Histopathology of Seed-Borne Infections - Applied Research Center ...

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Location of Fungal Hyphae in Seeds 105sorghum embryo (Figure 5.3C, D) is incited by C. lunata (Rastogi, Singh, and Singh,1990) and in that of wheat by B. sorokiniana (Yadav, 1984). In rubber (Heveabrasiliansis) seeds infected with B. theobromae, some cells in mesophyll of cotyledonsbecame hypertrophied and thick-walled (Varma, Singh, and Singh, 1990). Theembryo in heavily infected seeds shows conspicuous axial elongation, comprisingnarrow elongated cells in sorghum and wheat infected by C. lunata (Rastogi, Singh,and Singh, 1990) and D. tetramera (Yadav, 1984), respectively.Common histological manifestations at the subcellular level in heavily affectedcells of cotyledons in soybean by F. oxysporum and R. bataticola (Mathur, 1992;Sharma, 1992) are the loosening of cell wall fibrils, the broadening of plasmodesmata,the depletion of plasma membrane, the degradation of cytoplasm and cellorganelles, and the deformation of protein bodies, lipid bodies, and nuclear membrane.The soybean cotyledons infected with R. bataticola also revealed the appearanceof striated excretory bodies not found in uninfected cotyledons (Figure 5.3E,F). Thus, the changes at subcellular level show symptoms of disturbed metabolicactivity, including triggering of some new pathways.5.4. MIXED INFECTIONSSeeds usually do not have unifungal infection, but information on histopathologyof seeds infected with more than one fungus is limited (Wilson, Noble, and Gray,1945; Kunwar, Singh, and Sinclair, 1985; Sharma, 1992). Wilson, Noble, and Gray(1945) distinguished the hyphae of Gloetinia granigena (blind seed fungus) fromthat of the endophyte in rye grains on the basis of hyphal morphology. Gloetiniagranigena occurred in different parts of the seed and its expanse depended on thestage at which infection took place. But the mycelium of the endophyte was usuallyconfined to a layer immediately outside the aleurone layer (probably the seed coat).In germinating caryopsis, the endophyte spread to the plumule, while G. granigenawas usually restricted to the endosperm and scutellum.Kunwar, Singh, and Sinclair (1985) found Colletotrichum truncatum and Phomopsissp. or Cercospora sojina in soybean seeds. Based on hyphal color (unstained),width, presence or absence of oil globules, and reaction to stains (safranin-lightgreen and trypan blue), the mycelium of these fungi could be distinguished fromone another (Table 5.1). These pathogens compete with one another for colonizationof seed tissues. The hyphae of Phomopsis sp., an aggressive pathogen, are restrictedto seed coat layers when C. truncatum is present. Similarly, C. sojina hyphae aremore numerous in the seed coat than C. truncatum hyphae in seeds having mixedinfection of these pathogens. An additive effect is seen on deterioration of tissuesof seed coat when infected with C. truncatum and Phomopsis sp.Seeds of soybean can be infected with F. oxysporum and Papulaspora coprophila,a saprophyte. Hyphae of F. oxysporum are hyline, branched, septate, 2 to3.5 mm broad and stained green or light red, whereas those of P. coprophila arebrown to dark brown, much branched, shortly septate, 4 to 10.5 mm broad and darkred brown in safranin-fast green stained preparations. With trypan blue the hyphaeof F. oxysporum are stained blue, but those of P. coprophila retained the naturalbrown color. Both the fungi invade all the components, but F. oxysporum is more
106 Histopathology of Seed-Borne InfectionsABCDpbebcwlbEFFIGURE 5.3 Photomicrographs of normal and infected parts of embryo showing reaction ofhost tissue to infection. A, B, Ts part of cotyledons from adaxial surface of healthy andinfected sesame seeds by Macrophomina phaseolina. Note mycelium and microclerotiabetween cotyledons in B and pronounced cell divisions in cells. C, D, Ls embryo from normaland infected sorghum seeds by Curvularia lunata showing induced premature xylogenesis inthe mesocotyl region in D. E, F, TEM of cells from normal (E) and infected cotyledons ofsoybean infected by Rhizoctonia bataticola, the latter showing weakening of cell wall, dilatedprotein bodies, and ergastic bodies. The ergastic bodies are absent in cells of normal cotyledons.(Abbreviations: cw, cell wall; eb, ergastic bodies; lb, lipid bodies; pb, protein bodies.)(A, B, Singh, T. and Singh, D. 1979. In Recent Research in Plant Science. Bir, S.S., Ed.Kalyani Publishers, New Delhi; C, D, Rastogi, 1984; E, F, Mathur, R. 1992. Ph.D. thesis,University of Rajasthan, Jaipur, India.)
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Histopathology ofSeed-Borne Infecti
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PrefaceThe book deals with only one
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The AuthorsDalbir Singh, Ph.D., for
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ContentsChapter 1 Introduction ....
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4.3.2 Routes for Infection from Ova
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8.4 Survival in Seed ..............
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2 Histopathology of Seed-Borne Infe
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4 Histopathology of Seed-Borne Infe
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2Reproductive Structuresand Seed Fo
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Reproductive Structures and Seed Fo
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14 Histopathology of Seed-Borne Inf
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3Structure of SeedsThe seed habit i
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Structure of Seeds 49(1971) of usin
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Structure of Seeds 51is found in as
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Structure of Seeds 53dry seed of Ly
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Page 72 and 73: Structure of Seeds 57Endosperm: One
Page 74 and 75: Structure of Seeds 59scendembepsmuA
Page 76 and 77: Structure of Seeds 61Endosperm: Sca
Page 78 and 79: Structure of Seeds 63Chalaza simple
Page 80 and 81: Structure of Seeds 65stystypmerA Bc
Page 82 and 83: Structure of Seeds 67epsent endCADB
Page 84 and 85: Structure of Seeds 69perhscendembpe
Page 86 and 87: Structure of Seeds 71eposgepi′epo
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Page 90 and 91: Structure of Seeds 75Baker, D.M. an
Page 92 and 93: Structure of Seeds 77Maheshwari Dev
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156 Histopathology of Seed-Borne In
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7Seed Infection by VirusesViruses a
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Seed Infection by Viruses 201TABLE
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Seed Infection by Viruses 205Unlike
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Seed Infection by Viruses 2073. The
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Seed Infection by Viruses 209Wilcox
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Seed Infection by Viruses 213floret
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Seed Infection by Viruses 215ptowvv
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Seed Infection by Viruses 2177.4.2
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Seed Infection by Viruses 219seed(s
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Seed Infection by Viruses 221AMV fo
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Seed Infection by Viruses 223REFERE
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Seed Infection by Viruses 225Hunter
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Seed Infection by Viruses 227Wolf,
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