This Article Full Text (PDF) Other Versions of this Article: IAI.00724-08v1 76/11/5093    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 Google Scholar Articles by Seidl, K. Articles by Berger-Bächi, B. PubMed PubMed Citation Articles by Seidl, K. Articles by Berger-Bächi, B.

 Previous Article  |  Next Article 

Infect. Immun. doi:10.1128/IAI.00724-08
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

CcpA mediates the catabolite repression of tst in Staphylococcus aureus

Institute of Medical Microbiology, University of Zürich, Zürich, Switzerland; Institute of Medical Microbiology and Hygiene, University of Saarland Hospital, Homburg/Saar, Germany

^* To whom correspondence should be addressed. Email: bberger{at}immv.uzh.ch.

	Abstract

Some clinical isolates of Staphylococcus aureus produce the superantigenic toxic shock syndrome toxin TSST-1, encoded by tst and located on pathogenicity islands. The expression of tst is complex, and influenced by environmental conditions such as pH, CO₂ and glucose. We identified a putative catabolite responsive element (cre) in the promoter region of all known tst genes, indicating that tst transcription may be regulated by the catabolite control protein CcpA. By introducing tst-genes under their native promoter or tst-promoter-reporter gene fusions in wild type strain Newman, we showed that glucose was able to repress tst transcription and TSST-1 production, whereas glucose repression was abolished in the corresponding ccpA mutant. Stabilizing the pH ruled out a pH effect due to acid production during glucose catabolism. CcpA thus directly regulates tst transcription, linking carbohydrate utilization to virulence gene expression in S. aureus.