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Title: A PATHOGENICITY ISLAND ADRIFT? OVER-PRODUCTION OF TABTOXININE-B-LACTAM BY A CARNOSINASE MUTANT OF PSEUDOMONAS SYRINGAE BR2

Author
item KINSCHERF, THOMAS - UNIVERSITY OF WISCONSIN
item SAVAGE, A - UNIVERSITY OF WISCONSIN
item NARITA, E - UNIVERSITY OF WISCONSIN
item Willis, David

Submitted to: American Society for Microbiology
Publication Type: Abstract Only
Publication Acceptance Date: 6/1/1999
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Pseudomonas syringae BR2 causes wildfire disease on snap bean by virtue of its production of the b-lactam antibiotic tabtoxinine-b-lactam (TBL), better known by the name of the immediate toxin precursor, tabtoxin. The genes for tabtoxin production reside on a genetically dynamic region of the BR2 chromosome that fits the criteria for what are described as 'pathogenicity islands' in a variety of bacteria. A transposo mutant of BR2 was isolated that appeared to over-produce toxin as measured by bioassay with E. coli. The transposon insertion site was cloned and identified as an ortholog of a gene for carnosinase, a type of dipeptidase that can often hydrolyze multiple small peptide substrates. Southern hybridization analysis indicated that the BR2 carnosinase gene resides outside the tabtoxin pathogenicity island in the BR2 chromosome. Transconjugants that carried the BR2 carnosinase gene on a plasmid produced less tabtoxin than wild-type BR2 in both the BR2 and the over- producing mutant genetic backgrounds. Transconjugants of mutants deleted for the pathogenicity island that now carried plasmid copies of the carnosinase gene did not acquire resistance to TBL. Taken together, these results suggest that an endogenous carnosinase activity of BR2 degrades tabtoxin and/or one or more of the intermediates in the tabtoxin biosynthetic pathway before toxin release into the extracellular environment, rendering the process of tabtoxin production in BR2 inefficient to a point that raises intriguing questions about pathogen evolution.