The small nucleoid protein Fis is involved in Vibrio cholerae quorum sensing.

TitleThe small nucleoid protein Fis is involved in Vibrio cholerae quorum sensing.
Publication TypeJournal Article
Year of Publication2007
AuthorsLenz, DH, Bassler, BL
JournalMol Microbiol
Volume63
Issue3
Pagination859-71
Date Published2007 Feb
ISSN0950-382X
KeywordsFactor For Inversion Stimulation Protein, Gene Expression Regulation, Bacterial, Genetic Complementation Test, Promoter Regions, Genetic, Quorum Sensing, Repressor Proteins, RNA, Bacterial, Signal Transduction, Vibrio cholerae
Abstract

<p>Quorum sensing is a process of cell-cell communication that bacteria use to relay information to one another about the cell density and species composition of the bacterial community. Quorum sensing involves the production, secretion and population-wide detection of small signalling molecules called autoinducers. This process allows bacteria to synchronize group behaviours and act as multicellular units. The human pathogen, Vibrio cholerae, uses quorum sensing to co-ordinate such complex behaviours as pathogenicity and biofilm formation. The quorum-sensing circuit of V. cholerae consists of two autoinducer/sensor systems, CAI-1/CqsS and AI-2/LuxPQ, and the VarS/A-CsrA/BCD growth-phase regulatory system. Genetic analysis suggests that an additional regulatory arm involved in quorum sensing exists in V. cholerae. All of these systems channel information into the histidine phosphotransfer protein, LuxU, and/or the response regulator, LuxO. LuxO, when phosphorylated, activates the expression of four genes encoding the Qrr (quorum regulatory RNAs) small RNAs (sRNAs). The Qrr sRNAs destabilize the hapR transcript encoding the master regulator of quorum sensing, HapR. Here we identify the nucleoid protein Fis as playing a major role in the V. cholerae quorum-sensing circuit. Fis fulfils the predictions required to be the putative additional component that inputs information into the cascade: its expression is regulated in a growth phase-dependent manner; it requires LuxO but acts independently of LuxU, and it regulates all four qrr genes and, in turn, HapR by directly binding to the qrr gene promoters and modulating their expression.</p>

DOI10.1111/j.1365-2958.2006.05545.x
Alternate JournalMol. Microbiol.
PubMed ID17181781
Grant List5R01 G065859 / / PHS HHS / United States