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

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Location of Fungal Hyphae in Seeds 103pycperalmypycmyperalendendboldprrcvbsctcolpelsaloose/crackedpericarpshriveledAvbsaepiprrcmydiscoloredmysctmycolpmymymyBscvbCDmymyEFIGURE 5.2 Diagrammatic Ls of categorized infected wheat seeds. A, Ls bold, loose crackedpericarp, shriveled and discolored types of Stagnospora nodorum-infected wheat seeds showingthe expanse of mycelium. B, C, Ls of moderate and heavily infected wheat seeds byBipolaris sorokiniana. D, E, Ls wheat seeds moderate and heavily infected by Drechsleratetramera. The embryo damage is more by D. tetramera than B. sorokiniana or S. nodorum(Abbreviations: al, aleurone layer; colp, coleoptile; el, embryonic leaf; end, endosperm; epi,epiblast; my, mycelium; per, pericarp; pr, primary root; pyc, pycnidium; rc, root cap; sa, shootapex; sc, seed coat; sct, scutellum; vb, vascular bundle.) (A, From Agarwal, K. et al. 1985.Phytomorphology 35: 87–94; B to E, From Yadav, V. 1984. Ph.D. thesis, University ofRajasthan, Jaipur, India.)
104 Histopathology of Seed-Borne Infections5.2 PRIMARY SITES OF COLONIZATIONDevelopmental histopathological studies suggest that there is a primary site ofcolonization by the fungal mycelium in seed, depending on the course of penetrationand the availability of space or soft tissue. The infection through the micropylespreads readily in spaces between the components of the ovule and developing seed(Singh and Singh, 1979; Singh, Mathur, and Neergaard, 1980). This inoculumsubsequently infects cells in different components. The infection coming throughthe funiculus spreads first in the integument or developing seed coat or raphe, ifpresent. The hyphae further spreads from outside to the inside in different componentsof seeds, including the spaces between the components. The fungal myceliumentering directly through seed epidermis via natural openings, such as stomata andmicropores, or through cracks and wounds during late stages of seed development,predominantly occupies the cells with prominent air spaces and parenchymatouscells. In leguminous seeds, this infection is readily observed in hourglass cells withprominent air spaces (Ilyas et al., 1975; Singh and Sinclair, 1985, 1986; Mathur,1992; Sharma, 1992). If the fungus penetrates the ovule and seed through thefuniculus or micropyle, the infected seeds, particularly weakly infected ones, oftenlack hyphae or propagules of the fungus on the seed surface, whereas when infectiontakes place through the seed surface, the aggregation of mycelium on the seed surfaceis common. The fungal hyphae may follow more than one course of entry, as seenin soybean seeds infected with Alternaria sp. (Vaughan et al., 1988) and Cercosporasojina (Singh and Sinclair, 1985), Phomopsis longicolla (Roy and Abney, 1988),and Ranunculus asiaticus by Alternaria sp. (Halfon-Meiri, Kunwar, and Sinclair,1987).5.3 HOST–PATHOGEN INTERACTIONSThe reaction of seed tissues to different pathogens is variable. Usually heavy infectionof fungi, particularly necrotrophs, causes distortion and weakening of tissues,including thickenings of cuticles and cell wall (Singh, Mathur, and Neergaard, 1977,1980; Singh, 1983) and poor storage of reserve food material in the endospermand/or embryo, resulting in deformed and shriveled seeds. Several fungi, Alternariabrassicicola, A. tenuis, Trichothecium roseum in rape and mustard (Sharma, 1989),T. roseum in maize (Singh, Singh, and Singh, 1985), D. tetramera in wheat (Yadav,1984), C. lunata in sorghum (Rastogi, Singh, and Singh, 1990), R. bataticola inmothbean (Vigna aconitifolia) (Varma, Singh, and Singh, 1992b), and Fusariumoxysporum in mothbean and cowpea (Vigna unguiculata) (Varma, 1990), cause lysisof the cells of the embryo, forming cavities.Macrophomina phaseolina (R. bataticola) infection occurring in spaces betweenseed components in sesame seeds induces cell division in the endosperm and embryo(Singh and Singh, 1979). The divisions are conspicuous on the adaxial side ofcotyledons (Figure 5.3A, B). Cell divisions are also incited by C. dematium in theembryo of chili (Chitkara, Singh, and Singh, 1990), the epithelium of scutellum inwheat by B. sorokiniana (Yadav, 1984), and in the seed coat of rape and mustardby A. brassicicola (Sharma, 1989). Premature xylogenesis in the mesocotyl of
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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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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
Page 94: Structure of Seeds 79Vries, M.A. de
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154 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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