Nucleic Acids Research Advance Access originally published online on January 31, 2007
Nucleic Acids Research 2007 35(4):1279-1288; doi:10.1093/nar/gkl1154
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Nucleic Acids Research, 2007, Vol. 35, No. 4 1279-1288
© 2007 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.
RNA |
Sigma E controls biogenesis of the antisense RNA MicA
Department of Cell & Molecular Biology, Uppsala university, Biomedical Center, Box 596, S-75124 Uppsala, Sweden
*To whom correspondence should be addressed. Tel: +46 18 471 4579; Fax: +46 18 530396; Email: klas.udekwu{at}icm.uu.se Correspondence may also be addressed to E.Gerhart H.Wagner. Tel: +46 18 471 4579; Fax: +46 18 530396; E-mail: gerhart.wagner{at}icm.uu.se
Received October 30, 2006. Revised November 29, 2006. Accepted December 18, 2006.
Adaptation stress responses in the Gram-negative bacterium Escherichia coli and its relatives involve a growing list of small regulatory RNAs (sRNAs). Previous work by us and others showed that the antisense RNA MicA downregulates the synthesis of the outer membrane protein OmpA upon entry into stationary phase. This regulation is Hfq-dependent and occurs by MicA-dependent translational inhibition which facilitates mRNA decay. In this article, we investigate the transcriptional regulation of the micA gene. Induction of MicA is dependent on the alarmone ppGpp, suggestive of alternative
factor involvement, yet MicA accumulates in the absence of the general stress/stationary phase
S. We identified stress conditions that induce high MicA levels even during exponential growtha phase in which MicA levels are low (ethanol, hyperosmolarity and heat shock). Such treatments are sensed as envelope stress, upon which the extracytoplasmic sigma factor
E is activated. The strict dependence of micA transcription on
E is supported by three observations. Induced overexpression of
E increases micA transcription, an
rpoE mutant displays undetectable MicA levels and the micA promoter has the consensus
E signature. Thus, MicA is part of the
E regulon and downregulates its target gene, ompA, probably to alleviate membrane stress.
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