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Infection and Immunity, November 2008, p. 5093-5099, Vol. 76, No. 11
0019-9567/08/$08.00+0 doi:10.1128/IAI.00724-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Institute of Medical Microbiology, University of Zürich, Zürich, Switzerland,1 Institute of Medical Microbiology and Hygiene, University of Saarland Hospital, Homburg/Saar, Germany2
Received 9 June 2008/ Returned for modification 9 July 2008/ Accepted 6 August 2008
Some clinical isolates of Staphylococcus aureus produce the superantigenic toxic shock syndrome toxin 1 (TSST-1), encoded by tst, located on pathogenicity islands. The expression of tst is complex and is influenced by environmental conditions such as pH, CO2, and glucose. We identified a putative catabolite-responsive element (cre) in the promoter regions of all known tst genes, indicating that tst transcription may be regulated by the catabolite control protein CcpA. By introducing tst genes under the control of their native promoters 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.
Published ahead of print on 18 August 2008.
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