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

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Seed Infection by Nematodes 235Anther Gall: The young anther galls are oval to round with a prominent cavityoccupied by a large number of second stage larvae and the degenerating sporogenouscells (Figure 8.3A to C). The wall comprises four to seven layers, differentiated intotwo zones — an outer zone of two to three layers and an inner zone of two to fourlayers of richly protoplasmic cells. The sporogenous tissue is completely absorbedby the time the final molting takes place and males and females are formed(Figure 8.3D). Subsequently, the females lay eggs, which undergo embryogenesisand molt to form second-stage larvae. Simultaneously, the wall cells undergo hyperplasiaand become 12- to 14-layered. Inner layers remain parenchymatous, and theybecome absorbed during maturity. The outer layers become thick-walled and lignified.The mature galls are circular or slightly angular in transection, and the cavityhas numerous second-stage larvae (Figure 8.3E).Ovary Gall: The young ovary galls are more or less circular in outline intransections with a small cavity occupied by a few nematodes. The cavity enlargesand the larvae begin to molt, forming adult male and female nematodes. The wallcells undergo hyperplasia. They are thin-walled and parenchymatous. The femaleslay eggs (Figure 8.3F, G), which develop and molt to form second-stage larvae. Theinner layers remain thin-walled and are gradually absorbed, while the outer onesbecome thick-walled and lignified (Figure 8.3H).At maturity the ovary galls closely resemble the anther galls and are brown-black.The mature seed galls do show some differences in their morphology and color. Indry seed inspection, three categories of galls — bold, shriveled, and compound — arerecognized. Longitudinal sections of compound galls often show a multicavity condition.No distinction is observed in the portion of the wall contributed by differentorgans.8.2.2 ANGUINA AGROSTIS (STEINBUCH) FILIPJEV (BENT GRASSGALL NEMATODE)This nematode was recorded for the first time in 1797 from galls in spikes of colonialbent grass (Agrostis tenuis) and has been subsequently recorded in many grasses(Thorne, 1961; Southey, 1973). It is a serious pest of Lolium rigidum (Stynes andBird, 1982) and Leymus chinensis (Ma and Gu, 1987). The mode of infection anddevelopment of galls in the inflorescence of grasses by A. agrostis is similar to thatof A. tritici (Courtney and Howell, 1952; Stynes and Bird, 1982). Spindle-shapedpurple galls are produced in the inflorescence of the infected plants in A. tenuis andother grasses.8.2.2.1 Histology and Development of GallsThe infective second-stage larvae of A. agrostis colonizes the plant in the vegetativephase, migrates toward the main and lateral shoot apices, and remains in their vicinity.A large number of nematodes collect around the floret primordia (Figure 8.4A).Stynes and Bird (1982) believed that the nematodes feeding on the primordium ofthe gynoecium induce rapid cell division and enlargement. This growth and simultaneouslocal destruction of cells produce a depression, and then finally a gall with
236 Histopathology of Seed-Borne InfectionsanwmmcnABgwnC D EnngwF G HFIGURE 8.3 Histology of developing and mature galls caused by Anguina tritici in wheat.A to E, Anther gall. A, Ts part of young green gall showing nematode larvae and degeneratingsporogenous tissue. B, C, Parts from A magnified to show degenerating sporogenous cellsand second stage larvae. D, Ts green gall showing adult nematodes and eggs. E, Ts maturegall, cavity full of second-stage larvae and the wall of four to six lignified layers. F to H,Ovary gall. F, Part of gall showing eggs and adults. G, Ts gall at egg-laying stage. H, Ts partof mature gall showing second-tage larvae and thick and lignified cells of wall. (Abbreviations:anw, anther wall; gw, gall wall; mmc, microspore mother cells; n, nematode.) (Agarwal, K.1984. 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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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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TABLE 5.6Location of Mycelium of St
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Page 214 and 215: 7Seed Infection by VirusesViruses a
Page 216 and 217: Seed Infection by Viruses 201TABLE
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Page 222 and 223: Seed Infection by Viruses 2073. The
Page 224 and 225: Seed Infection by Viruses 209Wilcox
Page 228 and 229: Seed Infection by Viruses 213floret
Page 230 and 231: Seed Infection by Viruses 215ptowvv
Page 232 and 233: Seed Infection by Viruses 2177.4.2
Page 234 and 235: Seed Infection by Viruses 219seed(s
Page 236 and 237: Seed Infection by Viruses 221AMV fo
Page 238 and 239: Seed Infection by Viruses 223REFERE
Page 240 and 241: Seed Infection by Viruses 225Hunter
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