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

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Seed Infection by Viruses 221AMV forms rafts of short virus particles in the anthers, pollen, and cotyledons,and large crystalline bodies of long particles in the ovary wall, bud receptacle, andcotyledons. The crystalline bodies are crescent-shaped in cells of cotyledons, whilein pollen grains they form star-like aggregations (Wilcoxson, Johnson, andFrosheiser, 1975). Pesic, Hiruki, and Chen (1988) observed large crystalline bodiesin the cytoplasm of tapetal cells and pollen grains in anthers infected with AMV.Hoch and Provvidenti (1978) have reported areas of granular or fibrillar appearanceassociated with virus arrays of BCMV particles, virus-associated paracrystallinebodies, and arrays or undulating filaments in cells of infected seeds.7.6 INACTIVATION OR LONGEVITY OF VIRUSES INSEED DURING MATURATION AND STORAGEStability of viruses during seed maturation and dehydration has been shown to varywith the virus, host, and its cultivar. Inactivation of viruses in the seed coat duringmaturation has been observed in numerous cases, including AMV (Bailiss and Offei,1990), SMV (Bowers and Goodman, 1979), SBMV (Cheo, 1955), BSMV (Goldet al., 1954; Carroll, 1972), BCMV (Ekpo and Saettler, 1974), and PSbMV (Stevensonand Hagedorn, 1973).AMV is seed-transmitted in lucerne, and infectivity and ELISA tests have shownthat infective virus incidence decreases rapidly with seed maturation. But the antigenincidence (ELISA test) declined more slowly than the infective virus (Baillis andOffei, 1990). The incidence of infective virus and antigen was higher in seeds ofcultivar Maris Kabul than cultivar Europe. Incidence of seeds with infective AMVdecreased during maturation from 59 to 6.9% in cultivar Maris Kabul and 75 to1.7% in cultivar Europe.SMV is seed-transmitted at frequencies from 0 to 75%, depending on soybeancultivar and the virus strain (Tu, 1989). Bowers and Goodman (1979) found infectionin 94% and 58% of seeds of Midwest (highly seed transmitting cultivar) and Merit(poorly seed transmitting) at physiological seed maturity and 66% and 0.8% atharvest maturity, respectively. SMV was detected in the seed coat and embryos fromimmature seeds of both the cultivars, but in mature seeds it was detected in embryosof Midwest seeds, but not in those of Merit. SMV transmission showed only a slightdecline after storage for 6 months at 14°C.Cheo (1955) observed that during later stages of seed development, SBMVdecreased in the pods and seed coat, but increased in the embryo in Phaseolusvulgaris. During dehydration, the virus in the embryo was inactivated very rapidly,but not in the seed coat. In contrast, BCMV was inactivated in the pod wall andseed coat during maturation and drying in bean. It remained unaffected in the embryoduring maturation, drying, and also storage (Schippers, 1963). BCMV probablysurvives in seeds of navy bean as long as the seeds remain viable.The maize dwarf mosaic virus (MDMV) occurs in large proportions in immaturekernels (70%) from infected plants. MDMV was not detected in mature kernels andthe frequency of detection in the pericarp fell to 2% (Mikel et al., 1982).
222 Histopathology of Seed-Borne InfectionsThe longevity of viruses in seed during storage is also variable. Bennett (1969)has reported that the longevity of different viruses varies from 2 months to 6.5 years.TMV infection in tomato seeds declined rapidly in the first year, but was still presentafter 3 years of storage (Alexander, 1960). Frosheiser (1974) found little loss ofAMV in infected alfalfa seed after 5 years at room temperature. Scott (1961) found64% BSMV-infected seeds in seeds of barley stored for 6.5 years. An extremeexample is the detection of BCMV in a bean seedling grown from seeds after 30years of storage (Pierce and Hungerford, 1929).7.7 CONCLUDING REMARKSThe number of seed-borne and seed-transmitted viruses and viroids is quite large,and the present list (Tables 7.1 to 7.3) includes more than 120 of them. The histopathologicalinvestigations of virus-infected seeds using ultra-thin sections and electronmicroscopy are not only meager, confined to perhaps a dozen virus–seed interfaces,but except for BSMV in barley, the information is insufficient in most casesand often not supported by adequate photomicrographs or diagrams. Although cryptovirusesare only seed- and pollen-transmitted, and seed transmission of viroids islinked with their affinity to meristematic cells, there is virtually no information onhow these pathogens are introduced into the seed. Entry into seed is importantbecause the propagation and distribution of cryptic viruses occur only through cellmultiplication. Likewise, plant infection of more than a dozen viruses results in theproduction of symptomatic seeds (Phatak, 1974; Bos, 1977), but their histopathologyhas remained uninvestigated.The ovules and seeds, borne on the placenta, have contacts with tissues includingthe vascular supply of the pistil. The ovule has both symplastic and apoplasticsystems of transport of nutrients. Adequate histopathological data of infected reproductiveshoot (flower) and fertile floral appendages throughout their developmentallow proper understanding of the infection cycle of seed-transmitting virusesthrough the host (Figures 7.3 and 7.8). The infection of seed-transmitting strains ofBSMV spreads systemically in floral parts and exists in the egg, which developsinto an embryo (Carroll and Mayhew, 1976b; Carroll, 1981). The delayed invasionof ovule and seed by PSbMV is also direct from the mother plant. PSbMV appearsto be slow growing, does not reach the primordia of fertile appendages, and reachesthe ovule primarily through vascular tissue. The embryonic invasion takes placethrough the suspensor (Wang and Maule, 1994; Maule and Wang, 1996). How thevirus antigen traverses the embryo sac wall or the suspensor cell walls from theintegument remains unexplained; Wang and Maule (1994) think that it is unlikelyto occur apoplastically. The lack of histopathological investigation in such cases issorely felt because it could certainly yield corroborative evidence. The histopathologicalobservations on the infection cycle of seed-borne viruses in host plants,particularly the events leading to the infection of sporogenous cells, their survival,the infection of male and female gametophytic phases, and the passage of virus intothe seed and embryo are important, not only to gain insight into host–parasiteinteractions, but also to determine strategies to check the spread of viruses.
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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 238 and 239: Seed Infection by Viruses 223REFERE
Page 240 and 241: Seed Infection by Viruses 225Hunter
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