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Mg 2+ signalling defines the group A streptococcal CsrRS (CovRS) regulon
Author(s) -
Gryllos Ioannis,
Grifantini Renata,
Colaprico Annalisa,
Jiang Shengmei,
DeForce Emelia,
Hakansson Anders,
Telford John L.,
Grandi Guido,
Wessels Michael R.
Publication year - 2007
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.2007.05818.x
Subject(s) - regulon , two component regulatory system , biology , mutant , complementation , gene , virulence , genetics , histidine kinase , extracellular , regulation of gene expression , microbiology and biotechnology , transcriptome , gene expression
Summary CsrRS (or CovRS) is a two‐component system implicated in the control of multiple virulence determinants in the important human pathogen, group A Streptococcus (GAS). Earlier studies suggested that extracellular Mg 2+ signalled through the presumed sensor histidine kinase, CsrS. We now confirm those findings, as complementation of a csrS mutant restored Mg 2+ ‐dependent gene regulation. Moreover, we present strong evidence that Mg 2+ signals through CsrS to regulate an extensive and previously undefined repertoire of GAS genes. The effect of Mg 2+ on regulation of global gene expression was evaluated using genomic microarrays in an M‐type 3 strain of GAS and in an isogenic csrS mutant. Unexpectedly, of the 72 genes identified in the Mg 2+ ‐stimulated CsrRS regulon, 42 were absent from the CsrR regulon (the latter being defined by comparison of wild‐type and CsrR mutant transcriptomes at low Mg 2+ ). We observed CsrS‐dependent regulation of 72 of the 73 genes whose expression changed in response to elevated extracellular Mg 2+ in wild‐type bacteria, a result that identifies CsrS as the principal, if not exclusive, sensor for extracellular Mg 2+ in GAS. To our knowledge, this study is the first to characterize global gene regulation by a GAS two‐component system in response to a specific environmental stimulus.