Submitted to: Molecular Plant-Microbe Interactions
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/10/1995
Publication Date: N/A
Citation: N/A Interpretive Summary: Many plant-infecting viruses are capable of being transmitted from parent to progeny via the seed. A number of these viruses cause economically significant damage to crops. Thus, this mode of transmission can be of considerable economic importance in addition to being an important means of virus survival and spread in nature. Still, most viruses are not seed- transmitted. The specific mechanism by which some plant viruses are transmitted through seed, while others are excluded, is not known. Genetic tests designed to identify the viral genes which control seed transmission may aid in the discovery of this mechanism. This research was designed to determine the genes or parts of genes of barley stripe mosaic virus (BSMV) which determine its seed transmissibility in barley. By crossing BSMV strains which differ greatly in their ability to be seed transmitted, we were successful in identifying these specific portions of the BSMV genome. Our results uncovered some possible complex interactions among viral gene products and suggested that virus replication and movement play key roles in seed transmission of BSMV. Virus strains incapable of significant seed transmission in barley are apparently excluded from the plant reproductive tissues which provide the critical gateway to infection of the progeny.
Technical Abstract: 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 RNA gamma as the location of the primary determinants of seed transmission phenotype. RNA beta also played a role in seed transmission, but to a lesser extent than RNA gamma. Major genetic determinants of seed transmission on RNA gamma included the 5' untranslated leader, a 369nt repeat in the gamma-a gene, and the gamma-b gene. Important determinants of symptom phenotype mapped to the RNA gamma leader and the gamma-b gene as well. Some heterologous combinations of the RNA gamma leader and the gamma-b 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 RNA gamma leader, the gamma-b gene, and RNAs alpha and beta are involved in BSMV pathogenesis. Considering the putative regulatory role of the gamma-b gene and the trans effects that alterations in the gamma-b gene have on RNA beta gene expression, phenotypic effects attributed to elements of RNA gamma could result from cis or trans interactions involving the RNA gamma leader, the gamma-b gene, and RNAs alpha and beta. Clearly, virus replication and movement play pivotal roles in the seed transmission of BSMV.