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Microbiology 153 (2007), 1604-1608; DOI  10.1099/mic.0.2007/006247-0
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Microbiology 153 (2007), 1604-1608; DOI  10.1099/mic.0.2007/006247-0
© 2007 Society for General Microbiology

svrA, a multi-drug exporter, does not control agr

John Chen and Richard P. Novick

Program in Molecular Pathogenesis, Skirball Institute, and Departments of Microbiology and Medicine, New York University Medical Center, New York 10016, USA

Correspondence
Richard P. Novick
novick{at}saturn.med.nyu.edu

The Staphylococcus aureus svrA gene was identified in a signature-tagged mutagenesis screen for Tn917 insertions attenuated for mouse virulence, and subsequently found to be defective in agr expression. Its attenuation of virulence was attributed to its failure to express the agr regulon. In addition to the Tn917 insertion in svrA, the original svrA mutant strain (P6C63) has an adventitious frame-shift in agrC, which results in truncation of the AgrC peptide. Separation of the svrA mutation from the agrC frame-shift revealed that svrA has no detectable affect on agr activation, as assessed by exoprotein profiles and the production of haemolytic toxins. These results indicate that svrA does not play a role in Staphylococcus aureus infections via an agr-mediated pathway.


Abbreviations: AIP, autoinducing peptide; STM, signature-tagged mutagenesis; wt, wild-type







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