Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Mol Microbiol. 2003 Jul;49(1):1-9.

Control of rpoS transcription in Escherichia coli and Pseudomonas: why so different?

Author information

  • Bacteriology Group, International Centre for Genetic Engineering and Biotechnology, Area Science Park, Padriciano 99, 34012 Trieste, Italy. venturi@icgeb.org

Abstract

In Escherichia coli, the stationary phase alternative sigma factor sigmas controls the expression of genes involved cell survival in response to cessation of growth (stationary phase) and provides cross-protection to various stresses. Levels of sigmas increase dramatically at the onset of stationary phase and are regulated at the transcriptional, post-transcriptional and post-translational level, making this one of the most complex regulatory systems in bacteria. The basic mechanisms for the control of translation and sigmas proteolysis have been understood. However, studies on the transcriptional control in E. coli lag behind and are controversial. The cAMP-CRP complex and the two component BarA/UvrY system have been implicated and, ppGpp and polyphosphate appear to have a signalling role. sigmas has also been reported to be a general stress regulator in the fluorescent pseudomonads (Pseudomonas aeruginosa, P. fluorescens and P. putida) and recent studies on sigmas regulation highlight that transcriptional regulation in these bacteria apparently plays a major role. Global regulatory systems, the GacA/GacS two component system and quorum sensing all affect rpoS expression, as does the TetR family PsrA regulator that directly binds to- and activates the rpoS promoter in stationary phase. This striking difference in regulation between E. coli and Pseudomonas can be partly attributed to the differences in the functional role of sigmas in the two bacterial species. This report will review mainly recent studies on rpoS transcriptional regulation and will try to rationalize the current knowledge into a working model.

PMID:
12823806
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Icon for Blackwell Publishing
    Loading ...
    Write to the Help Desk