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

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.