| From a microbial perspective, the urinary tract is a stressful environment. Here, the chemical composition of urine, the host immune system, and a number of physical deterrents discourage the colonization and growth of microorganisms. Uropathogenic Escherichia coli (UPEC) strains, however, are able to overcome these stresses and colonize this environment. RpoS (sigma s), the general stress response sigma factor, directs the expression of genes in response to a variety of stressful conditions. About 10% of the genes in laboratory adapted E. coli K-12 are regulated by sigma s, either directly or indirectly. Here, we show that one of our previously used "wild type" stocks of UPEC strain CFT073 lacks functional rpoS . We subsequently show that sigmaS is needed by UPEC to cope with phagocyte oxidase-mediated oxidative stress during UTI and provide evidence that sigmaS -dependent genes may mitigate other stresses during UTI. A complex regulatory network exists to control sigma S levels and activity, commensurate with the magnitude and type of stress encountered. A manifestation of this regulatory network in K-12 is that levels of sigmaS are low during logarithmic phase growth and increase into and during stationary phase. Unlike K-12, CFT073 has comparable levels of sigmaS during both of these growth phases. We describe IraL, a novel RssB anti-adaptor that stabilizes sigmaS during logarithmic phase growth in CFT073. We show that iraL is present in many Escherichia and Shigella strains and that iraL is found more commonly in some pathotypes than others, suggesting that IraL-mediated sigmaS stabilization contributes to host and niche specificity of E. coli. Many genes are differentially regulated during logarithmic phase growth by sigma S and IraL, including the hyperosmotically inducible gene osmY. We demonstrate that osmY expression is affected by sigmaS and IraL under hyperosmotic stress and discuss future directions to study of IraL-mediated sigmaS stabilization, its regulation, and its physiological effects. Taken together, this work establishes a role for sigmaS during UTI, introduces the RssB anti-adaptor IraL, and suggests that strains containing iraL are able to respond to changes in environmental conditions differently from those without iraL. |
