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

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Location of Fungal Hyphae in Seeds 133myepsscicuendembecuAendBendembscCDFIGURE 5.14 Location of Alternaria sesamicola hyphae in sesame seeds. A, Ts seed througha weakly infected seed showing dark-colored mycelium in subepidermal cells of seed coat.B, A portion from A magnified. C, Ls micropylar part of severely infected seed showingfungal conidia in the space. D, Ls part of severely infected seed. The wall layers in the seedcoat are poorly differentiated, endosperm and embryo with mycelium all over. (Abbreviations:ecu, cuticle of endosperm; emb, embryo; end, endosperm; eps, seed epidermis; icu, innerenticle of seed coat; my, mycelium; sc, seed coat.) (From Singh, D., Mathur, S.B., andNeergaard, P. 1980. Seed Sci. Technol. 8: 85–93. With permission.)discolored, becoming black. Thick, dark brown, septate, knotty mycelium occur exoandendophytically in glumes of infected seeds. Curvularia lunata primarily colonizesthe pericarp and rarely invades the aleurone layer in moderately infected seeds.
134 Histopathology of Seed-Borne InfectionsIt is common in the persistent stylar tissue. Hyphae are distributed in all parts, i.e.,the pericarp, aleurone layer, and other layers of the endosperm and embryo in heavilyinfected seeds. Embryal infection occurs in the scutellum, coleoptile, mesocotyl,primary root, and coleorhiza. Cells in infected embryos are narrow and elongatedwith poor contents, and those of mesocotyl show premature xylogenesis. Rarely, theembryo remains undifferentiated, made up of small parenchyma cells with clumpsof mycelium. The heavily infected seeds fail to germinate.Symptomatic seeds of onion (Allium cepa) infected with C. lunata are dull black.Asymptomatic seeds rarely (about 20%) carry mycelium on the seed surface. Thick,brown, septate, and branched mycelium occurs in the seed coat and rarely in theendosperm of symptomatic seeds. Hyphal aggregation is more toward the micropylarend (Dwivedi, 1994).5.5.4.1.3 Bipolaris, Drechslera, and HelminthosporiumMost plant pathogenic species, initially described under Helminthosporium, wereplaced at one time under Drechslera (Subramanian and Jain, 1966; Ellis, 1971;Subramanian, 1971). Subsequently, these have been reclassified under Bipolaris,Drechslera, and Helminthosporium. These fungi cause leaf spots, blight, and crownor root rot in plants of Poaceae (Graminae). They are weak to potent pathogens andmany of them are seed-borne and seed-transmitted. Infection of such species wasprimarily recorded in the pericarp and seed coat in early studies, e.g., Bipolarissorokiniana in wheat (Weniger, 1925) and barley (Mead, 1942), Bipolaris oryzae inrice (Nisikado and Nakayama, 1943; Fazli and Schroeder, 1966), and Drechsleragraminiea in barley (Vogt, 1923; Genau, 1928; Platenkamp, 1975). Meffert (1950)reported Helminthosporium papaveris in the seed coat and endosperm of poppyseeds. Fazli and Schroeder (1966) also found B. oryzae hyphae in the endosperm.Recent investigations on seeds infected by Bipolaris and Drechslera species ofseveral crop plants have clearly shown that the expanse of mycelium in seed isdirectly correlated with the severity of infection (Yadav, 1984; Singh, Singh, andSingh, 1986a; Thakkar et al., 1991).Yadav (1984) divided the wheat seeds affected with B. sorokiniana into fourcategories: bold seeds, seeds with loose pericarp, shriveled seeds, and discoloredseeds. The mycelium is usually confined to outer layers of pericarp in bold seedsand rarely penetrates cross and tube cells (Figure 5.15H). Kernels with loose pericarpand shriveled type carry abundant mycelium in all the layers of the pericarp. Infectionoccurs in all components, i.e., pericarp, aleurone layer, endosperm (Figure 5.15I),and embryo in discolored seeds. The embryonal infection varies from weak to heavy.Weak infection is confined to the scutellum, but moderate to heavy infection spreadsto all parts of the embryo. Rarely, the cells of scutellar epithelium undergo two tothree transverse divisions, and premature xylogenesis is induced in the mesocotyledonarynode. Heavy infection of B. sorokiniana caused 62% pre- and postemergencelosses, and 28% of the 38% of the surviving seedlings developed symptoms (Yadav,1984).Wheat seeds from earheads artificially inoculated by D. tetramera carry myceliumin the pericarp, aleurone layer, endosperm, and rarely the embryo (Yadav, 1984).
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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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Structure of Seeds 553.3.2 SEED COA
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Structure of Seeds 57Endosperm: One
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Structure of Seeds 59scendembepsmuA
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Structure of Seeds 61Endosperm: Sca
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Structure of Seeds 63Chalaza simple
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Structure of Seeds 65stystypmerA Bc
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Structure of Seeds 67epsent endCADB
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Structure of Seeds 69perhscendembpe
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Structure of Seeds 71eposgepi′epo
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Structure of Seeds 73(Zea and Sorgh
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Structure of Seeds 75Baker, D.M. an
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Structure of Seeds 77Maheshwari Dev
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Structure of Seeds 79Vries, M.A. de
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184 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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