Quorum sensing-dependent biofilms enhance colonization in Vibrio cholerae

Vibrio cholerae is the causative agent of the diarrheal disease cholera. By an incompletely understood developmental process, V. cholerae forms complex surface-associated communities called biofilms. Here we show that quorum sensing-deficient mutants of V. cholerae produce thicker biofilms than those formed by wild-type bacteria. Microarray analysis of biofilm-associated bacteria shows that expression of the Vibrio polysaccharide synthesis (vps) operons is enhanced in hapR mutants. CqsA, one of two known autoinducer synthases in V. cholerae, acts through HapR to repress vps gene expression. Vibrio biofilms are more acid resistant than planktonic cells. However, quorum sensing-deficient biofilms have lower colonization capacities than those of wild-type biofilms, suggesting that quorum sensing may promote cellular exit from the biofilm once the organisms have traversed the gastric acid barrier of the stomach. These results shed light on the relationships among biofilm development, quorum sensing, infectivity, and pathogenesis in V. cholerae.     

Steps in the development of a Vibrio cholerae El Tor biofilm

We report that, in a simple, static culture system, wild-type Vibrio cholerae El Tor forms a three-dimensional biofilm with characteristic water channels and pillars of bacteria. Furthermore, we have isolated and characterized transposon insertion mutants of V. cholerae that are defective in biofilm development. The transposons were localized to genes involved in (i) the biosynthesis and secretion of the mannose-sensitive haemagglutinin type IV pilus (MSHA); (ii) the synthesis of exopolysaccharide; and (iii) flagellar motility. The phenotypes of these three groups suggest that the type IV pilus and flagellum accelerate attachment to the abiotic surface, the flagellum mediates spread along the abiotic surface, and exopolysaccharide is involved in the formation of three-dimensional biofilm architecture.     

Parallel quorum sensing systems converge to regulate virulence in Vibrio cholerae

The marine bacterium Vibrio harveyi possesses two quorum sensing systems (System 1 and System 2) that regulate bioluminescence. Although the Vibrio cholerae genome sequence reveals that a V. harveyi-like System 2 exists, it does not predict the existence of a V. harveyi-like System 1 or any obvious quorum sensing-controlled target genes. In this report we identify and characterize the genes encoding an additional V. cholerae autoinducer synthase and its cognate sensor. Analysis of double mutants indicates that a third as yet unidentified sensory circuit exists in V. cholerae. This quorum sensing apparatus is unusually complex, as it is composed of at least three parallel signaling channels. We show that in V. cholerae these communication systems converge to control virulence.