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Journal of Bacteriology, February 2006, p. 1049-1059, Vol. 188, No. 3
0021-9193/06/$08.00+0 doi:10.1128/JB.188.3.1049-1059.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Department of Environmental Toxicology,1 Center for Biomolecular Science and Engineering, University of California at Santa Cruz, Santa Cruz, California 95064,2 Department of Medicine, Division of Infectious Diseases and Geographic Medicine, and Department of Microbiology and Immunology, Stanford University Medical School, Stanford, California 943053
Received 29 July 2005/ Accepted 14 November 2005
Phase variation between smooth and rugose colony variants of Vibrio cholerae is predicted to be important for the pathogen's survival in its natural aquatic ecosystems. The rugose variant forms corrugated colonies, exhibits increased levels of resistance to osmotic, acid, and oxidative stresses, and has an enhanced capacity to form biofilms. Many of these phenotypes are mediated in part by increased production of an exopolysaccharide termed VPS. In this study, we compared total protein profiles of the smooth and rugose variants using two-dimensional gel electrophoresis and identified one protein that is present at a higher level in the rugose variant. A mutation in the gene encoding this protein, which does not have any known homologs in the protein databases, causes cells to form biofilms that are more fragile and sensitive to sodium dodecyl sulfate than wild-type biofilms. The results indicate that the gene, termed rbmA (rugosity and biofilm structure modulator A), is required for rugose colony formation and biofilm structure integrity in V. cholerae. Transcription of rbmA is positively regulated by the response regulator VpsR but not VpsT.
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