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

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Seed Infection by Nematodes 237ennnflpeAgwBnDgwCEFIGURE 8.4 Sections of spikelet and galls of Lolium rigidum caused by Anguina agrostis.A, Ls part of spikelet showing large number of nematodes (second-stage larvae) around afloret primordium. B, Ls of gall showing adult nematodes and large number of eggs. C, A partfrom B magnified. D, Ls almost mature gall showing gall cavity full of larvae and thin wall.E, Part from D magnified showing nematodes (second-stage larvae) and thick-walled cells ofgall wall. (Abbreviations: e, eggs; flp, floret primordium; gw, gall wall; n, nematode.) (A toE, From Stynes, B.A. and Bird, A.F. 1982. Phytopathology 72: 336–346. With permission.)a cavity and a distinct opening. Such galls that develop in place of ovules and lesscommonly in place of stamens contain usually three or four, rarely more, nematodes.Both Stynes and Bird (1982) and Courtney and Howell (1952) concluded that thegalls develop in the place of ovules and called them ovular galls. The authors wouldlike to point out here that the developing primordium of the gynoecium in itsontogeny is open at the apex, and the cavity is enclosed by the ovary wall. The gallsformed are the ovary galls since their wall is made up by the pericarp (ovary wall)
238 Histopathology of Seed-Borne Infectionsrather than any part of the ovule. The nematodes may enter through the opening atthe top or they may feed and enter after puncturing cells using their buccal stylet.After the gall initiation has taken place, the nematode larvae molt, forming malesand females (Figure 8.4B). Similar to A. tritici, this nematode is also amphimictic.The females lay eggs (Figure 8.4B, C) and finally second-stage larvae are hatched.Simultaneously, the galls enlarge, become 3 to 5 mm long and purplish due to theformation of anthocyanin pigment. Adults die in more advanced galls. The larvaeare closely pressed against each other in mature dried galls. The cells of the gallwall lose cytoplasmic contents, collapse, and develop weak thickenings. The cellslining the cavity have callose deposition (Figure 8.4D, E).In some florets, two galls occasionally develop. The additional gall may arisefrom stamen, glumes, or rachis. The structure of mature galls incited by A. agrostison other hosts is also similar to that described here (Stynes and Bird, 1982).8.2.3 ANGUINA AGROPYRONIFLORIS NORTON (WESTERNWHEATGRASS NEMATODE)Anguina agropyronifloris produces galls in the inflorescence of western wheat grass,Agropyron smithii (Lakon 1953; Norton and Sass, 1966) and in golden oatgrass,Trisetum flavescens (Lakon, 1953). The galls are elongated with a brittle wall.8.2.3.1 Origin and Histology of GallsNorton and Sass (1966) studied plant infection and gall formation in artificiallyinoculated seeds by placing 300 to 1000 juveniles of Anguina agropyronifloris perseed in the greenhouse. The nematodes invade the roots and scutellar node as bothecto- and endoparasites. They also reach the axils of leaf sheaths. The endoparasiticinfection of root and scutellar node does not cause floret infection. Ectoparasiticnematodes in leaf sheaths migrate to the apex and finally the inflorescence. Theypenetrate the undeveloped ovary as the earhead emerges from the boot leaf. Onlyfertile florets are invaded. Once the ovary is infected, other parts cease to develop.The larvae molt to produce adult males and females. The females lay eggs, whichmolt and form the second-stage larvae. The cells of the ovary wall elongate alongthe long axis. The wall is five- to six-layered, greatly compressed, weakly thickwalled,and brittle at maturity. The cavity is occupied by second-stage juvenile larvae(Norton and Sass, 1966).8.2.4 DITYLENCHUS DESTRUCTOR THORNE (POTATO NEMATODEIN GROUNDNUT)Ditylenchus destructor is an important pest of groundnut (Arachis hypogaea) in theRepublic of South Africa (De Waele et al., 1989; Jones and De Waele, 1988). Thegroundnut hulls have brown necrotic tissue at the point of connection with peg andblack discoloration along the longitudinal veins. The infected seeds are shrunken,and the testa and embryo show yellow to brown or black discoloration.Jones and De Waele (1990) determined the time and mode of entry, and thespread of D. destructor in pod and seed of groundnut under field and greenhouse
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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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100 Histopathology of Seed-Borne In
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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
Page 220 and 221: Seed Infection by Viruses 205Unlike
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
Page 242: Seed Infection by Viruses 227Wolf,
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