Sigma E controls biogenesis of the antisense RNA MicA.

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 sigma factor involvement, yet MicA accumulates in the absence of the general stress/stationary phase sigma(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 sigma(E) is activated. The strict dependence of micA transcription on sigma(E) is supported by three observations. Induced overexpression of sigma(E) increases micA transcription, an DeltarpoE mutant displays undetectable MicA levels and the micA promoter has the consensus sigma(E) signature. Thus, MicA is part of the sigma(E) regulon and downregulates its target gene, ompA, probably to alleviate membrane stress.