IraL Is an RssB Anti-adaptor That Stabilizes RpoS during Logarithmic Phase Growth in <named-content content-type="genus-species">Escherichia coli</named-content> and <italic toggle="yes">Shigella</italic>
ABSTRACT RpoS (σS), the general stress response sigma factor, directs the expression of genes under a variety of stressful conditions. Control of the cellular σS concentration is critical for appropriately scaled σS-dependent gene expression. One way to maintain appropriate levels of σS is to regula...
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| Autores principales: | , , , , |
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| Formato: | article |
| Lenguaje: | EN |
| Publicado: |
American Society for Microbiology
2014
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| Materias: | |
| Acceso en línea: | https://doaj.org/article/d4bf849e8bcb4c15960b7f487ac758ce |
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| Sumario: | ABSTRACT RpoS (σS), the general stress response sigma factor, directs the expression of genes under a variety of stressful conditions. Control of the cellular σS concentration is critical for appropriately scaled σS-dependent gene expression. One way to maintain appropriate levels of σS is to regulate its stability. Indeed, σS degradation is catalyzed by the ClpXP protease and the recognition of σS 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 σS. Unlike K-12, some E. coli isolates, including uropathogenic E. coli strain CFT073, show comparable cellular levels of σS during the logarithmic and stationary growth phases, suggesting that there are differences in the regulation of σS levels among E. coli strains. Here, we describe IraL, an RssB anti-adaptor that stabilizes σS 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 σS 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 σS 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 (σS), 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 σS levels and activity allows appropriately scaled σS-dependent gene expression. Here, we describe IraL, an RssB anti-adaptor that, unlike previously described anti-adaptors, stabilizes σS 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 σS-dependent gene expression under conditions under which strains without iraL cannot. Therefore, IraL-mediated σS stabilization may contribute to host and niche specificity in E. coli. |
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