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Journal of Bacteriology, November 2005, p. 7204-7213, Vol. 187, No. 21
0021-9193/05/$08.00+0     doi:10.1128/JB.187.21.7204-7213.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Stationary-Phase Regulation of RpoS Translation in Escherichia coli

Matthew Hirsch and Thomas Elliott*

Department of Microbiology, Immunology, and Cell Biology, West Virginia University Health Science Center, Morgantown, West Virginia 26506

Received 19 May 2005/ Accepted 15 August 2005

In enteric bacteria, adaptation to a number of different stresses is mediated by the RpoS protein, one of several sigma factors that collectively allow a tailored transcriptional response to environmental cues. Stress stimuli including low temperature, osmotic shock, nutrient limitation, and growth to stationary phase (SP) all result in a substantial increase in RpoS abundance and activity. The mechanism of regulation depends on the specific signal but may occur at the level of transcription, translation, protein activity, or targeted proteolysis. In both Escherichia coli and Salmonella enterica, SP induction of RpoS in rich medium is >30 fold and includes effects on both transcription and translation. Recently, we found that SP control of rpoS transcription in S. enterica involves repression of the major rpoS promoter during exponential phase by the global transcription factor Fis. Working primarily with E. coli, we now show that 24 nucleotides of the rpoS ribosome-binding site (RBS) are necessary and sufficient for a large part of the increase in rpoS translation as cells grow to SP. Genetic evidence points to an essential role for the leader nucleotides just upstream of the Shine-Dalgarno sequence but is conflicted on the question of whether sequence or structure is important. SP regulation of rpoS is conserved between E. coli and S. enterica. When combined with an fis mutation to block transcriptional effects, replacement of the rpoS RBS sequence by the lacZ RBS eliminates nearly all SP induction of RpoS.

* Corresponding author. Mailing address: Department of Microbiology, Immunology, and Cell Biology, West Virginia University Health Science Center, Morgantown, WV 26506. Phone: (304) 293-2676. Fax: (304) 293-7823. E-mail: telliott{at}hsc.wvu.edu.

Journal of Bacteriology, November 2005, p. 7204-7213, Vol. 187, No. 21
0021-9193/05/$08.00+0     doi:10.1128/JB.187.21.7204-7213.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Ranquet, C., Gottesman, S. (2007). Translational Regulation of the Escherichia coli Stress Factor RpoS: a Role for SsrA and Lon. J. Bacteriol. 189: 4872-4879 [Abstract] [Full Text]  
  • Bhagwat, A. A., Tan, J., Sharma, M., Kothary, M., Low, S., Tall, B. D., Bhagwat, M. (2006). Functional Heterogeneity of RpoS in Stress Tolerance of Enterohemorrhagic Escherichia coli Strains.. Appl. Environ. Microbiol. 72: 4978-4986 [Abstract] [Full Text]  


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