Submitted to: Molecular Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/27/1998
Publication Date: N/A
Citation: N/A 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. Ultimately, this understanding will provide information of use to breeders and plant molecular biologists that will enable them to develop plant lines resistant to disease organisms through the alteration of specific plant products that are required by the pathogen. This manucsript describes the isolation of a novel gene that regulates the ability of P. syringae pv. syringae to cause disease on bean. The analysis of this gene will identify additional genes required for the disease process.
Technical Abstract: The lemA and gacA genes encode members of a widely conserved two- component regulatory system that in Pseudomonas syringae pv. syringae strain B728a is required for lesion formation on snap bean, as well as for production of protease and the toxin syringomycin. A gene was discovered which, when present on a multiple-copy plasmid, restored syringomycin production to a lemA mutant. Disruption of the gene on the B728a chromosome resulted in loss of syringomycin production and lesion formation in laboratory assays. Sequence analysis of the gene, designated salA, suggests that it encodes a novel DNA-binding protein. Chromosomal reporter fusions revealed that lemA and gacA positively regulate salA , that salA upregulates its own expression, and that salA positively regulates the expression of a reported syringomycin biosynthetic gene, syrB. Loss of syringomycin production does not account for the salA mutant's attenuated pathogenicity, since a syrB mutant was found to retain full virulence. A homoserine lactone activity was detected that was dependent upon lemA and gacA for expression, but was unaffected by disruption of the salA gene. We have thus identified a novel regulator that activates the expression of a subset of lemA-regulated genes necessary for toxin production and lesion formation.