This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplemental material
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ranquet, C.
Right arrow Articles by Gottesman, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ranquet, C.
Right arrow Articles by Gottesman, S.

 Previous Article  |  Next Article 

Journal of Bacteriology, July 2007, p. 4872-4879, Vol. 189, No. 13
0021-9193/07/$08.00+0     doi:10.1128/JB.01838-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Translational Regulation of the Escherichia coli Stress Factor RpoS: a Role for SsrA and Lon{triangledown} ,{dagger}

Caroline Ranquet{ddagger} and Susan Gottesman*

Laboratory of Molecular Biology, National Cancer Institute, Bethesda, Maryland 20892

Received 7 December 2006/ Accepted 11 April 2007

Escherichia coli cell viability during starvation is strongly dependent on the expression of the rpoS gene, encoding the RpoS sigma subunit of RNA polymerase. RpoS abundance has been reported to be regulated at many levels, including transcription initiation, translation, and protein stability. The regulatory RNA SsrA (or tmRNA) has both tRNA and mRNA activities, relieving ribosome stalling and cotranslationally tagging proteins. We report here that SsrA is needed for the correct high-level translation of RpoS. The ATP-dependent protease Lon was also found to negatively affect RpoS translation, but only at low temperature. We suggest that SsrA may indirectly improve RpoS translation by limiting ribosome stalling and depletion of some component of the translation machinery.


* Corresponding author. Mailing address: Bldg 37, Room 5132, Laboratory of Molecular Biology, National Cancer Institute, Bethesda, MD 20892-4264. Phone: (301) 496-3524. Fax: (301) 496-3875. E-mail: susang{at}helix.nih.gov

{triangledown} Published ahead of print on 20 April 2007.

{dagger} Supplemental material for this article may be found at http://jb.asm.org/.

{ddagger} Present address: Laboratoire Adaptation et Pathogénie des Microorganismes, Institut Jean Roget-Faculté de Mèdecine-Pharmacie, Domaine de la Merci, F-38700 La Tronche, France.


Journal of Bacteriology, July 2007, p. 4872-4879, Vol. 189, No. 13
0021-9193/07/$08.00+0     doi:10.1128/JB.01838-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:

  • Paulander, W., Maisnier-Patin, S., Andersson, D. I. (2009). The Fitness Cost of Streptomycin Resistance Depends on rpsL Mutation, Carbon Source and RpoS ({sigma}S). Genetics 183: 539-546 [Abstract] [Full Text]  
  • Yoshida, H., Ueta, M., Maki, Y., Sakai, A., Wada, A. (2009). Activities of Escherichia coli ribosomes in IF3 and RMF change to prepare 100S ribosome formation on entering the stationary growth phase.. GENES CELLS 14: 271-280 [Abstract] [Full Text]