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Journal of Bacteriology, March 2008, p. 1956-1965, Vol. 190, No. 6
0021-9193/08/$08.00+0     doi:10.1128/JB.01677-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Variation in the Group B Streptococcus CsrRS Regulon and Effects on Pathogenicity{triangledown} ,{dagger}

Sheng-Mei Jiang,1,2 Nadeeza Ishmael,3 Julie Dunning Hotopp,3 Manuela Puliti,4 Luciana Tissi,4 Nikhil Kumar,3 Michael J. Cieslewicz,1,2 Hervé Tettelin,3 and Michael R. Wessels1,2*

Division of Infectious Diseases, Children's Hospital Boston,1 Harvard Medical School, Boston, Massachusetts 02115,2 The J. Craig Venter Institute, Rockville, Maryland 20850,3 Microbiology Section, Department of Experimental Medicine and Biochemical Sciences, University of Perugia, Perugia, Italy4

Received 16 October 2007/ Accepted 8 January 2008

CsrRS (or CovRS) is a two-component regulatory system that controls expression of multiple virulence factors in the important human pathogen group B Streptococcus (GBS). We now report global gene expression studies in GBS strains 2603V/R and 515 and their isogenic csrR and csrS mutants. Together with data reported previously for strain NEM316, the results reveal a conserved 39-gene CsrRS regulon. In vitro phosphorylation-dependent binding of recombinant CsrR to promoter regions of both positively and negatively regulated genes suggests that direct binding of CsrR can mediate activation as well as repression of target gene expression. Distinct patterns of gene regulation in csrR versus csrS mutants in strain 2603V/R compared to 515 were associated with different hierarchies of relative virulence of wild-type, csrR, and csrS mutants in murine models of systemic infection and septic arthritis. We conclude that CsrRS regulates a core group of genes including important virulence factors in diverse strains of GBS but also displays marked variability in the repertoire of regulated genes and in the relative effects of CsrS signaling on CsrR-mediated gene regulation. Such variation is likely to play an important role in strain-specific adaptation of GBS to particular host environments and pathogenic potential in susceptible hosts.

* Corresponding author. Mailing address: Division of Infectious Diseases, Children's Hospital Boston, 300 Longwood Ave., Boston, MA 02115. Phone: (617) 919-2900. Fax: (617) 730-0254. E-mail: michael.wessels{at}childrens.harvard.edu

{triangledown} Published ahead of print on 18 January 2008.

{dagger} Supplemental material for this article may be found at http://jb.asm.org/.

Journal of Bacteriology, March 2008, p. 1956-1965, Vol. 190, No. 6
0021-9193/08/$08.00+0     doi:10.1128/JB.01677-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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