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.




This article has been cited by other articles:

  • Somerville, G. A., Proctor, R. A. (2009). At the Crossroads of Bacterial Metabolism and Virulence Factor Synthesis in Staphylococci. Microbiol. Mol. Biol. Rev. 73: 233-248 [Abstract] [Full Text]  


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