A negative feedback loop involving small RNAs accelerates Vibrio cholerae's transition out of quorum-sensing mode.

TitleA negative feedback loop involving small RNAs accelerates Vibrio cholerae's transition out of quorum-sensing mode.
Publication TypeJournal Article
Year of Publication2008
AuthorsSvenningsen, SL, Waters, CM, Bassler, BL
JournalGenes Dev
Volume22
Issue2
Pagination226-38
Date Published2008 Jan 15
ISSN0890-9369
KeywordsBacterial Proteins, Base Sequence, Feedback, Molecular Sequence Data, Quorum Sensing, RNA, Bacterial, Signal Transduction, Vibrio cholerae
Abstract

<p>Quorum sensing is a cell-to-cell communication process that allows bacteria to measure their population numbers and to synchronously alter gene expression in response to changes in cell population density. At the core of the Vibrio cholerae quorum-sensing signal transduction pathway lie four redundant small RNAs (sRNAs), named the Quorum Regulatory RNAs (Qrr1-4). Expression of qrr1-4 is cell population density-dependent due to a requirement for the quorum-sensing controlled phosphorylated response regulator LuxO-P, which is abundant only at low cell population density. When expressed, Qrr1-4 repress translation of HapR, the "master" quorum-sensing transcription factor. Here we show a negative feedback loop in which HapR activates transcription of the qrr genes, which indirectly leads to hapR repression. Efficient feedback activation of the qrr genes requires the simultaneous presence of LuxO-P (present only at low cell population density) and HapR (present only at high cell population density). For this reason, the feedback loop does not influence quorum sensing at steady-state low or high cell population density. However, LuxO-P and HapR are simultaneously present immediately following the switch from high to low cell density conditions. In this state, the HapR feedback loop dramatically accelerates V. cholerae's transition from the high to the low cell density mode.</p>

DOI10.1101/gad.1629908
Alternate JournalGenes Dev.
PubMed ID18198339
PubMed Central IDPMC2192756
Grant List5R01 GM 065859 / GM / NIGMS NIH HHS / United States