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The LysR‐type transcriptional regulator, CidR, regulates stationary phase cell death in Staphylococcus aureus
Author(s) -
Chaudhari Sujata S.,
Thomas Vinai C.,
Sadykov Marat R.,
Bose Jeffrey L.,
Ahn Daniel J.,
Zimmerman Matthew C.,
Bayles Kenneth W.
Publication year - 2016
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/mmi.13433
Subject(s) - regulon , biology , operon , acetoin , staphylococcus aureus , regulator , transcriptional regulation , microbiology and biotechnology , regulation of gene expression , gene , transcription factor , genetics , escherichia coli , bacteria
Summary The Staphylococcus aureus LysR‐type transcriptional regulator, CidR, activates the expression of two operons including cidABC and alsSD that display pro‐ and anti‐death functions, respectively. Although several investigations have focused on the functions of different genes associated with these operons, the collective role of the CidR regulon in staphylococcal physiology is not clearly understood. Here we reveal that the primary role of this regulon is to limit acetate‐dependent potentiation of cell death in staphylococcal populations. Although both CidB and CidC promote acetate generation and cell death, the CidR‐dependent co‐activation of CidA and AlsSD counters the effects of CidBC by redirecting intracellular carbon flux towards acetoin formation. From a mechanistic standpoint, we demonstrate that CidB is necessary for full activation of CidC, whereas CidA limits the abundance of CidC in the cell.