IraL Is an RssB Anti-adaptor That Stabilizes RpoS during Logarithmic Phase Growth in Escherichia coli and Shigella

ABSTRACT RpoS (σ S ), the general stress response sigma factor, directs the expression of genes under a variety of stressful conditions. Control of the cellular σ S concentration is critical for appropriately scaled σ S -dependent gene expression. One way to maintain appropriate levels of σ S is to regulate its stability. Indeed, σ S degradation is catalyzed by the ClpXP protease and the recognition of σ S by ClpXP depends on the adaptor protein RssB. Three anti-adaptors (IraD, IraM, and IraP) exist in Escherichia coli K-12; each interacts with RssB and inhibits RssB activity under different stress conditions, thereby stabilizing σ S . Unlike K-12, some E. coli isolates, including uropathogenic E. coli strain CFT073, show comparable cellular levels of σ S during the logarithmic and stationary growth phases, suggesting that there are differences in the regulation of σ S levels among E. coli strains. Here, we describe IraL, an RssB anti-adaptor that stabilizes σ S during logarithmic phase growth in CFT073 and other E. coli and Shigella strains. By immunoblot analyses, we show that IraL affects the levels and stability of σ S during logarithmic phase growth. By computational and PCR-based analyses, we reveal that iraL is found in many E. coli pathotypes but not in laboratory-adapted strains. Finally, by bacterial two-hybrid and copurification analyses, we demonstrate that IraL interacts with RssB by a mechanism distinct from that used by other characterized anti-adaptors. We introduce a fourth RssB anti-adaptor found in E. coli species and suggest that differences in the regulation of σ S levels may contribute to host and niche specificity in pathogenic and nonpathogenic E. coli strains. IMPORTANCE Bacteria must cope with a variety of environmental conditions in order to survive. RpoS (σ S ), the general stress response sigma factor, directs the expression of many genes under stressful conditions in both pathogenic and nonpathogenic Escherichia coli strains. The regulation of σ S levels and activity allows appropriately scaled σ S -dependent gene expression. Here, we describe IraL, an RssB anti-adaptor that, unlike previously described anti-adaptors, stabilizes σ S during the logarithmic growth phase in the absence of additional stress. We also demonstrate that iraL is found in a large number of E. coli and Shigella isolates. These data suggest that strains containing iraL are able to initiate σ S -dependent gene expression under conditions under which strains without iraL cannot. Therefore, IraL-mediated σ S stabilization may contribute to host and niche specificity in E. coli.