Mapping of the seed transmission determinants of barley stripe mosaic virus

The specific mechanism(s) by which some plant viruses are transmitted through seed, while others are excluded, is not known. Using infectious barley stripe mosaic virus (BSMV) RNAs transcribed in vitro from full-length cDNA clones, the viral genetic determinants of seed transmission have been mapped. Both pseudorecombinant and chimeric viruses were constructed from BSMV strains ND18 (seed transmitted) and CV17 (not seed transmitted). The markedly different seed transmissibility of these two strains facilitated the identification of RNAgamma as the location of the primary determinants of seed transmission phenotype. RNAbeta also played a role in seed transmission, but to a lesser extent than RNAgamma. Major genetic determinants of seed transmission on RNAgamma included the 5' untranslated leader, a 369-nt repeat in the gammaa gene, and the gammab gene. Important determinants of symptom phenotype mapped to the RNAgamma leader and the gammab gene as well. Some heterologous combinations of the RNAgamma leader and the gammab gene resulted in dramatic changes in symptomatology and seed transmission, depending on the parental source of RNAs alpha and beta. These results suggest that a complex interaction of the RNAgamma leader, the gammab gene, and RNAs alpha and beta are involved in BSMV pathogenesis. Considering the putative regulatory role of the gamma gene (Donald and Jackson 1994, Plant Cell 6:1593-1606) and the trans effects that alterations in the gammab gene have on RNAbeta gene expression (Petty et al., 1990, EMBO J. 9:3453-3457), phenotypic effects attributed to elements of RNAgamma could result from cis or trans interactions involving the RNAgamma leader, the gammab gene, and RNAs alpha and beta. Clearly, virus replication and movement play pivotal roles in the seed transmission of BSMV.