IAI Accepts, published online ahead of print on 18 August 2008
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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

Kati Seidl, Markus Bischoff, and Brigitte Berger-Bächi*

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.


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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 {Delta}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.




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