Submitted to: Molecular Plant-Microbe Interactions
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: July 20, 2000
Publication Date: N/A
Interpretive Summary: We are studying the mechanism by which bacteria are able to cause plant disease. Towards this end, we are analyzing 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 paper describes the characterization of the role of a bacterial gene in plant disease.This gene is required for normal growth of bacteria in bean plants. The analysis of this gene illustrates the need for bacterial growth on plants as a prerequisite for the disease process. 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. The ultimate impact of this research will be the reduction of environmentally damaging and costly chemical inputs in agriculture.
KW3815, a previously identified Tn5 insertion mutant of the snap bean pathogen Pseudomonas syringae pv. syringae B728a, was subjected to further analysis. The mutant was initially identified in a screen for loss of the ability to form bacterial brown spot lesions. It was subsequently found that KW3815 is also impaired in its ability to grow when infiltrated into leaves of its susceptible host, Phaseolus vulgaris, in growth chamber assays, as well as for swarming on semisolid agar. The point of insertion of the Tn5 is in the P. syringae analog of ftsK/spoIIIE , a gene family previously described as being involved in spore formation, cell division, and stress tolerance. The gene order of the region of insertion is aat-ftsK lolA-ORF1-ORF2-serS, with ORF1 being a probable gene of unknown function that is highly conserved in both prokaryotes and eukaryotes. Subclones of the ftsK region containing only the intact ftsK gene are sufficient to complement the original Tn5 mutant for lesion formation, in planta growth, and swarming.