Submitted to: Applied and Environmental Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/19/2000
Publication Date: N/A
Citation: Interpretive Summary: We are studying the mechanism by which bacteria are able to cause plant disease. Towards this end, we are analyzing the Pseudomonas syringae pv. syringae (the causative agent of brown spot disease of snap bean - an important field disease in Wisconsin) as a model system. We hope to gain an understanding of the molecular biology of the genes and gene products that are required for the disease process. This manuscript describes characterization of the role of the ftsK gene in plant virulence. This gene is required for normal growth in bean plant. The analysis of this gene illustrates the need for bacterial growth on plants as a prerequisite for the disease process. The ultimate impact of this research will be the reduction of environmentally damaging and costly chemical inputs in agriculture. These results will be of interest to scientists who will use it for basic research into the prevention of plant disease.
Technical Abstract: Mutations in the global regulatory genes gacS or gacA render Pseudomonas syringae pv. syringae strain B728a completely avirulent in foliar infiltration assays on bean. It had been previously demonstrate that gac genes regulate alginate production in Pseudomonas species, while other published work indicated a requirement for alginate in the pathogenic interaction of P. syringae on bean. Together, these results suggested that the effects of gacS and gacA mutations on virulence in B728a might stem directly from a role in regulating alginate. In this report, we confirm a role for gac genes in both algD expression and alginate production in B728a. We were unable, however, to demonstrate a role for alginate in pathogenicity, instead finding that B728a mutants completely devoid of detectable alginate were as virulent as wild-type in our assay. Thus, factors other than, or in addition to, a deficiency of alginate must be involved in the avirulence of gacS/gacA mutants.