FIGURE 2.

The role of sRNAs in the major envelope stress responses. Gram-negative bacteria are diderm, with the OM and IM being separated by the periplasmic space containing the PG cell wall. (A) OM homeostasis is regulated by the RpoE response. A series of proteolysis steps results in the degradation of the anti-sigma factor RseA and concomitant release of RpoE. The large regulon of the alternative sigma factor also comprises at least three sRNAs: MicA and RybB function to downregulate the transcripts of all major OMPs to reduce the accumulation of misfolded porins within the periplasm. MicL specifically represses translation of the lpp mRNA. (B) Maintenance of the IM relies on the CpxA-CpxR TCS, which amongst other targets controls expression of at least three sRNAs, CyaR, RprA, and CpxQ. CpxQ is a stable fragment released by RNase E processing from the 3′ end of the cpxP mRNA. In association with Hfq, CpxQ functions to repress translation of several transcripts including skp mRNA, which encodes a periplasmic chaperone promoting the mistargeting of OMPs into the IM. (C) The IM-associated histidine kinase RcsC, phosphotransfer protein RcsD, and response regulator RcsB constitute the core of the Rcs system. The sRNA RprA is one highly induced component of the Rcs response, which is activated by LPS damage and perturbations of the cell wall. While acting as a negative regulator of the csgD mRNA, RprA also promotes translation of both the rpoS and the ricI messages. As transcription of ricI (encoding an inhibitor of the conjugation machinery) is dependent on RpoS, RprA functions at the heart of a posttranscriptional feedforward loop for RicI activity.