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The response regulator SsrB activates expression of diverse Salmonella pathogenicity island 2 promoters and counters silencing by the nucleoid-associated protein H-NS.
Mol Microbiol. 2007 Jul; 65(2):477-93.MM

Abstract

The two-component system SsrA-SsrB activates expression of a type III secretion system required for replication in macrophages and systemic infection in mice. Here we characterize the SsrB-dependent regulation of genes within Salmonella pathogenicity island 2 (SPI-2). Primer extension and DNase I footprinting identified multiple SsrB-regulated promoters within SPI-2 located upstream of ssaB, sseA, ssaG and ssaM. We previously demonstrated that ssrA and ssrB transcription is uncoupled. Overexpression of SsrB in the absence of its cognate kinase, SsrA, is sufficient to activate SPI-2 transcription. Because SsrB requires phosphorylation to relieve inhibitory contacts that occlude its DNA-binding domain, additional components must phosphorylate SsrB. SPI-2 promoters examined in single copy were highly SsrB-dependent, activated during growth in macrophages and induced by acidic pH. The nucleoid structuring protein H-NS represses horizontally acquired genes; we confirmed that H-NS is a negative regulator of SPI-2 gene expression. In the absence of H-NS, the requirement for SsrB in activating SPI-2 genes is substantially reduced, suggesting a role for SsrB in countering H-NS silencing. SsrB activates transcription of multiple operons within SPI-2 by binding to degenerate DNA targets at diversely organized promoters. SsrB appears to possess dual activities to promote SPI-2 gene expression: activation of transcription and relief of H-NS-mediated repression.

Authors+Show Affiliations

University of Illinois at Chicago, Department of Microbiology and Immunology, 835 S. Wolcott Ave M/C 790, Chicago, IL 60612, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.

Language

eng

PubMed ID

17630976

Citation

Walthers, Don, et al. "The Response Regulator SsrB Activates Expression of Diverse Salmonella Pathogenicity Island 2 Promoters and Counters Silencing By the Nucleoid-associated Protein H-NS." Molecular Microbiology, vol. 65, no. 2, 2007, pp. 477-93.
Walthers D, Carroll RK, Navarre WW, et al. The response regulator SsrB activates expression of diverse Salmonella pathogenicity island 2 promoters and counters silencing by the nucleoid-associated protein H-NS. Mol Microbiol. 2007;65(2):477-93.
Walthers, D., Carroll, R. K., Navarre, W. W., Libby, S. J., Fang, F. C., & Kenney, L. J. (2007). The response regulator SsrB activates expression of diverse Salmonella pathogenicity island 2 promoters and counters silencing by the nucleoid-associated protein H-NS. Molecular Microbiology, 65(2), 477-93.
Walthers D, et al. The Response Regulator SsrB Activates Expression of Diverse Salmonella Pathogenicity Island 2 Promoters and Counters Silencing By the Nucleoid-associated Protein H-NS. Mol Microbiol. 2007;65(2):477-93. PubMed PMID: 17630976.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The response regulator SsrB activates expression of diverse Salmonella pathogenicity island 2 promoters and counters silencing by the nucleoid-associated protein H-NS. AU - Walthers,Don, AU - Carroll,Ronan K, AU - Navarre,William Wiley, AU - Libby,Stephen J, AU - Fang,Ferric C, AU - Kenney,Linda J, PY - 2007/7/17/pubmed PY - 2007/10/30/medline PY - 2007/7/17/entrez SP - 477 EP - 93 JF - Molecular microbiology JO - Mol Microbiol VL - 65 IS - 2 N2 - The two-component system SsrA-SsrB activates expression of a type III secretion system required for replication in macrophages and systemic infection in mice. Here we characterize the SsrB-dependent regulation of genes within Salmonella pathogenicity island 2 (SPI-2). Primer extension and DNase I footprinting identified multiple SsrB-regulated promoters within SPI-2 located upstream of ssaB, sseA, ssaG and ssaM. We previously demonstrated that ssrA and ssrB transcription is uncoupled. Overexpression of SsrB in the absence of its cognate kinase, SsrA, is sufficient to activate SPI-2 transcription. Because SsrB requires phosphorylation to relieve inhibitory contacts that occlude its DNA-binding domain, additional components must phosphorylate SsrB. SPI-2 promoters examined in single copy were highly SsrB-dependent, activated during growth in macrophages and induced by acidic pH. The nucleoid structuring protein H-NS represses horizontally acquired genes; we confirmed that H-NS is a negative regulator of SPI-2 gene expression. In the absence of H-NS, the requirement for SsrB in activating SPI-2 genes is substantially reduced, suggesting a role for SsrB in countering H-NS silencing. SsrB activates transcription of multiple operons within SPI-2 by binding to degenerate DNA targets at diversely organized promoters. SsrB appears to possess dual activities to promote SPI-2 gene expression: activation of transcription and relief of H-NS-mediated repression. SN - 0950-382X UR - https://www.unboundmedicine.com/medline/citation/17630976/The_response_regulator_SsrB_activates_expression_of_diverse_Salmonella_pathogenicity_island_2_promoters_and_counters_silencing_by_the_nucleoid_associated_protein_H_NS_ L2 - https://doi.org/10.1111/j.1365-2958.2007.05800.x DB - PRIME DP - Unbound Medicine ER -