cm)12.419.611.414.414.218.6

The more extensive growth of the pathogen in thebloomless plants suggests that sorghums with littleor no waxy coating may be more predisposed toinfection by the organism. Since additional informationverifies that bloomless sorghums are lessdrought tolerant, we can assume the additionalstress encountered by these lines compared tonormal varieties provides a more favorable environmentfor charcoal rot development.If we can accept a threshold concept of physiologicalresistance, hybrids will then vary accordingto their drought tolerance. Additionally, morphologicalresistance and tolerance will contribute to afinal standability classification.Agricultural Experiment Station Research Report 93. LasCruces, New Mexico, USA: New Mexico State University.USDA. 1965. Losses in Agriculture. USDA Handbook 291.Washington, D.C., USA: U.S. Department of Agriculture.10 pp.ConclusionsAlthough charcoal rot is of less significance in theUnited States today than when hybrids firstappeared, we will continue to face a high percentageof cropped areas grown under stress. Whilethe initial yellow endosperm introductions seem tohave made a significant contribution, future progresswill also rely heavily on plant introductions.We need to determine the best approach for rapidand efficient improvement of adapted lines fromsuch germplasm.Once source material has been determined, themost practical approach to developing useablelines will be to combine this material with the twoprimary objectives of sorghum improvement in aridzones: improved yield and drought tolerance.Selection for the presence of a stiff stalk anddrought tolerance, especially of the nonsenescenttype, combined with high yield, will be more productivethan breeding for charcoal rot resistancealone. On the contrary, excellent progress indrought resistance has been possible by screeningfor charcoal rot under the appropriate late-seasonstress conditions. Finally, the breeder has muchless understanding of the mode of action of F.moniliforme than of M. phaseolina. The obviousseverity of diseases caused by this organism in themajor sorghum areas of the Americas suggeststhat equal attention be given F. moniliforme.ReferencesMALM, N.R., and HSI, D.C.H. 1964. New Mexico 31, acharcoal rot-resistant grain sorghum line. New Mexico224

Lodging, Stalk Rot, and Root Rotin Sorghum in AustraliaR.G. Henzell, R.L. Dodman, A.A. Done,R.L. Brengman, and P.E. Mayers*SummaryMost of the 600000 ha of grain sorghum in Australia is grown under dryland conditions, Waterdeficits during the growing season are common, and lodging associated with stress duringgrain filling is prevalent; this type of lodging is due to weakening and fracture of the stem base.Root lodging is of little significance. Stalk rots, predisposed by stress, are also common.Research and observations in Australia support evidence from elsewhere that the sourcesinkrelationships of the plant during grain filling greatly influence lodging and stalk rotdevelopment Physiological stress caused by a low source/sink ratio is a necessary conditionfor lodging and for the development of stalk rots.The source-sink relationship is important in selection for resistance to lodging, and charactersthat affect this relationship—particularly grain yield and maturity—are considered whenselecting for lodging resistance. Nonsenescence is closely correlated with lodging resistanceand is widely used as, an indicator characteristic during selection. The use of a tropicalenvironment is discussed.Little direct selection is practiced for resistance to stalk rots, although evidence exists forgenetic variation in resistance to Fusarium moniliforme and Macrophomina phaseolina.Some recommendations for future research are made.Approximately 600000 ha of grain sorghum aregrown in Australia each year, with about one third ineach of the northern New South Wales, southernQueensland, and central Queensland regions(Table 1 and Fig. 1). In addition, a large potential forincreased production is beginning to be realized inthe semi-arid tropics of north Queensland.Almost all sorghum in Australia is grown underdryland conditions in areas averaging 500 to 700mm annual rainfall. This is mainly summer rainfall,and it is unreliable both in total amount and distribution.Water deficits are therefore common, and theconsequent lodging is a significant factor insorghum production, particularly in centralQueensland. It is also expected to be a seriousproblem in the potential cropping regions of northernQueensland. Lodging resistance is an essentialcharacteristic of grain sorghums for these areasand is desirable in other parts of Australia. Rootlodging is of little significance in Australia.Although lodging and stalk rots are importantproblems in sorghum production, poor seedling*R.G. Henzell - Senior Plant Breeder, R.L. Dodman - Supervising Plant Pathologist, R.L.Brengman - Plant Breeder, andP.E. Mayers - Plant Pathologist, Department of Primary Industries, Hermitage Research Station, Warwick, Queensland4370, Australia; and A.A. Done - Sorghum Geneticist, Commonwealth Scientific and Industrial Research Organisation(CSIRO), Northern Territory, Australia.International Crops Research Institute for the Semi-Arid Tropics. 1984. Sorghum Root and Stalk Rots, a CriticalReview; Proceedings of the Consultative Group Discussion on Research Needs and Strategies for Control ofSorghum Root and Stalk Rot Diseases, 27 Nov - 2 Dec 1983, Bellagio, Italy. Patancheru, A.P. 502 324, India:ICRISAT.225

Table 1. Sorghum production in Australia, 1981/82 season. (Source: Australian Bureau of Statistics.)Area Production YieldState/region (ha) (tonnes) (t/ha)Queensland:Southern Queensland 257098 647418 2.518Central Queensland 228425 330437 1.447Northern Queensland 3621 4580 1.265Total Queensland 489144 982435 2.008New South Wales 152346 325689 2.140Western Australia 4928 5270 1.069Victoria 1537 2477 1.612Total Australia a 648574 1316706 2.030a. Includes small area and production from South Australia and the Northern Territory.emergence and root rots are also frequentlyencountered. The major planting period in southernQueensland and northern New South Walesoccurs in spring and early summer when soiltemperatures are frequently low. Seedling pathogensare commonly associated with poor emergenceand establishment under these conditions;replanting is often necessary. Root rots during cropdevelopment are widespread, and root systems areoften severely diseased; their effects on yield arenot known, however.T h e C a u s e s o f L o d g i n gSorghum crops grown under ideal conditions arestill green when the grain is physiologically mature.Extensive death of leaf or stem tissues ("senescence")at this time can be regarded as a stresssymptom.The most important type of lodging in grainsorghum in Australia occurs after a water deficitduring the grain-filling period. Plants senesce andthen lodge due to stems breaking at or just aboveground level. The stems are weakened by degradationof the pith and rind in the basal internodes,leaving unsupported vascular strands. Invasion bystalk-rotting fungi is common, but not universal, inlodged stalks.The causes of death and lodging are not wellunderstood, but three hypotheses can be proposed:(1) plants die as a direct result of waterdeficit, i.e., a physiological breakdown due to dehydration;(2) pathogens are the cause of death; or (3)death is due to an interaction between physiologicalstress and pathogens.The Role of PhysiologicalStress in LodgingIt has been proposed that physiological stress perse results in rapid senescence and subsequentlodging. This stress can be generated when a large"sink" for photosynthetic assimilate, such as arapidly growing organ (the grain), creates a highdemand in relation to the assimilate supply (photosyntheticcapacity). A crop is considered "sourcelimited" if the sink is capable of growing largerwhen the assimilate supply is increased; it is "sinklimited" if the sink does not respond in this way. If,for example, single-grain weight does not increasewhen the crop is thinned or panicles artificiallyreduced in size at anthesis, then the crop is said tobe sink limited with respect to grain yield, whereasan increase in grain weight would imply a sourcelimitation. Various factors can reduce assimilatesupply, including water deficit, leaf removal, leafdisease, insect damage, nutrient deficiency or toxicity,and low light intensity. The "physiologicalstress" is thought to result in a shortage of availablecarbohydrate in the stem (Chamberlin 1978). Celldeath occurs when the level is too low to supportsufficient maintenance respiration. Pith disintegrationthen begins at the base of the plant and mayextend upwards several internodes as conditionsworsen.There is good circumstantial evidence to supportthe hypothesis that high rates of senescence inresponse to water deficits are caused by the presenceof a relatively large grain-filling sink. This wasillustrated by Henzell and Gillieron (1973), whoaltered the source-sink relationship in two hybrids,Texas610 and DeKalb E57, and one inbred variety,226

12015010Darwin10KununurraBOTropic of CapricornNORTHERNTERRITORYQUEENSLANDEmeraldBiloelaWESTERN AUSTRALIASOUTH AUSTRALIAGattonB r i sbaneHermitage-30NEW SOUTHWALES30SydneyVICTORIA1 dot = 5000 ha40Main centers of sorghum researchTASMANIA40120 130 140 150Figure 7. Grain sorghum production in Australia in 1981-82.'Alpha,' by mechanically removing portions of theirpanicles at flowering. In each genotype, this reductionin sink size dramatically reduced the rate of leafsenescence in the presence of a water deficit. Therelationship for 'Alpha' is shown in Figure 2. Charcoalrot caused by Macrophomina phaseolina(Tassi) Goid. was associated with some deadplants, but the majority showed no obvious symptomsof infection by any stalk-rotting fungus (Table2). No isolations were made to determine the presenceof pathogens. A.A. Done has also observedthat nonf lowering plants senesce at a slow rate anddo not lodge even after extended periods ofdrought stress.The hypothesis that the source-sink relationshipaffects lodging is also supported by the associationbetween maturity type and lodging. Early floweringis often associated with a higher senescence rateand therefore with susceptibility to lodging. This Isprobably because early genotypes are likely to pro-227

80604020aaabAlphaa a a*aabcaabc100% p a n i c l e removed73% p a n i c l e removed42% p a n i c l e removed0% p a n i c l e removedc c cc010 20 30 40 50 60 70 80Days a f t e r treatment a p p l i e d*At a particular date, points followed by the sameletter are not significantly different (P < 0.05).Figure 2. Effect of panicle treatment on thedeath of leaves for the inbred variety 'Alpha' in1969-70. (Source: Henzell and Gillieron 1973.)abcbacabduce more grains per unit leaf area than later genotypes,This is at least partly due to a lowerprobability of water deficit at the time of panicledevelopment in early genotypes and therefore lesschance that a water deficit would inhibit panicledevelopment. Even in the absence of water deficitsduring panicle development, competition forassimilate between developing leaves and paniclemay be greater in late- than in early-flowering genotypesplanted at moderate to high population densities.This results in a lower grain number to leafarea ratio in later genotypes.It might be conjectured that later maturing genotypeswould have a higher probability of encounteringend-of-season water deficits and therefore agreater chance of lodging. Experience has shown,however, that the morphological and physiologicalcharacteristics associated with later maturityapparently contribute more to lodging resistancethan phenological characteristics might beexpected to contribute to susceptibility. This associationbetween lodging resistance and late maturitycan be seen in Tables 5,8,9, and 10, which arediscussed later.It is frequently observed that there is a negativecorrelation between days to flower and harvestindex, as illustrated for four locations in Table 3.This observation supports the proposed explana-Table 2. Percentage of dead plants and charcoal-rot-diseased plants (% of dead plants) for four panicletreatments for DeKalb E57 and Texas610 at Biloela, Queensland, Australia.PanicleFull panicleTwo-thirds panicleOne-third panicleNo panicleDeKalb E57% dead % rottedplantsplants58 452 01 00 0%deadplants503600Texas610% rottedplants91300Table 3. Correlation between days to flower and harvest index in four experiments in Australia.Test locationCorrelationcoefficientKununurra (dry-season tropics restricted irrigation) -0.63**Hermitage (irrigated temperate) -0.56Hermitage (dryland temperate) -0.87**Dalby (dryland temperate) -0.80** P

tion of the relationship between maturity andsenescence rate. Plants with a high harvest indexare more likely to have a low source/sink ratio andaccording to the hypothesis are therefore morelikely to senesce when the source's capacity to fillthe sink is reduced.On the other hand, Brown (1978) has data that donot support this proposition. He found that theeffect of adverse conditions during the panicledevelopment was in the direction of enhancingpanicle (sink) relative to leaf (source) development.However, plants in his study were grown in pots in aglasshouse, with stress usually being sudden andsevere and applied during brief segments of theperiod of panicle development.Because of the apparent importance of thesource-sink relationship in determining senescencerate, it is of interest to consider the relationshipfor genotypes of known lodging resistance.Muchow and Wilson (1976) examined, under favorablegrowing conditions, the source-sink relationshipsin the grain yield of four hybrids: DeKalb E57,Pacific Goldfinger, Texas610SR (ATx3197/RTAM422), and Texas626 (ATx3197/RTx415). DeKalbE57 is resistant to lodging, whereas the other threeare very susceptible. Muchow and Wilson's analysisshowed that the hybrids susceptible to lodgingwere source limited, whereas the resistant hybridwas partially limited by both source and sink—afinding that is consistant with our physiologicalhypothesis. The small number of genotypes limitsgeneral conclusions, and the source-sink relationshipof particular genotypes is likely to vary withenvironmental stresses. Brown (1978) found, however,little if any evidence to suggest that sourcecapacity was limiting grain yield in DeKalb E57subjected to varying levels of water deficit duringpanicle development.Done and Muchow (1983) found in an irrigatedwinter planting in northwest Australia that all genotypes(20 inbred lines and F 1 hybrids) except Ramada(a tall, late, sweet inbred) were source limitingfor grain yield. The degree of limitation varied, butthis did not appear to be related to the knownlodging resistance of the genotypes. However,DeKalb E57 was less source limited than mostgenotypes.It is also of interest to examine the hypothesisthat lodging-susceptible genotypes, under conditionsof photosynthate shortage, relocate dry matterfrom the stems to the developing grain. Suchgenotypes may also preferentially partition newlyproduced photosynthate to the grain (more so thanunder good conditions) to the detriment of the stem.Chamberlin (1978) examined this hypothesis usingthe lodging-resistant and lodging-susceptiblehybrids DeKalb E57 and Texas610, respectively.He found very little evidence that a water shortageduring grain filling resulted in increased mobilizationof reserves assimilated prior to anthesis. Therewas also no indication that stress caused changesin the distribution patterns of current assimilates,favoring the grain at the expense of the stem. Heconcluded that "lodging seems rather to haveresulted from the assimilate supply being too towunder conditions of water shortage during grainfilling to provide the substrate for stem maintenancerespiration." His results and conclusionsstrongly support the physiological hypothesis.Chamberlin (1978) showed in glasshouse experimentsthat Texas610 lodged more than DeKalbE57, as has also been observed in the field.Although the causes were not clear, there weresignificant differences. Texas610 had a greateremphasis on grain production when assimilateswere partitioned at the expense of the lower stem.Also there was a more gradual depletion ofreserves from DeKalb E57 stems during grain filling.These reserves were higher in DeKalb E57than in Texas610 at anthesis. As pointed out above,this pattern was not altered by water deficit inChamberlin's test. Once again, however, the generalconclusion from this work may be limited in thatonly two hybrids were tested and the plants weregrown in pots in a glasshouse, resulting in a relativelyrapid onset of stress.As previously pointed out, Done and Muchow(1983) observed that while most genotypes weresource limiting with respect to grain yield, themajority produced more dry matter during grainfilling than was used to fill the grain. Stover drymatter yield at physiological maturity was higherthan anthesis dry matter yield. In this experiment,grain yields were high (up to 7.6 t/ha), with litttesenescence and no lodging at physiological maturity.Done found in another experiment that low grainyields associated with increased water deficitcaused a reduction in the net amount of nongrain(surplus) dry matter produced during grain filling.Senescence and lodging occurred in the highlystressed treatments, but differences in dry matterpartitioning could not be distinguished betweengenotypes susceptible and resistant to lodging.Failure to detect such an effect, however, could beattributed to large experimental errors and does notprovide conclusive evidence for its absence.229

It can therefore be conjectured that in a healthy,high-yielding sorghum crop, surplus dry matter willbe produced during grain filling, and any reductionin this surplus could represent a "stress" situationresulting in senescence and lodging susceptibility.This argument can be extended to suggest that anyattempt to genetically improve grain yields by usingpreanthesis assimilate or by increasing the proportionof assimilate partitioned to grain during grainfilling would have the undesirable side effects ofincreased senescence and susceptibility tolodging.The Role of Pathogens in LodgingStalk rots are often, but not always, associated withlodged stalks. Where stalk rot does occur, it is notclear what effect it has on grain yield and subsequentlodging.In Australia, there are few reports of detailedsurveys to identify the causes of lodging and itsassociation with stalk rots and other factors. Thepathogens involved with the characteristic symptomsof stalk rot have been examined, and it hasbeen found that M. phaseolina is readily recoveredfrom stalks with blackened piths typical of charcoalrot, while Fusarium moniliforme Sheldon is the predominantfungus from stalks with a very dark-red todeep-purple discoloration of the pith tissue (Burgesset al. 1981). These fungi are sometimes presentin the same stalk. In addition, Nigrosporasphaerica (Sacc.) Mason can occasionally be recoveredfrom discolored stalks, usually where oneor both of the other pathogens are present (Mayers,unpublished data; Dodman, unpublished data;Trimboli1981).Although these fungi are consistently associatedwith discolored stalks, they often cannot be recoveredfrom lodged stalks that show no discoloration.In central Queensland, G.S. Purss(Department of Primary Industries, Brisbane,Queensland, Australia; personal communication)examined the stalks of a number of grain sorghumgenotypes and found that although pith disintegrationhad occurred, M. phaseolina was rarely presentand no other organism could consistently berecovered. Similarly, Henzell and Gillieron (1973)reported that charcoal rot was rarely seen in plantsthat were dead at the base. From surveys in NewSouth Wales in 1978 and 1979, Trimboli (1981)reported that no fungi were isolated from nonlodgedstalks exhibiting a hard, dry, brittle stalksyndrome (the frequency of occurrence of suchstalks was not indicated). Severe water deficitsoccurred in 1982/83 in southern Queensland, andlodging was widespread. Most lodged stalksshowed no discoloration, although the basal internodeswere shrivelled and collapsed. F. moniliformewas the predominant fungus recovered, butit could be isolated from only about half of thesestalks.In contrast to these reports, Mayers found a highincidence of stalk rot in a detailed examination of acrop at Brookstead in southern Queensland in1977/78. A sample of 1400 stalks was collectedfrom randomly located quadrats and examined forsymptoms of stalk rot. More than 80% of thesestalks showed typical symptoms of invasion by F.moniliforme, and Mayers estimated that between20 and 50% would have lodged before harvest.Trimboli (1981) reported that F. moniliforme wasthe fungus most commonly found in lodgedsorghum stalks in New South Wales. M. phaseolinaand N. sphaerica were isolated much less frequently,and he concluded that they probably play aminor role in stalk rot development in the regionssurveyed. However, there were indications that M.phaseolina occurred more often in areas of lightersoils. No information was provided on the amountof lodging or the proportion of lodged stalks withsymptoms of stalk rot.It is apparent from these observations that infectionwith stalk rot pathogens and symptoms of invasionare not always associated with lodging.However, the frequency of lodging with and withoutstalk rot and that of stalk rot without lodging has notbeen defined. Surveys should be conducted overseveral seasons to clarify the situation.Recent research in Queensland by Mayers (from1978-1981) and Dodman since 1981 has aimed atclarifying some of these issues by manipulatingenvironmental conditions and inoculum levels ofsoilborne pathogens. The importance of soil moisturewas studied in plots receiving adequate rainfallor irrigation and in plots where rainfall wasexcluded with plastic-covered shelters. The role ofpathogens was examined in untreated plots andplots fumigated with the granular fumigant dazomet(tetrahydro-3,5-dimethyl-2H-1,3,5-thiadiazine-2-thione).Our trials at Hermitage in southern Queenslandin 1978/79 and 1980/81 showed that stalk rotdeveloped only when the pathogen F. moniliformewas present in the soil and when this was accompaniedby water deficits (Table 4). Fumigation230

231Table 4. The effect of moisture regime and soil fumigation on the incidence (%) of fusarium stalk rot In twosorghum hybrids at Hermitage, Queensland, in 1978/79.Soil treatmentNot fumigated:Fumigated:MeanCultivarTropicDeKalb E57MeanTropicDeKalb E57MeanNatural rainfall(low stress)6.54.05.23.00.51.73.5Moisture regimeRain excluded(high stress) aa. Rainfall was excluded with a rain-out shelter erected 5 weeks after planting; symptoms of water deficit (wilting and senescence of leaves)developed soon after anthesis.69.033.051.03.30.01.626.3Mean28.11.7reduced both the inoculum level and the incidenceof stalk rot even where a severe water deficitoccurred, whereas no stalk rot developed in theabsence of a water deficit. It was found that waterdeficits reduced grain yield by 36% through effectson both single grain weight and grain number. Stalkrot produced an additional yield loss of 6.5% byreductions in single grain weight. Where lodgingoccurs in commercial production, losses can bemuch greater due to harvesting problems.In the 1981 /82 and 1982/83 growing seasonswe extended our research to an examination of thesusceptibility of a wide range of genotypes. Despitethe imposition of severe water deficits through theuse of rain-out shelters, disease development waslower than in the earlier work, particularly with theearly-maturing genotypes. Although disease levelswere low in 1982/83, the incidence of severe stalkrot in seven genotypes of medium maturity rangedfrom 0 to 40% (stalks with severe stalk rot havemore than three diseased internodes). No relationshipwas found between reaction to stalk rot and astandability rating obtained from observations ofhybrid-evaluation trials at many sites over severalseasons.Although water deficits are usually associatedwith lack of rainfall, the inability of plants to absorbsoil moisture due to poor root systems is often acontributing factor. Root rots caused by fungalpathogens can develop soon after seed germinationand continue to affect the roots during allstages of plant development. Severe destruction ofcrown (or prop) roots is often seen around anthesisand may restrict water uptake, even where soilmoisture reserves are adequate for crop growth.Trimboli (1981) indicated that lesions on crownroots are initially small (0.5-4 mm), dark-red to purple,and usually restricted to one side of the cortex.These enlarge, girdling the root and extendingalong it for several centimeters. On large crownroots the cortex may eventually slough away andthe necrosis may extend into the stele. He foundthat F. moniliforme and Periconia circinata (Mangin)Sacc. were the fungi most commonly recoveredfrom such lesions. Similar observations werepreviously reported from Queensland (Mayers1976).Our research carried out in Queensland supportsthe hypothesis that pathogens invade stalktissue that has been predisposed by a physiologicalstress. In Queensland the major cause of suchstress is a plant moisture deficit associated withinadequate supplies of soil water and inability toabsorb water because of root rots. At present it hasnot been resolved whether physiological stress orstalk rot is the main cause of lodging. It seemsprobable that there is one type of lodging associatedwith severe moisture deficits and little stalkrot, and another where there is a close associationbetween physiological stress and pathogens.Breeding for Resistanceto Lodging and Stalk RotsVariation in the CharactersProgress in selection for stalk rot and lodging resistance,or indeed any character, is dependentupon the presence of genetic variation for that

character. Fortunately, large genetic differencesexist in sorghum for lodging caused by water deficits.The data in Table 5 illustrate the range ofvariation available. Unfortunately, most genotypesare susceptible. Table 6 lists some commonly usedgenotypes and their lodging reaction in Australia.Of these, KS19 is outstanding. It is a selection byW.M. Ross (University of Nebraska, USA) from across between CK-60 and Short Kaura made byO.J. Webster (Professor Emeritus, University ofArizona, Tucson, USA). KS19 is one parent in thepedigree of QL10, QL11, QL12, QL25, and QL27(Table 6). We have not yet tested genotypes suchas SC35-6, SC56-6, SC56-14, and SC599-6,reported as resistant in Texas (Rosenow 1977).Information on resistance to stalk rots caused byF. moniliforme and M. phaseolina is less conclusive.Variation in stalk rot severity has been found,but the presence of inherent differences in resistanceto the pathogen(s) has not been proved. Variationsmay have been caused by differences in thepredisposing physiological stress because of differencesin maturity. The data in Table 4 show thatDeKalb E57, a lodging-resistant hybrid, had a lowerlevel of disease than did Tropic, a lodgingsusceptiblehybrid. However, DeKalb E57 flowersearlier than Tropic and probably experienced lesssevere water deficits than Tropic in this test.Table 5. Percentage of lodged plants, leaf senescence, grain yield, and days to flower of some grain sorghumgenotypes at Hermitage, Queensland, in 1982/83.Lodged plants a Leaf Yield Days toGenotype (%) nonsenescence b (t/ha) flowerNK150 85 9.7 3.85 68Texas610SR 71 8.6 3.53 72ATx624/RTx430 69 8.0 3.73 79DK55 68 8.6 3.79 74AKS4/KS19 22 8.0 3.39 73ATx624/QL10 15 8.3 3.81 75Goldrush 8 8.3 4.31 77AKS4/QL12 6 7.7 3.97 75DeKalb E57 5 5.7 3.84 82Pride 2 7.0 5.16 79A378/QL12 0 5.4 4.78 80Dorado 0 6.0 3.90 84a. Severe water deficits occurred during grain filling; lodged plants showed no visible symptoms of stalk rot.b. Leaf nonsenescence ratings: 1 = all leaves green, 10 = all leaves dead. Ratings were made 105 days after planting.Table 6. Lodging reaction in Australia of some sorghum genotypes, obtained over years and sites.LodgingLodgingGenotype reaction a Genotype reactionKS19 R RTx2536 VSQL10 R RTx430 VSQL11 R IS2816C(SC120C) VSQL12 R IS12608C(SC108C) VSQL25 R IS12664C(SC173C) VSQL27 R RTx7000 VSB399 MS NM31 VSSC170C-6-8-4 S TAM428 VSBTx3197 S BTX3042 VSRTx7078 VS BTx378 VSTAM422 VS BTx622,623,624 VSa. R = resistant; MS = moderately susceptible; S = susceptible,; VS = very susceptible.232

Table 7. Percent incidence of macrophomina (M) and fusarium (F) stalk rot in nine sorghum hybrids grown over 2years under water deficit in a rain-out shelter at Emerald, Queensland. (Source: G.D. Reefer and P.E.Mayers, Department of Primary Industries, Emerald, Queensland, Australia).Trial 1 Trial 2 M/FresistanceHybrid M FM Findicated aLodgingresistance bGoldrush 56 66 8 31 sSM8 NA c NA 31 39 R/S RAKS4/KS19 29 72 NA NA R/HS HRDeKalb E57 29 84 32 73 R/HS HRSundowner NA NA 57 80 S/HS RDeKalb F64a 66 59 NA NA S/S RTexas610SR 84 52 68 65 HS/S HSGoldfinger 90 44 NA NA HS/S HSDorado 90 41 65 54 HS/S Sa. HR = highly resistant; R = resistant; S = susceptible; HS = highly susceptible.b. Classification based on long-term field tests.c. Not available.G.D. Keefer (Department of Primary Industries,Emerald, Queensland, Australia) and Mayers havemore positive evidence of the existence of M. phaseolinaresistance genes since differences in diseaseincidence went across maturity classes. Thedata shown in Table 7 suggest that reaction ofgenotypes to the two pathogens may be inheritedindependently and that there may be a correlationbetween lodging resistance (as measured in longtermfield tests) and resistance to M. phaseolina,but not to F. moniliforme.Selection for the CharactersOur discussion on the causes of lodging and stalkrots clearly implicates the source-sink relationshipsof grain growth in their occurrence. It isessential that this be kept firmly in mind whenselecting for resistance to them. For example,because of their apparent effect on the source-sinkrelationship, characters such as grain yield andmaturity, particularly, must be considered. Plantswith a high grain yield and early maturity are morelikely to be source limited and therefore susceptibleto the lodging and stalk rot syndrome. A considerationof lodging and stalk rot resistance alone wouldprobably result in the selection of late-flowering,low-yielding genotypes. This would be particularlyso if high grain yield was due to greater partitioningof dry matter to the grain (i.e., increased harvestindex), rather than to an overall increase in thebiological yield of the plant. Maturity differences arealso important because of the influence they mayhave on severity of water deficits experienced bygenotypes in different maturity classes.Most breeding programs in Australia take a similarapproach to evaluating lodging resistance. Thatis, hybrids rather than inbred lines are evaluatedbecause the low grain yield of inbreds tends tomake them lodging resistant. The genotypes undertest are grown at a number of sites at which grainyield, maturity, nonsenescence, and lodging aremeasured if differences are expressed. Severalsites are used to increase the chances of encounteringlodging conditions. Then subjective selectionis made for resistance to lodging withinmaturity and yield classes.Often lodging does not occur, yet differences inrate of leaf and plant death (senescence) areexpressed. Selection is then made for nonsenescence,again within maturity and grain yieldclasses. Evidence in Australia is similar to thatreported by Rosenow (1977) in Texas: a significantpositive association exists between nonsenescenceand lodging resistance (Tables 8,9, and 10).This association is expected because plants diebefore they lodge, What is surprising is that thecorrelation coefficients are not higher. It seemsother factors besides senescence rate areinfluencing lodging. Tables 8, 9, and 10 show thecorrelation matrices of lodging with some otherfactors, including yield, days to flower, and height atHermitage in 1982 and 1983 and at Banana in233

Table 8. Correlation coefficients between five characters in 81 hybrids at Hermitage, Queensland, in 1981/82.CharacterGrainyieldDays toflowerNonsenescencea% lodging at18 Feb 1983% lodging at28 Feb 1983Grain yieldDays to flowerNonsenescence% lodging on 18 Feb 1982% lodging on 28 Feb 1982-0.04-0.02-0.18-0.16-0.82**-0.66**-0.71**0.56**0.64** 0.94**a. Leaf nonsenescence ratings: 1 = all leaves green, 10 = all leaves dead.* * P < 0 0 1 .Table 9. Correlation coefficients between five characters in 72 hybrids at Hermitage, Queensland, in 1982/83.Grain Days to Non % lodging at % lodging atCharacter yield flower senescence a 11 Feb 1983 18 Feb 1983Grain yieldDays to flower -0.28Nonsenescence 0.10 -0.86**% lodging on 11 Feb 1983 -0.01 -0.36** 0.42**% lodging on 18 Feb 1983 -0.08 -0.46** 0.53** 0.96**a. Leaf nonsenescence ratings: 1 = all leaves green, 10 = all leaves dead.* * P < 0 . 0 1 .Table 10. Correlation coefficients between five characters in 28 hybrids at Banana, Queensland, in 1979/80.CharacterGrainyieldDays toflowerHeightNonsenescenceaLodging(%)Grain yieldDays to flowerHeightNonsenescence% lodging-0.39*0.190.100.100.07-0.18-0.50**-0.150.20 0.44*a. Leaf nonsenescence ratings; 1 = all leaves green, 10 = all leaves dead.* * P < 0 . 0 1 .* P

expected because of the different environmentalconditions encountered in the winter dry seasonand in the summer of Queensland, the latter beingthe normal growing period for grain sorghum inAustralia. Low grain yields are a feature of suchout-of-season plantings with restricted irrigation,but it seems the source-sink relationships have notbeen altered substantially, as evidenced by harvestindex values in excess of 0.50. Such an environmentmay in fact be superior to normal summerplantings in determining inherent differences inlodging resistance because maturity differencesbetween genotypes are reduced by the short winterdays. It is interesting that the correlation betweenlodging and days to flower in a test at Kununurrawas only -0.27, whereas it is usually higher in thesummer in Queensland (Tables 8, 9, and 10). Thepredictability of the environment at Kununurra isreflected in the high correlations (0.71-0.84)obtained between scores in different years. Done'sresults exclude particular genotypes that in someseasons fail to flower and do not senesce or exhibitstem lodging.Very little direct screening for resistance to stalkrot pathogens is practiced in Australia. Someworkers doubt its usefulness. Brengman and Dodmanhave had very limited success with toothpickinoculation with M. phaseolina because of maturitydifferences in genotypes and the unpredictable climate.Brian Hare (Pacific Seeds, Toowoomba,Queensland, Australia; personal communication)is attempting to establish a reliable procedure forscreening for resistance to stalk-rotting pathogens.To this end he is looking at pathogenicity tests (toensure organisms are causal agents), conditionsfor infection, and conditions in the plant for diseasedevelopment.Recommendationsfor Future Research1. More information is needed on the cause(s) ofgenetic variation in lodging resistance andstalk rot resistance. Consideration should begiven to how such information may be utilizedin a breeding program. For example, differencesin physiological responses to water deficitsneed to be examined. Differences inosmotic adjustment have been implicated byWright (1981 ), and dry matter partitioning duringgrain filling may be of considerableimportance.2. More information is needed on the role of pathogensin the type of lodging caused by waterdeficits. For example, surveys could be conductedover several seasons to establish thisrole.3. If it is established that pathogens are involved,then tests need to be devised for reliably identifyinggenetic differences in resistance.ReferencesBROWN, R.F. 1978. Environmental effects on panicledevelopment in grain sorghum (Sorghum bicolor (L.Moench)). Ph.D. thesis, University of Queensland,Australia.BURGESS, L.W., DODMAN, R.L., PONT, W., and MAYERS, P.E. 1981. Fusarium diseases of wheat, maize andgrain sorghum in Eastern Australia. Pages 64-76 in Fusarium:diseases, biology and taxonomy (eds. P.E. Nelson,T.A. Toussoun, and R.J. Cook). University Park, PA 16802,USA: Pennsylvania State University Press.CHAMBERLIN, R.J. 1978. The physiology of lodging ofgrain sorghum (Sorghum bicolor L Moench). Ph.D. thesis,University of Queensland, Australia.DONE, A.A., and MUCHOW, R.C. [1983]. Yield limitationsin a range of inbred and F 1 hybrid cultivars of Sorghumbicolor (L Moench). Australian Journal of AgriculturalResearch (in press).HENZELL, R.G., and GILLIERON, W. 1973. Effect of partialand complete panicle removal on the rate of death ofsome Sorghum bicolor genotypes under moisture stress.Queensland Journal of Agricultural and Animal Sciences30:291-299.MAYERS, P.E. 1976. The first recordings of Milo diseaseand Periconia circinata on sorghums in Australia. AustralianPlant Pathology Society Newsletter 5:59-60.MUCHOW, R.C., and WILSON, G.L. 1976. Photosyntheticand storage limitations to yield in Sorghum bicolor (LMoench). Australian Journal of Agricultural Research27:489-500.ROSENOW, D.T. 1977. Breeding for lodging resistance insorghum. Pages 171-185 in Proceedings of the 32ndAnnual Corn and Sorghum Research Conference.Washington, D.C., USA: American Seed TradeAssociation.TRIMBOLI, D.S. 1981. The fungi associated with stalk androot rot of grain sorghum in New South Wales. M.Sc.Agriculture thesis, University of Sydney, Australia.WRIGHT, G.C. 1981. Adaptation of grain sorghum todrought stress. Ph.D. thesis, University of New England.Armidale, Australia.235

QuestionsMaranville:I am confused about source/sink definition. Whatis source and what is sink? Can you quantify this,and what are the units? I don't think grains afterphysiological maturity can be a sink, so theycouldn't be used as a factor in calculation. Do youagree or disagree? Why?Henzell:Join the club. However, we talk specifically aboutthe source/sink ratio during grain filling. Underthose conditions the sink is almost entirely thedeveloping grain. A limited amount of experimentationsuggests that most, if not all, the dry matterproduced during grain filling ends up in the grain.The source we talk about is the nongrain part of theplant. In sorghum it appears as though the majorcomponent of this source is the leaves and not thestems, roots, glumes, etc., even under moisturestress conditions.Odvody:There seemed to be no pathogens isolated fromdead stalks. Is it possible that root death due topathogens was responsible, in part, for plant death,although there was no progression to stalk tissue?Henzell:Yes, it is possible. In many cases only stems wereexamined.Odvody:Based on your diagram of the physiological stresshypothesis, do you feel that all of the stalk and rootrot occurrence is due to colonization of dead cells(i.e., strictly a saprophytic process)?Henzell:I don't really know. However, at least with Fusariummoniliforme infection the fact that anthocyanin productionoccurs would indicate to me that the cellsare not entirely dead.236

Control of Sorghum Root and Stalk RotsSummary and Synthesis IR.W. Schneider*Biological and Cultural ControlBiological ControlFor the purposes of this review, biological control isdefined as the suppression of disease or inoculumdensity of the pathogen by an introduced biologicalagent. Two strategies for biological control may beemployed: The agent must be effective against thepathogen apart from the host, or the agent mustprotect at the site of infection.Apart from the HostA review of the extensive literature on this aspect ofbiocontrol (Baker and Cook 1982, Cook and Baker1983) indicates that there is no precedent for successin controlling soilborne plant pathogensexcept under highly artificial conditions. However,foliar pathogens are amenable to control by thisstrategy. The primary difference between thesetwo classes of pathogens is that in the soil relativelyhigh populations of the introduced agent must bemaintained tor extended periods of time. Becausethe soil is well buffered with respect to abruptchanges in microbial constituents (Baker and Cook1982), it is unlikely that an introduced agent willbecome established and maintain a population sufficientlylarge to eliminate target pathogens. Furthermore,stalk and root rots of sorghum are causedby several pathogens that are effective saprophyticcompetitors, and they may infect the plant anytimeduring the season (Reed et. al. 1983).At the Site of InfectionIn this case, high populations of the biocontrolagent need not be maintained. Rather, the agentmust be capable of propagating itself as a rootparasite or be an effective rhizosphere competitor.There are numerous success stories with thistype of biocontrol (Cook and Baker 1983). Seedlingdiseases are particularly amenable to control bythis strategy because the seeds or other propagativematerial can be coated with the agent. Theintroduced organism need only colonize theemerging roots for a short period of time. Actinomycetes,Trichoderma, other fungi, and certain bacteriahave been successfully tested against Pythium,Fusarium, Rhizoctonia, and other pathogens (Cookand Baker 1983).In the case of root and stalk rot of sorghum, rootsmay become infected weeks or months after planting.This requires that the introduced agent must beable to grow with the developing root system tor anindefinite period of time. Weller (1983) recentlydemonstrated that an introduced pseudomonad,which was antagonistic to Gaeumannomyces gra~minis on wheat, colonized and displaced the nativemicroflora from field-grown wheat roots for theduration of the season. This represents a signifi-* Assistant Professor, Department of Plant Pathology, University of California, Berkeley, CA 94720, USA.International Crops Research institute for the Semi-Arid Tropics. 1984. Sorghum Root and Stalk Rots, a CriticalReview: Proceedings of the Consultative Group Discussion on Research Needs and Strategies for Control ofSorghum Root and Stalk Rot Diseases, 27 Nov - 2 Dec 1983, Bellagio, Italy. Patancheru, A.P. 502 324, India:ICRISAT.237

cant advance toward the eventual use of biocontrolagents for soilborne plant pathogens.incidence is thought to be related to physical andbiological factors.Disease Suppressive Soilsand Cultural ControlSuppressive SoilsDisease suppressive soils are those that suppressspecific diseases even though the pathogen andsusceptible host may be present (Schneider 1982).The suppressive agent(s) may be biological orphysical/chemical.Perhaps the most studied example of this phenomenonis take-all of wheat (Schippers and Gams1979), In this case disease suppression has beenattributed to, among other things, the competitiveexclusion of virulent strains of the pathogen byavirulent strains, the development of populations ofpseudomonads that suppress the pathogen, andchanges in certain soil chemical characteristicsthat suppress disease development. Any one or allof these and other factors may be responsible forthe decline of take-all. Elucidation of one or moremechanisms could lead to an effective diseasecontrol strategy in which disease suppressioncould be induced at will.Such a phenomenon has not been described forroot and stalk rots of sorghum. Perhaps these diseasesare not amenable to suppression because ofthe diverse pathogens involved. However, pathologistsmust be alert to the possibility and investigatewell-documented cases of disease remission overtime or the lack of disease development in certainareas.Cultural ControlCultural control is defined as a reduction in diseaseincidence or severity by a specific cultural or agronomicpractice, even though a susceptible host isused. Agronomic practices may include alteredirrigation schedules the use of specific plant nutrientsand forms of nitrogen, and crop rotations.Ecofallow, as developed by Doupnik and Boosalis(1980) and Doupnik et al. (1975), is particularlyrelevant to root and stalk rot diseases of sorghum.A combination of reduced tillage and a specificcrop rotation resulted in significantly less stalk rot ingrain sorghum than with conventional agronomicpractices. The cause of this reduction in diseaseBreeding for ResistancePrograms, philosophies, and strategies in breedingfor resistance to root and stalk rots were ablyreviewed by authors in these proceedings. However,the difficulty in working with root and stalk rotsof mature plants should be reemphasized. Not onlyis it impossible to grow a representative matureplant under controlled greenhouse conditions, butthe task is made even more difficult by the fact thatthese diseases occur only in senescing plants.The breeding program of Henzell et al. (theseproceedings) takes account of this fact and incorporatesnovel means of measuring senescencepotential. They also screen their entries underenvironmental conditions that accelerate senescence,namely high temperature and water deficits.Interestingly, they are more concerned withsenescence-induced lodging than with root andstalk rot and consider the disease to be secondaryto the physiological problem.The physiology and biochemistry of senescenceare not completely understood. Thus, factors thataffect this process (Thomas and Stoddart 1980),including growth regulators, source:sink ratios,drought stress, and the environment, cannot bereproducibly imposed. Differences in senescencemay account for the high variability over time andspace in disease severity following inoculation ofsorghum with various root- and stalk-rottingorganisms.Assimilate PartitioningAnother topic that has been discussed in theseproceedings is assimilate partitioning, or harvestindex (HI). It is generally accepted that domesticationand selection of modern varieties of cropplants have not resulted in increased rates of CO2exchange per unit leaf area; rather increased yieldshave come primarily from changes in HI (Hanson1979, Gifford and Evans 1981). This is known to betrue for maize, sorghum, pearl millet, and numerousother crops. Therefore past improvements in yieldhave been derived largely by affecting the proportionof dry weight accumulated in the harvestedorgan. HI is thus genetically controlled. It appearsthat there is an optimum value for HI for any pro-2 3 8

duction environment, and today's elite genotypesare often close to this optimum.In the case of sorghum, roots and stalks mayserve as sources of assimilates during periods ofrapid grain fill or stress-induced decreases in rateof photosynthesis. Thus, the very process that mayaccount for a high HI, namely accelerated senescence,also conditions the plant to susceptibility.Furthermore, stresses of various types, such asnutritional, water, and biotic, are known to acceleratethe senescence process (Beevers 1976,Schneider and Pendery 1983, Thomas and Stoddart1980).As discussed by Rosenow and Henzell et al. inthese proceedings, senescence and susceptibilitymay be inextricably related such that one wouldhave to accept a slightly lower HI in order to maintainjuvenility and resistance in the roots and stalks.Yet, in one recent review article (Evans and Wardlaw1976) it was stated that assimilates remainingin the vegetative organs represent unused yieldpotential and should be diverted genetically to thegrain. However, we know very little about the potentialbiological yield of wild relatives. Of course, thesacrifices one would be willing to make in terms ofHI would depend on the area in which the crop is tobe grown. Factors to be considered include theprobability of a water deficit, anticipated availabilityof nutrients at the proper time, and pressure fromother pests, which may induce senescence.Because of the relationship between HI andsenescence, several breeding programs havebeen developed to assess the quantity of reserveassimilates. A small-grains breeding program isnow being implemented in which plants are chemicallydefoliated at a specific physiological age(Blum et al. 1983). Grain fill is then measured andcompared to nondefoliated controls. A similar programis being used to screen for septoria leafblotch in wheat (Zilberstein et al. 1984). Previousauthors in these proceedings described otherapproaches. Thus, varieties can be selected forareas in which a high level of reserve assimilatescan be made available during periods of acceleratedsenescence.Perhaps a topic that should be explored in muchgreater depth is the potential for increasing biologicalyield. This could be done by measuring the CO 2exchange rate in wild relatives and incorporatingany superiority in this trait into cultivars with anacceptable HI. This probably represents a longtermbreeding commitment, but the results shouldjustify the effort.Another area that may be worthy of investigationconcerns the induction of senescence by exogenouslyapplied growth regulators. This would providea means of testing resistance during advancedstages of senescence without the complications ofa nonreproducible adverse environment Promotersof senescence include abscisic acid and ethylene(Beevers 1976). Ethephon, a commerciallyavailable precursor of ethylene, can be sprayed onplants. This product is used to promote uniformripening of fruits.Chemical ControlWilliams and Nickel (these proceedings) thoroughlyreviewed the strategies and potential usesof traditional fungicides. However, in light of whatwe know about the relationships between senescenceand susceptibility, and between droughtstress and predisposition, it is worthwhile to examineother possibilities related to the use of chemicalsthat affect the host rather than the pathogen.This is particularly important with stalk rotsbecause the pathogen is active in dead tissues(Pappelis, these proceedings), sites which may beinaccessible to fungicides.One of the natural causes of physiological agingand senescence is a decreased supply of cytokins from the root to the shoot (Thomas and Stoddart1980). Kinetin, one of the cytokinins, is the mosteffective senescence-retarding growth regulatorsknown (Beevers 1976). Is it possible to apply sucha compound to retard the onset of senescence andsusceptibility? What would be the cost in terms ofHI? There are many questions to be answered, butcertainly this topic is deserving of a major researcheffort.Furthermore, one of the metabolic breakdownproducts of benzimidazole fungicides is a kinetinlikecompound that retards senescence (Wang etal. 1960). Thus, it may be possible to synthesize acompound that is both fungicidal and effective as agrowth regulator.Finally, work done with Cyclocel or CCC (2-chloroethyl trimethyl-ammonium chloride) shouldbe mentioned. This material is used in the ornamentalsindustry to induce short, thick stems inshrubs. When applied to leaves of cereals, itcauses the stalks to become shorter and thickerand thereby more resistant to breaking and lodging(Nilsson 1969). There are no reports of this materialbeing used to control lodging associated with stalkrot of sorghum.239

ReferencesBiochemical Research Communications 2:92-101.BAKER, K.F., and COOK, R.J. 1982. Biological control ofplant pathogens. San Francisco, California, USA: W.H.Freeman. 433 pp.BEEVERS, L. 1976. Senescence. Pages 771 -794 in Plantbiochemistry (eds. J. Bonner and J.E Varner). New York,New York, USA: Academic Press. 925 pp.BLUM, A., MAYER, J., and GOZLAN, G. 1983. Chemicaldesiccation of wheat plants as a simulator of postanthesisstress: II. Relations to drought stress. Field CropsResearch 6:147-155.COOK, R.J., and BAKER, K.F. 1983. The nature and practiceof biological control. St. Paul, Minnesota, USA: AmericanPhytopathological Society. 550 pp.DOUPNIK, B., and BOOSALIS, M.G. 1980. Ecofallow—areduced tillage system—and plant diseases. Plant Disease64:31-35.DOUPNIK, G., BOOSALIS, M.G., WICKS, G.A., andSMIKA, D. 1975. Ecofallow reduces stalk rot in grainsorghum. Phytopathology 65:1021 -1022.EVANS, L.T., and WARDLAW, I.F. 1976. Aspects of thecomparative physiology of grain yield in cereals. Advancesin Agronomy 28:301 -359.GIFFORD, R.M., and EVANS, C.T. 1981. Photosynthesis,carbon partitioning and yield. Annual Review of PlantPhysiology 32:485-509.HANSON, A. 1979. Plant breeding and partitioning incereals and grain legumes. Pages 18-23 in Partitioning ofassimilates. Rockville, Maryland, USA: American Societyof Plant Physiology. 23 pp.NILSSON, H.E. 1969. Studies of root and foot rot diseasesof cereals and grasses. Annals of the Agricultural Collegeof Sweden 35:275-807.REED, J.E., PARTRIDGE, J.E., and NORDQUIST, P.T.1983. Fungal colonization of stalks and roots of grainsorghum during the growing season. Plant Disease67:417-420.SCHIPPERS, B., and GAMS, W. (eds.). 1979. Soil-borneplant pathogens. San Francisco, California, USA: AcademicPress. 686 pp.SCHNEIDER, R.W. (ed.). 1982. Suppressive soils andplant disease. St. Paul, Minnesota, USA: American PhytopathologicalSociety. 88 pp.SCHNEIDER, R.W., and PENDERY, W.E. 1983. Stalk rot ofcorn: Mechanism of predisposition by an early-seasonwater stress. Phytopathology 73:863-871.THOMAS, H., and STODDART, J.L. 1980. Leaf senescence.Annual Review of Plant Physiology 31:83-111.WANG, D., HAO, M.S., and WAYGOOD, E.R. 1960. Theeffect of benzimidazole on the biosynthesis of chlorophyll.WELLER, D.M. 1983. Colonization of wheat roots by afluorescent pseudomonad suppressive to take-all. Phytopathology73:1548-1553.ZILBERSTEIN, M., BLUM, A., and EYAL, Z. [1984.] Chemicaldesiccation of wheat plants as a simulator of postanthesis Septoria leaf blotch stress. Phytopathology74:(in press).240

Control of Sorghum Root and Stalk RotsSummary and Synthesis IIJ.F. Scheuring*This commentary is based on the three breeders'papers presented by Drs Rosenow, Maunder, andHenzell.The summary comments and generalizations wehave read in these three papers represent extensivefield experience spanning the past twodecades in Australia, North America, and SouthAmerica. In spite of the sharply contrasting environmentsin which these scientists have worked,there is a remarkable similarity in their breedingstrategies, field screening, and selection criteria.Major PointsAll three breeders have had to wrestle with thefollowing problems:1. identification of what resistance is desired—charcoal rot, fusarium root rot, lodging,drought, or all at once;2. lack of reliable field screening techniques foridentifying sources and derivatives of heritableresistance;3. identification of plant characters that eitherimpart or indicate resistance.The three authors are interested in breeding outyield limiters (stalk rots, lodging, or drought susceptibility)at the postfloral stage. Henzell reiteratedseveral times that lodging ("stem collapse") is theultimate effect of stalk rots and drought in Australia.Therefore he breeds directly for lodging resistanceand thus indirectly for stalk rot resistance.Rosenow (personal communication, 1983) hascome to the same conclusion. He no longer cutsstems to verify the presence of charcoal rot sclerotia.He takes lodging scores. Although Maunderplaces due importance on standability, he identifiesseparate sources of charcoal rot, fusarium root rot,and drought resistance. He takes charcoal rotmeasurements even on standing plants.These authors agreed that reliable field screeningis difficult. Consequently, all three breedersmake multilocational plantings with large numbersof entries under a range of growing conditions.They are all interested in locations with disease ordrought occurrence. In at least some of their nurseriesthey try to create a boom and bust situationwith high plant populations, high fertility, and optimumirrigation, followed by postfloral heat andmoisture stress. In Australia, an off-season location(at the Kimberley Research Station) has beenfound that, under irrigation manipulation, can accuratelypredict the lodging performance of mainseasonlocation nurseries. Excellent fusarium rootrot "hot spots" have been identified in Argentina.Rosenow has made considerable progress bymaking lodging scores in nurseries left standingover winter.Plant maturity differences can confound lodgingand stalk rot response. If stress occurs too soonbefore or after flowering then stalk rots or stemcollapse may not occur even in susceptible sorghums.To overcome the problem of plant maturity,these authors try to group their materials accordingto maturity and base their decisions on largenumbers of multilocational observations.Maunder and Rosenow make use of the tooth-*Cereal Breeder, ICRISAT/Mali Program, c / o Ambassade Arnericaine, B.P. 34, Bamako, Mali, West Africa (Via Paris).International Crops Research Institute for the Semi-Arid Tropics. 1984. Sorghum Root and Stalk Rots, a CriticalReview: Proceedings of the Consultative G r o u p Discussion on Research Needs and Strategies f o r Control ofS o r g h u m Root a n d Stalk Rot Diseases, 27 Nov - 2 Dec 1983, Bellagio, Italy. Patancheru, A.P. 502 324, India:ICRISAT.241

pick method of charcoal rot inoculation in at leastsome replications of some nurseries. However,Henzell has found little success with that practicein Australia.Nonsenescence was identified by all threeauthors to be the single most important plant characterindicative of stalk rot, lodging, and postfloraldrought resistance. Maunder and Rosenow relatenonsenescence closely with drought resistance.Henzell and Rosenow point out the significantassociation between nonsenescence and diseaseresistance. In the case of SC-599-6 nonsenescenceis also linked with fusarium root rot resistance.Nonsenescence is used as a selectioncriterion per se by all three breeders.The stiff stalk character is emphasized byMaunder and Henzell for both charcoal rot andlodging resistance. The lodging-resistant lines SC-56-6 and NSA 663 have been described byRosenow as having an elastic stalk.Short stature was related to lodging and stalk rotresistance. Maunder proposes that the shortenedintemodes slow down stalk rot development in thestem.Late maturity was also related to stalk rot andlodging resistance by Henzell and Rosenow. Henzellinsists that the reason for late maturity resistanceis due to a happy source-sink balance.Henzell and his colleagues place considerableimportance on the role of the source-sink equilibriumduring grain fill. They propose that stem collapseduring grain fill is due primarily to sourcelimitations and that the problem of stalk rots andlodging can be best understood through sourcesinkdynamics.Additional InformationSome recent observations of Malian local sorghumsmay shed additional light on the foregoingsummary:During the past 5 years we have made extensivemultilocational observations of local varieties,introduced varieties and hybrids, and local x introducedhybrids. White-seeded exotic hybrids (U.S.and Indian) are generally susceptible to charcoalrot. Durra x exotic hybrids are highly susceptibleand Guineense x exotic hybrids are highlyresistant.We have never seen a local Guineense or Guineensex exotic hybrid succumb to charcoal rot.The Guineenses are 3-5 m tall, relatively nonsenescent,and have elastic, dry stems. Under themicroscope the cortex cells appear completelyempty, In contrast, juicy- and intermediate-juicystemsorghums have cortex cells filled with sap.It isclear that the Guineense stalk rot and lodgingresistance is related neither to short stature nor tostiff stalk. Since their grain straw ratio is only about20%, their resistance may be related to the favorablesource-sink balance. However, their resistancemay also be related to empty cortex cells. Without areadily available substrate, how can a stalk rotpathogen grow in the pith?In juicy-stem sorghums, sudden changes ofosmotic pressures in the sap during grain fill maycause cortex cell hemorrhage and stem collapse.That eventuality may be prevented by the absenceof sap in the cortex cells.Gaps in Knowledgeand Research1. Very little anatomical work has been done toclearly describe the stems and leaves of resistantvs susceptible varieties or senescentvs nonsenescent varieties. Schertz andRosenow's article (1977) was a beginning, butonly a beginning. These studies should bedone with known separate sources of resistanceto charcoal rot, fusarium root rot, andlodging. Parallel studies could trace the growthof stalk rot pathogens in stem tissues to accuratelyidentify which tissues are affected.2. The physiologists need to distinguish betweencortex, vascular tissue, and sclerenchymatissue in describing stem carbohydratedynamics, so that pathogenic, physiological,and botanical descriptions of the stem can becoherently understood.3. Nonsenescence needs to be more clearlydefined and assessed. Many local Malian durrascan show severe leaf firing and be ratedhighly senescent, yet they make immediateregrowth after late rains. On the other hand,CSH-5 (and 2077A hybrids in general) is nonsenescentwhen it does not succumb to charcoalrot.4. A systematic screening of representativegroups of the sorghum world collection isneeded to identify separate and multiple sourcesof resistance to charcoal rot, fusarium rootrot, lodging, and postfloral drought.242

Possible Issues for Discussion1. Should we breed for stalk rot resistance, lodgingresistance, drought resistance, and yield instepwise fashion or all at once?2. If a source-sink equilibrium is essential forstalk rot and lodging resistance in stressedenvironments, are there yield limits for givenplant statures and maturities?3. Are all nonsenescent sorghums stalk rot, lodging,and drought resistant? If not, how does thenonsenescence of susceptible sorghumsdiffer from the nonsenescence of resistantsorghums?ReferencesSCHERTZ, K.F., and ROSENOW, D.T. 1977. Anatomicalvariation in stalk intemodes of sorghum. Crop Science 17:628-631.DiscussionFungicidesPartridge:There seems to be an interest in growth regulators,and when these are discussed in reference tochemical control, kinetin and IAA are often mentionedbecause these compounds are extremelylethal to cell protoplasts and callus tissues insorghum.Odvody:Dr. Williams, since most of the systemic fungicidesare acropetally transmitted, do you see any continuingproblem in controlling diseases that occur inroots and stalks, and do you think that soil treatmentsfor long-term control and seed treatmentsfor short-term control will basically overcome that?Williams:You're probably right. This is a major difficulty.Granular fungicides with a slow release componentcan perhaps do a very good job in that regard.Partridge:What is the potential for using chemicals to studyfacets of stalk rot?Williams:There is plenty that we don't know, but we havefungicides that are specific to Pythium. So we couldpossibly use these chemicals to take apart theetiology and the interrelationships between theimplicated fungi We could also use fungicides totry to focus on just when the critical infectionoccurs, like treating different plants at differenttimes during their growth stage. There are severalways we could use these effective fungicides asresearch tools to fill gaps that still exist.Frederiksen:When we first had to diagnose Pythium from deadplants and dead roots without knowing whatcaused the disease, we used 10 kg/ha of a varietyof selected fungicides. We found Pythium in thePCNB plots. We eliminated a series of other soilmicroflora and were able to select out the keypathogen. This approach might be useful in successionresearch and could give a better understandingof the role of specific organisms in theseproblems.Biological and Cultural ControlSeetharama:Dr. Doupnik, one of the things you suggested wasto keep soil moisture at 80% of field capacity atflowering to control stalk rot. How widely can this beapplied?Doupnik:Moisture conservation will reduce stalk rot incidenceregardless of the location.Rosenow:You referenced the fact that plant population andnot row spacing was important under your conditions.We have some data from Texas that are243

somewhat to the contrary. We looked at narrowrows versus wide rows. At yield levels below 3000kg/ha, we got poorer yield performance whenplants were spaced equidistant than when theywere planted in 1-meter rows. At low yield levels,plant spacing became important—not just plantpopulation. At low yield levels they performed betterin 1-meter rows than in solid equidistant plantspacings. At high yield levels under good moistureconditions, there was some advantage to equidistantspacing. With low yield levels under moisturestress, we were not taking moisture out of the lowersoil depths. We had apparently enough competitionof rooting in the upper surface that we were notusing all the lower-profile moisture. The plants justcollapsed and lodged when stress occurred.Recent data from Chillicothe, Texas, show a consistentadvantage in the skip-row technique—1-meter rows with two rows planted and one rowskipped—over solid plantings of 1 -meter rows withthe same number of plants per hectare.Clark:To overcome high nitrogen, do you have anyrecommendations as to the form of N applied orwhen it is applied that might overcome diseaseincidence?Doupnik:No, we don't have any data. Purdue has some dataon maize.McBee:From the standpoint of rotations and cultural control,to what extent has allelotrophy been consideredalong with the effects of pathogens? It hasbeen shown to be a factor in rotations involvingmonocots and dicots. In sorghum and specificlegume rotations, yields have been reduced significantly.Other legumes have no effect and there is abenefit from the residual nitrogen.Doupnik:This is a problem in continuous cropping, especiallywith the same genotype. Herbicide carryoverand root exudates may be involved andconfound the problem.Schneider:When there is residue on the soil surface and thesorghum comes up through this material, is thesorghum stunted for the first 4 weeks?Doupnik:There appears to be a slower growth rate and asmaller root system due to cooler soiltemperatures.Schneider:J.M. Lynch in England [at Agricultural ResearchCouncil, Letcombe Laboratory, Oxford] worked onbarley in crop residue, and he attributed the stuntedplants to the anaerobic or cold-soil degradation ofthe residue, which results in the accumulation ofanaerobic metabolic by-products, such as propionicand lactic acids. The plants are stunted onlyuntil these organic acids are metabolized and thesoil warms up again.Doupnik:By the time the canopy develops, the plants simplydo not look that different.Eastin:It's soil temperature as it relates to growth. We didsome research on screening for plants that growunder cool temperatures. At 15°C the seed willgerminate, but the plants don't grow very well andthere's a big difference among genotypes. Respirationincreases about 15% per degree from 15 to30°C.Mukuru:Dr. Doupnik, you obtained good disease control,and lodging was reduced. Was this due to moistureconservation or because the organisms werereduced?Doupnik:We think it was due to soil moisture and soil temperature.Under the high residue, we were storing 7.6cm more of soil moisture. During the growing season,it takes 22.9 cm of soil moisture to produce thefirst 62.8 kg/ha of sorghum grain. Every 2.5 cmabove that, you can add about 628 kg/ha yield. Soin the average years with 35.6-38.1 cm of rain,there's a potential of 3140-3768 kg of grain/ha. Ifyou can conserve an extra 7.6 cm, you can gain anextra 1884 kg /ha. The heat reflection of sunlight offthe residue may affect the physiological activity ofthe plant.Pappelis:In the no-till systems, the nodes stay alive at thebase of the plants. This may be restricting pathogenpenetration of the stalk.244

Jordan:Differences between the ecofallow and conventionalsystems in between-row soil-temperaturecan be 6-17°C based on your research. What aboutthe effect of temperature directly in terms of heatstress on the root systems, particularly near the soilsurface?Doupnik:Both temperature and moisture are important, andinteractions may be involved.Pappelis:One study involving sandy soils and heat buildupon seedlings in a greenhouse showed a buildup ofblight.Schoeneweiss:Reflected heat from media surfaces on succulentseedling parts is a problem. I don't know the mechanisminvolved, but with heat comes a disturbancein water relations—desiccation injury. This mightoccur on sorghum seedlings.Pappelis:Has anyone put a temperature probe on sorghumstalks or roots at the soil line to see how hot it is?Seetharama:I found no differences between stalk and soiltemperatures, and the leaf sheath may have been afactor.Schneider:In a study involving fusarium hypocotyl rot in pineseedlings, soil surface temperature and temperatureat the hypocotyl rose to 45°C, predisposing theplant to disease. Control methods included sprinkling,shading, and whitewashing. After 1 hour atcooler temperatures, the tissue was notsusceptible.McBee:Temperatures in sorghum leaves do fluctuate duringflowering and pollination. The temperature mayrise during pollination.Eastin:Temperature effects must be evaluated on totalgrowth. This may result in infection differences asthe plant growth is suppressed under cool temperatures.What temperature has an effect on fungalgrowth or infection?Schoeneweiss:Considerable work on other host-pathogen systemshas been reported. Heat shock treatmentshave been shown to alter the host's resistance. Insoybean, leaves placed in a water bath at 50°C for10 minutes were shown to predispose the host toPhytophthoca megasperma. The heat shock suppressedphytoalexin production, and after removalof the leaves from the heat treatment, phytoalexinproduction was resumed.Eastin:Cool soils and high moisture conditions will result ina reduction of plant growth, as it's more difficult forpathogens to invade roots in cool and wet soils.Schoeneweiss:The range of temperatures for growth is highlyvariable among pathogenic organisms. Fusarium isactive at high temperature and Verticillium is moreactive at low temperature. Most will grow at a reasonablerate at moderate temperatures (18-20°C).At 15°C or below, they will grow more slowly.Odvody:The optimum temperature for Macrophomina is35°C. This is not necessarily the best temperatureunder soil conditions, as it can't grow at lowertemperatures due to soil microflora, host susceptibility,etc.Maranville:Mulching conserves heat during the warmer portionsof the season, and mulched soils are warmerthroughout the fall. This may create ideal conditionsfor disease development.Breeding for ResistancePappelis:Are breeding plots being grown under no-till ormulched conditions?Eastin:A limited amount is being grown under theseconditions.Rosenow:We started using no-till plots in our dryland breedingprogram last year.Doupnik:Paul Nordquist routinely conducts screening pro-245

grams under no-till conditions at the North Platte,Station near North Platte Nebraska. Variety testingis also conducted by Russell Moomaw under no-tillat the Northeast Station near Concord, Nebraska.Pappelis:More corn [maize] borer tunnels were noted inmaize plants grown under mulched conditions. Nodifferences were noted in pith; however the rindcharacteristics of these plants were changed.Rosenow:In Texas, Southwestern corn [maize] borer populationsare reduced by tillage that exposes the overwinteringlarvae to moisture and temperaturefluctuations.Partridge:Dr. Maunder, are DeKalb-Pfizer's breeding programsdesigned for maximum yields or consistentyields?Maunder:Maximum yield is difficult to define. We strive for acontinuity of maximum yield over several years.The hybrid C-46 was not a maximum-yield type buthad a consistent yield over 5 to 10 years.Partridge:Are there different materials for different areas?Maunder:There are different breeding approaches for eachtarget area. Each genotype will be tested in eachenvironment. What works for one thing may notwork for another.Vidyabhushanam;Are hybrids more susceptible than their inbredparents?Maunder:Hybrids may be more susceptible. In screeningtests conducted during 1960-64, one parent wassusceptible, and the resulting hybrid was more susceptiblethan the worst parent due to dominance forsusceptibility. In DK-46, one parent is a charcoalrot-resistantline, and the other parent is a nonsenescingline with a stiff stalk that is not susceptible.If one parent is really bad, the hybrid may be evenworse. If one parent is good and the other carriescharcoal rot resistance, you can have a goodhybrid. It's not a really clear-cut inheritance wheresusceptibility is always dominant. It's'also verypolygenic.Vidyabhushanam:If you want a resistant hybrid, I believe you shouldhave resistance in both parents.Maunder:That would be optimum. But when you start requiringthis, you have problems in bringing along theother favorable traits, and this is why we have goneto the intermediate x resistant approach. You'remore likely to get more things you want in the endresult. Anytime you have a new requirement, youdouble the effort to get what you want.Rosenow:We use a very stay-green, charcoal-rot-resistantparent on one side, and the other parent is a veryhigh-yield-potential line with wide adaptation. TheF 1 combines many of the good traits of both: Thisinvolves the dominant type of stay-green trait.Vidyabhushanam:These stay-green types are low yielders and sinklimiting.Henzell:They are not necessarily low-yielding. But theyhave a source-grain sink relationship such that theplant is nonsenescing. You can indeed have ahigh-yielding nonsenescing plant, but it likely wouldnot be source limited.Vidyabhushanam:If the source is not limiting, can high yield beobtained?Henzell:High yields can be obtained, but the option ofincreasing grain yield via increasing harvest indexwould probably result in a plant that is relativelysource limited and therefore senescent.Mukuru:I have looked at a number of Guineense and noneof them have succumbed to charcoal rot. Incrosses, the derivatives are not as resistant as theoriginal parents. Of those lines converted in theU.S., are any resistant to charcoal rot?Rosenow:We have not looked at the charcoal rot resistance246

of the converted Guineense. They don't have goodlodging resistance. We don't really know whetherthey have the stay-green characteristic. It could bemasked in them.Scheuring:I know it's expedient in breeding programs to go forlodging resistance and hope you can bring alongeverything else. In the long run we might makemore progress by identifying different sources ofcharcoal rot resistance, recombining among these,and selecting against lodging at the end of theprocess.Rosenow:An effort was made this past year to select outearly-maturing genotypes from converted materialsthat appeared to have drought tolerance.Maunder:The greatest asset to a breeding program is theutilization of the world sorghum germplasm collection,but to use it in the converted form can be a realdisadvantage because you get one trait that iswanted and a lot that are not wanted.Drought ResistanceJordan:What characteristics are best for different environmentsto promote drought resistance in associationwith stalk rot resistance?Rosenow:In the context of overall drought resistance—whenI use the term drought resistance related to stalk rotresistance, I'm only talking about drought resistanceat the Iate stage of grain fill—I don't know if theplant is avoiding drought due to efficient utilizationof moisture. Soil water extraction work doesn'tshow big differences in amount of water extracted.Slight differences occur where nonsenescingtypes extract less water during early growth andgreater proportions during later growth. The rootsremaining active may be a key. There are no differencesin genotypes in total amount of waterextracted. There is no explanation of why one plantlives and the adjacent one dies.Henzell:The whole gamut of mechanisms involved withdrought resistance are probably important in promotingresistance to stalk rot. Roots are a factor indrought avoidance. In drought tolerance, you wanta plant that continues to operate at low leaf waterpotentials, and osmoregulation is important. E-57 isnonsenescent, lodging-resistant, and an osmoregulator,with resultant continuing photosynthesisand an actively growing root system. With an osmoregulationsystem, desiccation tolerance becomesimportant in the drought resistance mechanism. Inlimited surveys in Australia, lodged plants havebeen found to have pathogens present eventhough there were no symptoms. Other plantslacked the pathogens and had no symptoms, butthey were lodged.Maunder:It's a very complex, quantitative problem. We haveconcentrated on roots too heavily. Our best rootsystem is in a hybrid that requires irrigation. RS-610and DK-46 have poor root systems but gooddrought tolerance: not using water excessivelyearly in the season is a good trait. Tillering shouldbe avoided. Osmoregulation may need moreattention.Jordan:Do we have unique genetic variability forosmoregulation?Henzell:It is likely that every plant osmoregulates, but someare more efficient than others.Mukuru:We screened under moisture stress and selectedthe unscorched genotypes that recovered. Wehave selected against avoidance.Seetharama:Morphological and ecological considerations aremore important in our drought resistance and stalkrot resistance programs, while physiological andbiochemical factors are less important.Stress StudiesPartridge:Maize stalks lodged under greenhouse conditionswithout any internal parasites detected in the collapsedportion. It's also possible that sorghum willlodge under similar conditions if stressed severelyand without pathogens being detected.247

Pappelis:Hydroponic units (gravel) can be used to measurestress factors under greenhouse conditions.Temperature, moisture gradients, herbicides, fertilizers,can all be measured.Jordan:Osmotic solutions to induce stress have been utilizedin a useful manner. Carbowax used to inducestress is not a good choice, as water is still available.In a decreasing soil moisture situation, both therate of transport of water and energy problems areimportant.McBee:Changes in alternating light from high to low withhigh and low temperature frequently producedesiccation and may result in collapse of plants.Plants differ slightly at different growth stages andthe effects of nonsenescence and stalk rot need tobe studied at each growth stage.Charcoal RotRosenow:It appears that the local types grown in variouscountries possess charcoal rot tolerance. Theintroduced types from the U.S., ICRISAT, and otherprograms seemingly have an increased incidenceof charcoal rot. Is this attributable to the highyielding,photoperiod-insensitive, grain/strawratios possessed by the introduced accessions, ordo the local types possess resistance due to adifferent plant configuration and other factors?Mukuru:When the converted line was compared to the originalin charcoal rot tests, the original line wasresistant. When the photoperiod-insensitive linewas crossed, the progeny were not resistant.Rosenow:Would you agree that some local types may beresistant, while others may escape due to othermechanisms?Scheuring:The resistance of the Guineense parents is presentand can be transferred. However, lateness mightbe one factor masking escapes. We often get a2-week drought toward the end of the rainy season.That drought often occurs at or after flowering ofthe early lines but before the flowering of the lates.The earlier lines often collapse because they are ata vulnerable stage of development. The slowergrowing late sorghums seem to be less sensitive todrought even during the vulnerable grain fill stage.Mughogho:Local landraces need to be examined under controlledconditions to determine if they have charcoalrot resistance. There were reports of stalk rotproblems on local landraces in West Africa.Mukuru:This appears to be something different, as there arevarious sorghum types in the areas that are susceptible.We haven't seen any local landraces ofsorghum with charcoal rot.Scheuring:We must emphasize that local landraces are thetopic and not other types.Mughogho:Some of these local landraces of the Guineensesorghums possess resistance to grain molds and, ifthey are resistant to charcoal rot, they would bemost useful in breeding programs.Rosenow:Were the changes due to insensitivity per se or acomplete change of the plant?Scheuring:We have a number of F 5 s and F 6 s from crossesbetween tall, late, local, and short, early exoticmaterials that are holding up well to charcoal rotpressure. The progeny are short and phenotypicallyquite different from the local parents.248

Group Discussionsand Recommendations

Group AGroup BGroup C

Report of Group Discussions and Recommendationson Charcoal Rot, Fusarium Root and Stalk Rot,and Anthracnose Stalk RotFollowing the presentation and discussion of thefour sets of background papers, participants wereassigned to one of three groups A, B, and C. Eachgroup consisted of nine persons. The nominalgroup technique, which provides a structuredapproach for considering specific problems andenhances productivity of conferences (Dalbecq etal. 1975), was used to arrive at recommendationson priority research areas on the three major rootand stalk diseases: charcoal rot, fusarium root andstalk rot, and anthracnose stalk rot.For each disease, the procedure followedinvolved five steps:1 presentation of the problem in the form of aquestion; the questions presented to the threegroups were:a. What information must be acquired beforecontrol of is possible?b. In the absence of constraints, what shouldbe done to control ?c. What are the major opportunities for interdisciplinaryand collaborative researchon ?2. recording of ideas generated by each memberof the group (see Appendix at the end of thischapter);3. discussion of each idea for clarification;4. ranking (by vote) of the most important ideasas recommendations of each group;5. presentation of each group's findings to ameeting of all participants, and steps 3 and 4repeated in order to arrive at specific finalrecommendations for future research.In accordance with the above procedure, thispresents the priority research problems identifiedby groups and final recommendations of the wholeworkshop on the three diseases.Charcoal RotPriority Research ProblemsIdentified by GroupsGroup A: What information must be acquiredbefore control of charcoal rot is possible?1. Understand host-parasite-environment interactions.2. Establish optimum parameters for uniformscreening techniques.3. Identify immune genera and new resistancesources for incorporation into varieties byclassical or biotechnical methods,4. Quantify stress and the plant's reaction as itaffects pathogenesis.5. Investigate the inheritance of resistance.6. Identify plant traits responsible for resistance.7. Determine chemical-physiological propertiesof plants that enhance disease.Group B: In the absence of constraints whatshould be done to control charcoal rot?1. Collect, select, and screen germplasrn withemphasis on accessions from regions withhigh natural selective pressure.2. Determine causes of genotype variation in251

host plant resistance and lodging resistancewith particular emphasis on physiological(e.g., source/sink relationships, osmoregulation,photosynthetic efficiency, living cell resistance)and anatomical aspects.3. Develop more effective and relevant screeningtechniques.4. Characterize the predisposing stress environmentutilizing controlled stress techniques,e.g., hydroponics, gravel culture.5. Study the biology of the pathogen, includingthe role of root exudates and its interactionwith other organisms.6. Study the genetic differences among charcoalrot resistance sources (inheritance) and theirstability across environments (heritability).7. Establish special interdisciplinary varietaldevelopment nurseries using presenttechniques,8. Evaluate and utilize chemical and culturalpractices to develop crop management systemsfor control.9. Determine disease severity/crop loss relationships.10. Examine the potential for biological control(e.g., suppressive soils).Group C: What are the major opportunities forinterdisciplinary and collaborative research oncharcoal rot?1. Develop reliable, sound inoculation techniquesfor field evaluation of resistance.2. Predict disease incidence and loss.3. Investigate the relationship between Macrophominaand other organisms at soil-plantinterface.4. Identify mechanisms of physical and physiologicalresistance.5. Determine the effect of genotype and environmentinteraction on disease, particularlytemperature and water.6. Study the genetics and stability of the nonsenescencetrait.7. Investigate the epidemiology and etiology ofdisease.Final Recommendationsfor Priority Research Areas1. Investigate host-parasite-environment interactions,with emphasis on temperature, moisture,and nutrient stress, and predisposingfactors in disease development.2. Develop more effective and relevant screeningtechniques for resistance.3. Determine physical and physiological plantcharacteristics associated with resistance tothe pathogen and to lodging.4. Determine the relevance of the nonsenescentcharacter to charcoal rot resistance and thestability of this trait across environments.5. Collect, select, and screen germplasm for resistance,with emphasis on accessions fromregions with high natural selection pressure.6. Establish interdisciplinary nurseries for varietydevelopment.7. Determine the inheritance and heritability ofresistance.8. Develop models to predict onset and developmentof the disease and resulting yield loss.9. Identify and utilize exotic sources of resistanceby classical or innovative methods (biotechnological/geneticengineering).10. Evaluate and utilize chemicals (e.g., fungicides,plant growth regulators) and culturalpractices to develop crop management systemsfor control.11. Elucidate the biology and variability of thepathogen in its interaction with the host.12. Elucidate the epidemiology of the disease.Fusarium Root and Stalk RotPriority Research ProblemsIdentified by GroupsGroup A: What information must be acquiredbefore control of fusarium root and stalk rot ispossible?1. Determine the inheritance and heritability ofresistance.2. Identify immune genera and new sources of252

esistance for incorporation of genetic materialby classical or biotechnical methods.3. Understand host-parasite-environment interactionsfor various geographical locations.4. Identify plant traits conferring resistance.Group B: In the absence of constraints, whatshould be done to control fusarium root and stalkrot?1. Improve screening techniques for resistance,including the examination of development ofthe initial screening program using controlledwater and heat stress.2. Determine regionally the importance of fusariumdisease(s) and the relative importance ofthe different Fusarium spp.3. Determine causes of genotype variation inhost plant resistance to lodging, with particularemphasis on physiological (e.g., source/sinkrelationship, assimilate partitioning, photosyntheticefficiency, etc.) and anatomical aspects.4. Identify sorghum lines with relative resistanceand susceptibility through a selected screeningof the world collection.5. Study host-parasite interactions, includingpredisposition and mechanisms of resistance.6. Develop integrated management systems tocontrol the problem.7. Examine the potential for control with fungicides,plant growth regulators, and relatedchemicals.8. Relate cell death patterns to susceptibility andresistance in roots and stalks, especially insenescing and nonsenescing (stay-green)genotypes.9. Determine inheritance of different sources ofresistance.10. Determine root and stalk rot incidence andyield losses in no-till, conservative-till, andconventional tillage (include inoculation andpith condition rating when possible).Group C: What are the major opportunities forinterdisciplinary and collaborative research onfusarium root and stalk rot?1. Investigate the epidemiology and etiology ofthe fusarium disease complex.2. Determine environmental factors responsiblefor predisposition.3. Determine the relationship of nonsenescenceto resistance.4. Investigate the effect of crop managementfactors in disease incidence.5. Develop and standardize screeningtechniques.6. Analyze interactions among Fusarium sppcomplex, host, and environment in disease.7. Study the relationship between Fusarium sppand other root/stalk rot pathogens.Final Recommendationsfor Priority Research Areas1. Investigate host-parasite-environment interactions,with emphasis on temperature, moisture,and nutrient stress as predisposingfactors in disease development.2. Develop more effective and relevant screeningtechniques for resistance.3. Identify physical and physiological plant characteristicsassociated with resistance to thepathogen(s) and to lodging.4. Determine the regional importance of fusariumstalk rot and the relative importance of thedifferent Fusarium spp in each region.5. Determine the relationships between Fusariumspp and other root/stalk rot pathogens.6. Determine the inheritance and heritability ofresistance.7. Evaluate and utilize chemicals (e.g., fungicides,plant growth regulators) and culturalpractices to develop crop management systemsfor control.8. Identify sorghum groups with relative resistanceand susceptibility through selectivescreening of the world sorghum germplasmcollection.9. Identify and utilize exotic sources of resistanceby classical or innovative methods (biotechnological/geneticengineering).10. Relate cell death pattern to susceptibility andresistance in roots and stalks, especially in253

254senescing, and nonsenescing (stay-green)genotypes.11. Elucidate the etiology and epidemiology of thedisease.AnthracnosePriority Research ProblemsIdentified by GroupsGroup A: What information must be acquiredbefore control of anthracnose is possible?1. Understand host-pathogen-environmentinteractions.2. Determine the inheritance and heritability ofanthracnose stalk rot resistance.3. Incorporate improved sources of resistanceusing classical and biotechnical methods.4. Determine the relative importance of grain andleaf anthracnose to stalk rot.5. Determine the relative advantages of culturalcontrol, chemical control, and biocontrol ofanthracnose.Group B: In the absence of constraints, whatshould be done to control anthracnose?1. Evaluate known sources of resistance worldwideand screen untested world collectionitems at known ''hot spots''.2. Determine mechanisms of resistance in arange of genotypes.3. Determine race/genotype interactions inmajor sorghum-producing regions, using a setof common genotypes and regionally importantadditions.4. Determine regionally the relative importanceand virulence of the disease, including differentphases of the disease.5. Accelerate and coordinate breeding programsfor resistance at strategic locations.6. Evaluate and utilize chemical and culturalpractices to develop crop management systemsfor control.Group C: What are the major opportunities forinterdisciplinary and collaborative research onanthracnose?1. Identify sources of resistance.2. Analyse the relationship of stalk rot to otherdisease phases.3. Evaluate collected isolates at containmentfacilities.4. Compare the economic losses caused byanthracnose with the losses caused by otherstalk rot pathogens.5. Determine the role of seedborne inoculum indisease development and dissemination.6. Identify the races of Colletotrichum.Final Recommendationsfor Priority Research Areas1. Investigate host-parasite-environment interactions.2. Evaluate known sources of resistance worldwideand screen untested world collectionitems at known "hot spots."3. Monitor pathogen variability using standarddifferential varieties and regionally importantcultivars.4. Determine the relationship of grain and foliaranthracnose to stalk rot.5. Determine mechanisms of resistance.6. Evaluate and utilize chemicals (e.g., fungicides,plant growth regulators), cultural practicesand biological control to develop cropmanagement systems for control.7. Develop more effective and relevant screeningtechniques for resistance.8. Determine the role of seedborne inoculum ondisease development and dissemination.9. Identify and utilize improved and exotic sourcesof resistance by classical or innovativemethods (biotechnological/genetic engineering).10. Determine the inheritance and heritability ofresistance.1.1. Compare the economic losses caused byanthracnose with losses caused by other stalkrot pathogens.12. Elucidate the etiology and epidemiology of thedisease.

13. Evaluate collected isolates at containmentfacilities to determine the variability of thepathogen.3. Determine the role of other soil microorganismsassociated with charcoal rot.Appendix: ProblemsRecorded by Groups (Step 2)Charcoal RotYield/Crop Loss1. Apportion loss of yield caused by drought anddisease.2. Determine disease severity/crop loss relationships.3. Develop a predictive model for losses.Biology of Macrophomina phaseolina1. Study fungal properties that induce diseasesymptoms.2. Conduct field and laboratory studies of thefungus.3. Evaluate the distribution of fungal propagulesin the soil.4. Investigate the rate of physiological change inM. phaseolina.5. Determine the role of root exudates on thepathogen.6. Study the role of root exudates in microbialecology.7. Assess kinetics of extracellular fungalenzymes in pathogenesis.8. Study fungal succession in the diseasecomplex.9. Assess the rate of mutation in M. phaseolina.10. Determine pathogen variability.Associated Organisms1. Determine nematode-pathogen-host interactions.2. Obtain a better understanding of the epidemiologyand etiology of M. phaseolina and itsinteraction with other microorganisms, particularlyat the soil/plant interface.Epidemiology1. Identify major predisposing factors in differentcropping systems.2. Quantify stress and the plant's reaction as itaffects pathogenesis.3. Determine the predisposing level and durationof water stress.4. Determine time and location of host infection.5. Determine the role of high temperature in diseasedevelopment.6. Study the chemical-physiological propertiesof plants that enhance disease.7. Understand host-parasite-environment interaction.8. Investigate seedborne dissemination of thepathogen.9. Conduct a thorough in situ study of the biologyof the pathogen.10. Investigate the effect of plant architecture ondisease development.11. Determine the inoculum threshold.12. Identify factors promoting infection andcolonization.13. Carry out studies of pathogenesis.14. Determine time (development stage) ofpathogenesis.15. Determine the methods of penetration andestablishment in the host.16. Analyse the host maturity/susceptibilityrelationship.17. Relate types and levels of carbohydrates insorghum to environmental factors—i.e., stressand diseases.18. Create gravel culture system(s) to study host /pathogen-stress interactions.19. Develop accurate host-parasite models.20. Model disease development (simulation).21. Obtain a better description of the stressenvironment.256

22. Understand response and adaptation tostress,23. Quantify the stress level necessary for predispositionto infection.24. Obtain a better understanding of the worldwideepidemiology and etiology of charcoalrot.25. Study the interrelationship of heat/moisturestress and variety on disease.26. Elucidate the epidemiology and biology ofinfection and disease development.27. Understand the factors predisposing the plantto disease.28. Gain a better understanding of epidemiologyworldwide.29. Analyse the pathogen's influence on plantmetabolism.Screening Techniquesand Identification of Resistance1. Develop reliable field screening techniques.2. Formulate a uniform method of diseasescoring.3. Improve screening techniques for resistance.4. Devise cell-culture or in vitro screening techniquesbased on mechanism of pathogenicity.5. Establish optimum parameters for uniformscreening techniques.6. Screen all available genotypes for resistance.7. Collect and screen germplasm from regionswith high selection pressure.8. Monitor uniform genotypes in screeningnurseries.9. Identify stable resistance sources.10. Develop screening techniques, after establishingthe causes of genetic variability in hostresistance.11. Study resistance to nonhosts.12. Establish special interdisciplinary varietaldevelopment nurseries, using presenttechniques.13. Systematize knowledge of unaffected plantgenera for possible gene transfer.14. Determine stability of charcoal rot resistanceacross environments.15. Identify immune genera and new resistancefor incorporation of genetic material by classicalor biotechnical methods.Plant Traits Associated with Resistance1. Identify plant traits responsible for resistance.2. Determine inheritance of the stay-green trait.3. Understand the relationship of senescenceand nonsenescence with stalk disease.4. Study the genetics and stability of the nonsenescencecharacter under drought stress.5. Establish the relationship between nonsenescence,senescence, and cell death patterns inroots and stalks.6. Relate the spread of the disease in the host tocell death patterns.7. Determine the importance of root/stalksenescence.8. Examine stay-green/ charcoal rot resistancemultilocationally.Nature of Resistance1. Determine resistance mechanisms.2. Determine the causes of genetic variability ofresistance.3. Analyse inheritance of resistance.4. Study inheritance of genetic differencesamong resistance sources.5. Study the physiology and biochemistry of resistanceand pathogenecity.6. Determine the role of osmoregulation in resistanceand susceptibility.7. Identify defense mechanisms of living cells.8. Characterize all known sources of resistance(and susceptibility)—including stay-green andsenescent types—anatomically, pathologically,physiologically, and biochemically.9. Determine the relationship between resistanceto Macrophomina and resistance toFusarium.256

10. Study the genetics of pathogenicity and pathogenvariability.10. Determine the influence of soil and fertilityfactors.Drought Tolerance and Disease Resistance1. Study the physiological mechanisms involvedin postflowering drought tolerance.2. Improve the tolerance of the host to drought.3. Correlate drought resistance/infection/disease.4. Determine whether selection for drought resistanceincludes charcoal rot resistance.5. Obtain a better understanding of the role ofdrought resistance, root and stalk senescence,and cropping systems on charcoal rotdevelopment.6. Work towards improved environmental stresstolerance.Chemical Control1. Examine the potential for fungicidal and/orplant growth regulators or related chemicalsas control components.2. Determine the effects of antisenescencechemicals on host-pathogen interactions.Biocontrol1. Find biological control systems.2. Study mechanisms of suppressive soils.3. Develop crop management for diseasecontrol.4. Determine whether rotation with nonhostcrops reduces disease.5. Determine host-parasite interactions underno-till, conservative-till, and conventionaltillage.6. Determine fertilizer effects on host response.7. Carry out specific studies on nutrientinteraction.8. Study management influence on diseases.9. Elucidate synergistic effects of genotype andmanagement factors.Research Collaboration1. Conduct studies in laboratory and fieldthrough teamwork of physiologists; pathologists,and breeders.2. Aim for a better understanding of disease etiologyby breeders and physiologists.3. Stimulate fellow scientists to increase output.4. Publish collaborative research jointly.5. Obtain a better understanding of the diseasecomplex.6. Promote greater public and private supportfunding.7. Determine how results could be useful internationally.8. Establish collaborative research programs betweenINTSORMIL and ICRISAT.Fusarium Root and Stalk RotCrop Loss1. Clarify the relationships between disease andcrop loss.2. Develop methods to predict losses due todisease.3. Estimate grain yield and quality reductionscaused by fusarium stalk rots.4. Determine root and stalk rot losses in no-till,conservative-till, and conventional tillage(include inoculation and pith condition ratingswhen possible).Biology of the Pathogen1. Identify the Fusarium spp in the diseasecomplex.2. Determine the role of the different Fusariumspp penetrating roots and causing disease.3. Determine regionally the importance of fusariumdisease(s) and relative importance of differentFusarium spp.257

4. Specify the species of Fusarium important incausing root and stalk rot.5. Examine the synergism hypothesis amongFusarium spp.6. Outline the role of Fusarium spp in root andstalk senescence.7. Determine whether the Fusarium spp/sorghum stalk rot interactions follow the Diplodiamaydis model.8. Determine why Fusarium moniliforme appearsto be inhibited in its systemic phase.9. Analyze the interaction between the variousFusarium spp involved in the host tissue.10. Determine the importance of seedborne Fusariumin the disease.11. Gain a better understanding of the worldwideepidemiology and etiology of the Fusarium diseasecomplex.12. Undertake a multilocational and multicultivarstudy of fungal succession and systemicity.13. Determine host differentials for speciesseparation.Pathogens1. Determine the mechanisms of pathogenesis.2. Describe in detail penetration, establishment,and spread of pathogens in living and deadcells of roots.3. Determine relationships between plant stressand pathogenesis.4. Correlate the association of quantity and qualityof carbohydrates with severity of thedisease.5. Conduct physiological-pathological studiesdifferentiating pathogenic and saprophyticattack.Etiology and Epidemiology1. Determine the "where" and "when" of primaryinfection.2. Investigate the survival of inoculum in soil.3. Study the epidemiology and etiology of theFusarium spp involved.4. Study host-parasite interactions, includingpredisposition and mechanisms of resistance.5. Quantify host-pathogen-environment combinationsfavoring infection and pathogenesis.6. Characterize environments in which the diseaseis a problem.7. Quantify environmental conditions enhancingstalk and root rots.8. Describe environmental conditions leading tostalk rot.9. Determine the precise environment(s) necessaryfor infection in the field.10. Determine which environmental factors predisposeplants to the disease.11. Understand the host-parasite-environmentinteractions for various geographic areas.12. Describe the interaction between plant Stressand inoculum levels.13. Identify factors responsible for predispositionto the disease.14. Determine the effects of soil nutrients on diseasedevelopment.15. Understand host-parasite-environment interaction.16. Determine the mechanisms for predispositionand disease resistance.17. Determine the effects of plant injuries on fusariumroot and stalk rot.18. Study the host/parasite relationships indiverse sorghum areas.19. Examine the occurrence and importance ofthe systemic phase.20. Quantify the pathogen-host-soil-microfloraenvironmentinteraction for disease development.21. Explore the relationship between root andstalk rots.22. Compare sorghum and maize stalk rotscaused by Fusarium spp.23. Study the similarities between fusarium andcharcoal rots.24. Examine the relationships between fusariumand macrophomina root and stalk rotcomplexes.258

25. Determine the interaction of other fungi withFusarium spp.26. Determine the relationship between Fusariumspp and other root and stalk rot pathogens.Resistance Screening Techniquesand Identification of Resistance1. Develop effective screening techniques.2. Devise screening techniques for all stages ofplant growth.3. Improve screening techniques for resistance,including the examination of an initial screeningprogram using controlled water and heatstress.4. Identify sorghum groups with relative resistanceand susceptibility through a selectedscreening of the world collection.5. Identify cultivars with specific reactions foruse in standardized nurseries.6. Identify sources of resistance.7. Identify immune species and new sources ofresistance for incorporation of genetic materialby classical or biotechnical methods.8. Determine the causes of genotype variation inhost plant resistance, with particular emphasison physiological and anatomical aspects.9. Formulate scoring scales for measuring differentkinds of damage.Nature of Resistance1. Study the inheritance and heritability of resistance.2. Examine the genetics of host resistance.3. Identify the physiological plant factors relatedto host resistance.4. Determine the inheritance of several sourcesof resistance.5. Determine whether free and glycocidic phenolsare involved in resistance.6. Investigate the genetics of resistance andsusceptibility of stalk and root rots.7. Determine the causes of genotypic variation inhost plant resistance and lodging, with particularemphasis on physiological aspects (e.g.,source-sink relationships, assimilate partitioning,photosynthetic efficiency) and anatomicalaspects.8. Define the relationships between grain moldresistance (Fusarium) and fusarium stalk androot rot resistance.9. Identify plant traits conferring resistance.10. Determine the relationship of senescence andnonsenescence to the resistance or susceptibilityof the genotype to disease.11. Relate cell death patterns to susceptibility andresistance in roots and stalks, especially insenescing and nonsenescing (stay-green)genotypes.12. Undertake a comprehensive study of assimilatepartitioning with respect to senescence,harvest index, susceptibility, and lodging.13. Search for differences in photosyntheticefficiency.Chemical Control1. Examine potentials for control with fungicides,plant growth regulators, and relatedchemicals.2. Investigate control of senescence with appliedchemicals.Crop Management and Disease1. Develop integrated management systems tocontrol the problem.2. Develop cultural methods for disease management.3. Study crop management factors influencingthe disease.4. Identify cultural practices that might alleviatethe impact of the disease.5. Define the role of cultural and locationspecificfactors on disease incidence in contrastinggenotypes.6. Determine the effects of row spacing and populationon disease expression.259

AnthracnoseCrop Loss1. Explore the relationship between infectionseverity and yield loss by geographic areas.2. Make separate assessments of yield lossesdue to infection of individual plant parts.Biology1. Describe the taxonomy of the pathogen and itsrelationship to other cereal anthracnoses.2. Determine regionally the relative importanceand virulence of the disease, including its differentphases.3. Study genetic variability of the pathogen.4. Determine the race/genotype interactions inmajor sorghum-producing regions, using a setof common genotypes and regionally importantgenotypes.5. Estimate the mutation rate of the pathogen.6. Devise improved methods for identification ofphysiological races.7. Identify predominant races of the pathogen bygeographical area.8. Identify physiological races of anthracnose.9. Collectively evaluate isolates at a containmentfacility for pathogen variability.Phases of the Disease1. Elucidate the causes of different phases ofanthracnose.2. Explain the relationship of stalk rot to otherphases of the disease,3. Determine whether there is a relationshipbetween anthracnose stalk rots of maize andsorghum.4. Examine correlations of resistance to leaf,peduncle, and panicle phases.5. Establish the relationship of grain and leafanthracnose to stalk rot.Epidemiology1. Investigate the temperature/plant growth/ diseaseinteraction.2. Correlate plant nutrient balance with diseaseincidence.3. Determine and quantify optimum environmentalfactors necessary for infection and pathogenesis.4. Study host-pathogen-environment interaction.5. Analyse environmental parameters in pathogenesisof anthracnose stalk rot.6. Identify factors affecting inoculum survival inthe soil.7. Establish the relationship of seedborne inoculumto foliage infection, grain infection, andstalk rot.8. Determine the importance of seedborne inoculumin epidemiology and seed exchange.9. Study seedborne dissemination of new pathotypes.10. Estimate the rate of growth of different phasesof anthracnose in different cultivars under differentenvironmental conditions.11. Describe mechanisms of survival of the pathogenunder natural conditions.12. Determine how anthracnose spreads fromleaves to stalk in senescent and nonsenescentgenotypes, with emphasis on locatinggenotypes to resist this spread.13. Examine the spread of the pathogen within thestalk.14. Identify the mode of infection of leaf, grain,stalk, and root.15. Determine which factors are favorable or unfavorablefor the incidence of anthracnoseand fusarium and charcoal rot.Physiology of Host-Parasite Interaction1. Conduct biochemical studies on host plantresistance.2. Study the physiology of host response toinfection.260

3. Investigate the biochemistry of pathogenesis.4. Relate the osmotic potential of the host plant tothe degree of infection at different growthstages.Control1. Evaluate growth regulators as chemicalcontrols.2. Develop cost-effective chemicals for control.3. Evolve methods for cultural control, chemicalcontrol, and biocontrol of anthracnose.4. Evaluate and utilize chemicals and culturalpractices to develop crop management systemsfor control.5. Evaluate fungicides, plant growth regulators,and related chemicals as control agents.6. Study the effect of conservation tillage on diseasedevelopment.7. Determine the role of preformed fungistaticcompounds and phytoalexins and other postinfectionresistance chemicals in resistance.8. Study host disease reaction before and aftertreatment with ethylene.9. Accelerate and coordinate breeding programsfor resistance at strategic locations.Screening Techniques andIdentification of Resistance8. Test multilocationally a carefully selected setof genotypes for stability of identifiedresistance.Nature of Resistance1. Determine ''r'' for various cultivars or cultivarmixtures, and its value in reducing damage.2. Study the genetics and stability of resistance.3. Study the inheritance and heritability ofanthracnose stalk rot resistance.4. Analyze mechanism(s) of resistance related tostability of heritable character(s).5. Identify plant factors conferring resistance.6. Identify plant morphological factors affectingresistance.7. Determine the mechanism of resistance in arange of genotypes, including preformed postinfectioncompounds.8. Determine the relationship of senescence/nonsenescence in resistance.ReferencesDALBECQ, A.L., VAN DER VEN, A.H., and GUSTAFSON,A.H. 1975. Group techniques for program planning: aguide to nominal group and delphi processes, Glenview,Illinois, USA: Scott, Foreman.1. Develop effective and relevant laboratory andfield screening techniques.2. Determine germplasm susceptibility/resistanceto multiple disease.3. Screen the world sorghum germplasm collectionfor resistance at locations where there aredifferences in pathogen variability.4. Identify stable and durable anthracnose resistancefor incorporation into improved cultivars.5. Screen all known available sources ofresistance.6. Identify broad-spectrum resistance sources.7. Determine the value of known sources of resistancefor sorghum improvement programs.261

Meeting Organizationand Participants

Meeting OrganizationOrganizing CommitteeChairperson: C.R. Jackson, Director, International Cooperation, ICRISATCoordinator: L.K. Mughogho, Principal Sorghum Pathologist, ICRISATR.A. Frederiksen, Professor of Plant Pathology, Texas A&M UniversityL.R. House, Leader, Sorghum Program, ICRISATJ.M. Peacock, Principal Sorghum Physiologist, ICRISATN. Seetharama, Sorghum Physiologist, ICRISATH.L. Thompson, Head, Information Services, ICRISATS. Krishnan, Senior Admin. Officer, International Cooperation, ICRISATR.A. FrederiksenA.B. MaunderL.K. MughoghoSession ChairpersonsS.Z. MukuruA.J. PappelisD.T. RosenowLE. ClaflinR.B. ClarkB. DoupnikR.R. DuncanR.G. HenzellRapporteursA.B. MaunderG.N. OdvodyR.W. SchneiderJ.B. SinclairR.V. VidyabhushanamR.A. FrederiksenR.J. WilliamsGroup ChairpersonsW.R. JordanR.R. DuncanJ.D. EastinSZ. MukuruGroup RecordersJ.F. ScheuringN. SeetharamaN. ZummoSecretariesG.V.S. GurunadhK.M. SharmaParticipantsL.E. ClaflinAssociate ProfessorDepartment of Plant PathologyKansas State UniversityManhattan, KS 66506USAR.B. ClarkResearch Chemist, USDA-ARSKiesselbach Crops Research LaboratoryUniversity of NebraskaLincoln, NE 68583USAB. Doupnik, Jr.Professor of Plant PathologyUniversity of NebraskaSouth Central StationBox 66Clay Center, NE 68933USAR.R.DuncanSorghum Breeder/PhysiologistUniversity of GeorgiaGeorgia Experiment StationGriffin, GA 30212USA265

J.D. EaatinProfessor of AgronomyUniversity of Nebraska205 Kiesselbach Crops Research LaboratoryLincoln, NE 68583-0817USAR.A. FrederiksenProfessor of Plant PathologyDepartment of Plant Pathology and MicrobiologyTexas A&M UniversityCollege Station, TX 77843USAR.G. HenzellSenior Plant BreederDepartment of Primary IndustriesHermitage Research Station, Warwick, Qld. 4370AUSTRALIAW.R.JordanProfessor of Plant Physiology andDirector, Texas Water Resources InstituteTexas A&M UniversityCollege Station, TX 77843-2118USAJ.W. MaranvilleProfessor, Department of Agronomy102C Kiessetbach Crops Research LaboratoryUniversity of NebraskaLincoln, NE 68583-0817USAA. Bruce MaunderVice PresidentDekalb-Pfizer GeneticsRoute 2, Lubbock, TX 79415USAG.G. McBeeProfessor of Plant PhysiologyDepartment of Soil and Crop SciencesTexas A&M UniversityCollege Station, TX 77843-2474USAL.K. MughoghoPrincipal Plant PathologistICRISATPatancheru P.O., A.P. 502 324INDIAS.Z. MukuruPrincipal Plant BreederICRISATPatancheru P.O., A.P. 502 324INDIAG.N. OdvodyPlant Pathologist/Assistant ProfessorTexas A&M UniversityAgricultural Research and Extension CenterRt.2, P.O. Box 589Corpus Christi, TX 78410USAE.H. OmerPlant PathologistAgricultural Research Corp.Botany and Plant Pathology SectionGazira Agricultural Research StationWad MedaniSUDANS. PandePlant PathologistICRISATPatancheru P.O., A.P. 502 324INDIAA.J. PappelisProfessor, Department of BotanySouthern Illinois UniversityCarbondale, IL 62901USAJ.E. PartridgeAssistant ProfessorDepartment of Plant PathologyUniversity of NebraskaLincoln, NE 68583-0722USAGloria RosenbergPublication EditorP.O. Box 303State College, PA 16804USAD.T. RosenowProfessor, Sorghum BreederTexas A&M UniversityTexas Agricultural Experiment StationRt.3, Lubbock, TX 79401USAJ.F. ScheuringCereal BreederICRISAT/Mali ProgramC/o. Ambassade AmericaineB.P. 34BamakoMALI, West Africa (Via Paris)R.W. SchneiderAssistant Professor266

Department of Plant PathologyUniversity of CaliforniaBerkeley, CA 94720USAD.F. SchoeneweissPlant PathologistIllinois State Natural History Surveyand University of Illinois607 E. Peabody DriveChampaign, IL 61820USAN. SeetharamaPlant PhysiologistICRISATPatancheru P.O., A.P. 502 324INDIAK.M. SharmaSecretaryICRISATPatancheru P.O., A.P. 502 324INDIAJ.B. SinclairProfessor of Plant PathologyUniversity of IllinoisN-519 Turner HallUrbana-Champaign, IL 61801USAPhoto CreditsCover:S.C. Dalmacio, University of the Philippines atLos Banos: bacterial stalk rotD.T. Rosenow: nonsenescent and senescentsorghum linesR.J. Williams: stalk lodgingFrontispieces:S. Pande: charcoal rotN. Zummo: fusarium stalk rot and pokka boengG.N. Odvody: pythium root rotR.A. Frederiksen: anthracnose stalk rot; acremoniumwiltG.N. Odvody: periconia root rotLE. Claflin: nematode and nematode damage tosorghumR.V. VidyabhushanamPlant Breeder and Head of StationIARI Regional Research StationRajendranagarHyderabad, A.P. 500 030INDIAR J. WilliamsPhytopathologistCiba-Geigy AGAgricultural Division, AG 2-82CH-4002, BaselSWITZERLANDN. ZummoResearch Plant Pathologist, USDA-ARSand Adjunct Professor of Plant PathologyMississippi State UniversityP.O. Drawer PGMississippi State, MS 39762USA267

I C R I S A TInternational Crops Research Institute for t h e Semi-Arid TropicsICRISAT Patancheru P.O.Andhra Pradesh 5 0 2 3 2 4 , India

Sorghum Root and Stalk Rots - Agropedia

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