Abstract
Bacteria can rapidly and reversibly respond to changing environments via complex transcriptional and post-transcriptional regulatory mechanisms. Many of these adaptations are specific, with the regulatory output tailored to the inducing signal (for instance, repairing damage to cell components or improving acquisition and use of growth-limiting nutrients). However, the general stress response, activated in bacterial cells entering stationary phase or subjected to nutrient depletion or cellular damage, is unique in that its common, broad output is induced in response to many different signals. In many different bacteria, the key regulator for the general stress response is a specialized sigma factor, the promoter specificity subunit of RNA polymerase. The availability or activity of the sigma factor is regulated by complex regulatory circuits, the majority of which are post-transcriptional. In Escherichia coli, multiple small regulatory RNAs, each made in response to a different signal, positively regulate translation of the general stress response sigma factor RpoS. Stability of RpoS is regulated by multiple anti-adaptor proteins that are also synthesized in response to different signals. In this review, the modes of signaling to and levels of regulation of the E. coli general stress response are discussed. They are also used as a basis for comparison with the general stress response in other bacteria with the aim of extracting key principles that are common among different species and highlighting important unanswered questions.
Highlights
Bacteria can rapidly and reversibly respond to changing environments via complex transcriptional and post-transcriptional regulatory mechanisms
In the environment, bacteria will generally not be in the type of rich and uncrowded conditions we provide in the lab, and many bacteria may be in a stationary phase-like state for much of the time
The gene for rpoS is downstream from nlpD, encoding an outer membrane lipoprotein involved in cell division via an effect on peptidoglycan metabolism, and the primary promoter for rpoS is embedded in the middle of nlpD (Fig. 2) [19]
Summary
The definition I will use here for a general stress response requires evidence that, upon induction by a given stress, cells become resistant to multiple stress treatments that are, to the best of our current knowledge, in different repair or adaptation pathways than the response to the original inducing stress. If the sigma factor is needed rapidly, under conditions when energy and nutrients are running out, it may be very useful for the cell to have the sigma factor ready for activation when it is needed, rather than starting the induction process when a stress is encountered with new transcription and translation. In E. coli K12, the lab strain that has been most studied, RpoS ( called S or 38) is the sigma factor that mediates the general stress response, called the stationary phase response. Over the 25 years since that paper, experiments by many groups have uncovered some of the pathways for each of these levels of regulation, but we are still far from a full understanding of the ways in which cells induce and recover from the general stress response
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