This Article Full Text (PDF) Other Versions of this Article: JB.01843-07v1 190/9/3225    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Pulliainen, A. T. Articles by Finne, J. Search for Related Content PubMed PubMed Citation Articles by Pulliainen, A. T. Articles by Finne, J.

 Previous Article  |  Next Article 

J. Bacteriol. doi:10.1128/JB.01843-07
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Deficiency of the Rgg regulator promotes H₂O₂ resistance, AhpCF-mediated H₂O₂ decomposition and virulence in Streptococcus pyogenes

Department of Medical Biochemistry and Molecular Biology, University of Turku, Kiinamyllynkatu 10, FI-20520 Turku, Finland; Department of Medical Microbiology and Immunology, University of Turku, Kiinamyllynkatu 13, FI-20520 Turku, Finland

^* To whom correspondence should be addressed. Email: arto.pulliainen{at}unibas.ch.

	Abstract

Streptococcus pyogenes (GAS), a catalase-negative gram-positive bacterium, is aerotolerant and survives H₂O₂ exposures that kill many catalase-positive bacteria. The molecular basis of the H₂O₂ resistance is poorly known. Here, we demonstrate that serotype M49 GAS lacking the Rgg regulator is more resistant to H₂O₂, and also decomposes more H₂O₂ than the parental strain. Sub-genomic transcriptional profiling and genome-integrated GFP-reporters show that a bi-cistronic operon, a homolog of the Streptococcus mutans ahpCF-operon, is transcriptionally up-regulated in the absence of Rgg. Phenotypic assays with ahpCF-operon knockouts demonstrate that the gene products decompose H₂O₂ and protect GAS against peroxide stress. In a murine intraperitoneal infection model, Rgg-deficiency increases the virulence of GAS, although in an ahpCF-independent manner. Rgg-mediated repression of H₂O₂ resistance is divergent of the previously characterized peroxide resistance repressor PerR. Moreover, Rgg-mediated repression of H₂O₂ resistance is inducible by cellular stress of diverse nature – ethanol, organic hydroperoxide and H₂O₂. Rgg is thus identified as a novel sensoregulator of streptococcal H₂O₂ resistance with potential implications in the virulence of the catalase-negative GAS.