Abstract
The general stress sigma factor RpoS (sigma s) is induced during entry into stationary phase and in response to multiple stress conditions. RpoS is regulated at the levels of transcription, translation, proteolysis and protein activity. A key factor in RpoS control is the two-component response regulator RssB, which acts as a direct recognition and targeting factor for ClpXP-mediated RpoS proteolysis. A major, but not the only phosphodonor for RssB is the complex histidine sensor kinase ArcB. ArcB coordinates RpoS proteolysis with rpoS transcription by also phosphorylating the response regulator ArcA, which besides controlling a large regulon, also acts as a transcriptional repressor for rpoS. ArcB activity depends on the redox state of the respiratory chain, which links RpoS control to the balance between energy supply and available respiratory electron acceptor. In addition, the BarA/UvrY and Rcs phosphorelay systems can activate rpoS transcription and translation, respectively. These systems are involved in the control of motility, biofilm formation and/or virulence, suggesting that further studying a potential role of RpoS in these physiological functions may be rewarding.
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