Nucleic Acids Research Advance Access published online on January 31, 2007
Nucleic Acids Research, doi:10.1093/nar/gkl1154
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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 growth—a 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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