Antimicrobial Agents and Chemotherapy, August 2003, p. 2558-2564, Vol. 47, No. 8
0066-4804/03/$08.00+0 DOI: 10.1128/AAC.47.8.2558-2564.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.
MsrR, a Putative Cell Envelope-Associated Element Involved in Staphylococcus aureus sarA Attenuation
Jutta Rossi,1 Markus Bischoff,1 Akihito Wada,2 and Brigitte Berger-Bächi1*
Institute of Medical Microbiology, University of Zürich, CH-8028 Zürich, Switzerland,1
Department of Microbiology, National Institute of Infectious Diseases, Toyama 1-23-1, Shinjuku-ku, 162-8640 Tokyo, Japan2
Received 3 February 2003/
Returned for modification 7 April 2003/
Accepted 24 May 2003
A novel membrane-associated protein, MsrR, was identified in Staphylococcus aureus which affects resistance to methicillin and teicoplanin, as well as the synthesis of virulence factors. MsrR belongs to the LytR-CpsA-Psr family of cell envelope-related transcriptional attenuators and was shown to be inducible by cell wall-active agents, such as ß-lactams, glycopeptides, and lysostaphin. The expression of msrR peaked in the early exponential growth phase and decreased sharply thereafter. msrR mutants showed increased sarA transcription and an earlier and higher expression of RNAIII, resulting in altered expression of virulence factors such as alpha-toxin and protein A. These observations suggest that MsrR is a new component involved in sarA attenuation and the regulatory network controlling virulence gene expression in S. aureus.
* Corresponding author. Mailing address: Institute of Medical Microbiology, University of Zürich, Gloriastr. 32, Postfach, CH-8028 Zürich, Switzerland. Phone: 41 1 634 26 50. Fax: 41 1 634 49 06. E-mail: bberger{at}immv.unizh.ch.
Antimicrobial Agents and Chemotherapy, August 2003, p. 2558-2564, Vol. 47, No. 8
0066-4804/03/$08.00+0 DOI: 10.1128/AAC.47.8.2558-2564.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.
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Copyright © 2003 by the American Society for Microbiology. All rights reserved.