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

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<strong>Seed</strong> Infection by Viruses 2177.4.2 BEAN COMMON MOSAIC VIRUS (BCMV)Early infection <strong>of</strong> BCMV on bean plants causes necrosis and dropping <strong>of</strong> buds. Thepistils at the ovule primordial stage lack virus particles, but these could be detected4 or 5 days before flowering when the ovules contain the eight-nucleate embryo sac.Infectious virus reaches the ovules 2 or 3 days before flowering. Cross-pollinationexperiments using pollen and pistils <strong>of</strong> infected plants have shown that the embryomight get infection from infected eggs or pollen grains (Schippers, 1963). BCMVhas been reported in immature and mature seeds from infected plants. It occurs inthe cotyledons and plumule (Ekpo and Saettler, 1974).BCMV has also been reported in embryos <strong>of</strong> urdbean (Vigna mungo) and cowpea(Vigna unquiculata) by Agarwal, Nene, and Beniwal (1979) and Patil and Gupta(1992), respectively.7.4.3 LETTUCE MOSAIC VIRUS (LMV)LMV particles are seen throughout the ovary and ovular tissues, except the embryosac, in infected plants <strong>of</strong> lettuce cultivar Salinas. High levels <strong>of</strong> LMV infection occurin the integumentary tapetum (Hunter and Bowyer, 1994). In mature seeds (cypsil),LMV particles occur in the endosperm (Figure 7.7D), cotyledons (Figure 7.7E),hypocotyl-radicle axis, and pericarp (Figure 7.7A to C). The virus particles are eitherscattered in the cytoplasm (Figure 7.7C) or seen in association with protein bodies.Cylindrical and pinwheel-shaped cytoplasmic inclusions have been observed in thecells <strong>of</strong> the integument, ovary wall, endosperm (Figure 7.7D), and embryo(Figure 7.7E, F), but not in those <strong>of</strong> the pericarp (Hunter and Bowyer, 1993, 1994).7.4.4 PEA SEED-BORNE MOSAIC VIRUS (PSBMV)Figure 7.8 gives a schematic representation <strong>of</strong> the infection cycle <strong>of</strong> PSbMV in ahigh seed-transmitting cultivar <strong>of</strong> pea. The virus infection in unfertilized flowersoccurs in sepals, petals, anther-epidermis, and carpel, but none in the pollen grainsand ovule except the funiculus (Wang and Maule, 1992, 1994). In fertilized ovules,the virus antigen was initially detected in cells close to the vascular supply <strong>of</strong> theovule, from where it spread throughout the integument. Subsequently, it reached theendospermic fluid and suspensor <strong>of</strong> the embryo. In the embryo proper, in spite <strong>of</strong>abundant virus in the embryo sac fluid, the infection was seen initially in cells thatwere in contact with the suspensor, indicating that it had traversed through thesuspensor (Wang and Maule, 1994). The spread <strong>of</strong> infection <strong>of</strong> PSbMV from carpelto embryo clearly shows that the virus enters the ovule through the funiculus,probably via its vascular supply. From the ovular supply it spreads in the integumentin permissive cultivar–virus interaction systems as in cultivar Vedette. Finally, thevirus enters the embryo with the suspensor as its main route (Figure 7.9A). In acultivar with a nonpermissive interaction, e.g., cultivar Progreta, virus enters theovule through the funicular vascular supply, but is unable to invade the cells <strong>of</strong> theintegument in the nonvascular region. Thus, the infection fails to reach the micropyleregion crucial for the transmission <strong>of</strong> virus to the embryo via suspensor (Figure 7.9B).Although it is shown that the transmission <strong>of</strong> PSbMV occurs exclusively through

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