Quorum sensing controls biofilm formation in Vibrio cholerae through modulation of cyclic di-GMP levels and repression of vpsT.

TitleQuorum sensing controls biofilm formation in Vibrio cholerae through modulation of cyclic di-GMP levels and repression of vpsT.
Publication TypeJournal Article
Year of Publication2008
AuthorsWaters, CM, Lu, W, Rabinowitz, JD, Bassler, BL
JournalJ Bacteriol
Date Published2008 Apr
KeywordsBacterial Proteins, Biofilms, Cyclic GMP, Electrophoretic Mobility Shift Assay, Flow Cytometry, Gene Expression Regulation, Bacterial, Green Fluorescent Proteins, Models, Biological, Protein Binding, Quorum Sensing, Trans-Activators, Vibrio cholerae

<p>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 the transcription of 14 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 the 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. In addition, HapR binds to and directly represses the 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.</p>

Alternate JournalJ Bacteriol
PubMed ID18223081
PubMed Central IDPMC2293178
Grant ListR01 GM065859 / GM / NIGMS NIH HHS / United States
5R01GM065859 / GM / NIGMS NIH HHS / United States
/ HHMI / Howard Hughes Medical Institute / United States
F32-AI0586492 / AI / NIAID NIH HHS / United States