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A search for homologs of theBacillus subtilis PhoP response regulator in the group A streptococcus (GAS) genome revealed three good candidates. Inactivation of one of these, recently identified ascsrR (J. C. Levin and M. R. Wessels, Mol. Microbiol. 30:209–219, 1998), caused the strain to produce mucoid colonies and to increase transcription ofhasA , the first gene in the operon for capsule synthesis. We report here that a nonpolar insertion in this gene also increased transcription ofska (encoding streptokinase),sagA (streptolysin S), andspeMF (mitogenic factor) but did not affect transcription ofslo (streptolysin O),mga (multiple gene regulator of GAS),emm (M protein),scpA (complement C5a peptidase), orspeB orspeC (pyrogenic exotoxins B and C). The amounts of streptokinase, streptolysin S, and capsule paralleled the levels of transcription of their genes in all cases. Because CsrR represses genes unrelated to those for capsule synthesis, and because CsrA-CsrB is a global regulatory system inEscherichia coli whose mechanism is unrelated to that of these genes in GAS, the locus has been renamedcovR , for “control of virulence genes” in GAS. Transcription of thecovR operon was also increased in the nonpolar insertion mutant, indicating that CovR represses its own synthesis as well. All phenotypes of thecovR nonpolar insertion mutant were complemented by thecovR gene on a plasmid. CovR acts on operons expressed both in exponential and in stationary phase, demonstrating that the CovR-CovS pathway is separate from growth phase-dependent regulation in GAS. Therefore, CovR is the first multiple-gene repressor of virulence factors described for this important human pathogen.

A Response Regulator That Represses Transcription of Several Virulence Operons in the Group A Streptococcus