This Article Full Text (PDF) Other Versions of this Article: JB.01756-07v1 190/7/2527    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Waters, C. M. Articles by Bassler, B. L. Search for Related Content PubMed PubMed Citation Articles by Waters, C. M. Articles by Bassler, B. L.

 Previous Article  |  Next Article 

J. Bacteriol. doi:10.1128/JB.01756-07
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Quorum Sensing Controls Biofilm Formation in Vibrio cholerae through Modulation of Cyclic Di-GMP Levels and Repression of vpsT

Departments of Molecular Biology and Chemistry, and Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, NJ 08544, USA; Howard Hughes Medical Institute, Chevy Chase, MD 20815-6789, USA

^* To whom correspondence should be addressed. Email: bbassler{at}princeton.edu.

	Abstract

Two chemical signaling systems, quorum sensing (QS) and 3',5'-cyclic diguanylic acid (c-di-GMP), reciprocally control biofilm formation in Vibrio cholerae. QS is the process by which bacteria communicate via the secretion and detection of autoinducers, and in V. cholerae, QS represses biofilm formation. C-di-GMP is an intracellular second messenger that contains information regarding local environmental conditions, and in V. cholerae, c-di-GMP activates biofilm formation. Here we show that HapR, a major regulator of QS, represses biofilm formation in V. cholerae through two distinct mechanisms. HapR controls transcription of fourteen genes encoding a group of proteins that synthesize and degrade c-di-GMP. The net effect of this transcriptional program is a reduction in cellular c-di-GMP levels at high cell density, and consequently a decrease in biofilm formation. Increasing c-di-GMP concentration at high cell density to the level present in the low-cell-density QS state restores biofilm formation, showing that c-di-GMP is epistatic to QS in the control of biofilm formation in V. cholerae. Additionally, HapR binds to and directly represses expression of the biofilm transcriptional activator, vpsT. Together, our results suggest that V. cholerae integrates information about the vicinal bacterial community contained in extracellular QS autoinducers with the intracellular environmental information encoded in c-di-GMP to control biofilm formation.

This article has been cited by other articles:

• Fong, J. C. N., Yildiz, F. H. (2008). Interplay between Cyclic AMP-Cyclic AMP Receptor Protein and Cyclic di-GMP Signaling in Vibrio cholerae Biofilm Formation. J. Bacteriol. 190: 6646-6659 [Abstract] [Full Text]