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Nucleic Acids Research Advance Access originally published online on October 25, 2008
Nucleic Acids Research 2008 36(21):6781-6794; doi:10.1093/nar/gkn742
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Nucleic Acids Research, 2008, Vol. 36, No. 21 6781-6794
© 2008 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Gene regulation, Chromatin and Epigenetics

The 5' end of two redundant sRNAs is involved in the regulation of multiple targets, including their own regulator

Maude Guillier and Susan Gottesman*

Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA

*To whom correspondence should be addressed. Tel: +1 301 496 3524; Fax: +1 301 496 3875; Email: susang{at}helix.nih.gov

Received July 31, 2008. Revised October 1, 2008. Accepted October 3, 2008.

Small RNAs are widespread regulators of gene expression in numerous organisms. This study describes the mode of action of two redundant Escherichia coli sRNAs, OmrA and OmrB, that downregulate the expression of multiple targets, most of which encode outer membrane proteins. Our results show that both sRNAs directly interact with at least two of these target mRNAs, ompT and cirA, in the vicinity of the translation initiation region, consistent with control of these targets being dependent on both Hfq and RNase E. Interestingly, these interactions depend on short stretches of complementarity and involve the conserved 5' end of OmrA/B. A mutation in this region abolishes control of all OmrA/B targets tested thus far, thereby highlighting the crucial role of the OmrA/B 5' end. This allowed us, by looking for mRNA sequences complementary to the OmrA/B 5' end, to identify ompR as an additional direct target of these two sRNAs. Since the OmpR transcriptional regulator activates expression of both omrA and omrB genes, this newly identified control should result in an autoregulatory loop limiting the amount of OmrA/B sRNAs.

Present address: Maude Guillier, UPR 9073 du CNRS, Institut de Biologie Physico-chimique, 13 rue Pierre et Marie Curie, 75005 Paris, France.


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