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MsrR contributes to cell surface characteristics and virulence in Staphylococcus aureus

Hübscher, Judith ; McCallum, Nadine ; Sifri, Costi D. ; Majcherczyk, Paul A. ; Entenza, José M. ; Heusser, Roni ; Berger-Bächi, Brigitte ; Stutzmann Meier, Patricia

In: FEMS Microbiology Letters, 2009, vol. 295, no. 2, p. 251-260

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    Titre
    • MsrR contributes to cell surface characteristics and virulence in Staphylococcus aureus
    Auteur
    • Hübscher, Judith. Institute of Medical Microbiology, University of Zürich, Zürich, Switzerland
    • McCallum, Nadine. Institute of Medical Microbiology, University of Zürich, Zürich, Switzerland
    • Sifri, Costi D.. Division of Infectious Diseases and International Health, University of Virginia Health System, Charlottesville, VA, USA
    • Majcherczyk, Paul A.. Department of Fundamental Microbiology, University of Lausanne, Lausanne, Switzerland
    • Entenza, José M.. Department of Fundamental Microbiology, University of Lausanne, Lausanne, Switzerland
    • Heusser, Roni. Institute of Medical Microbiology, University of Zürich, Zürich, Switzerland
    • Berger-Bächi, Brigitte. Institute of Medical Microbiology, University of Zürich, Zürich, Switzerland
    • Stutzmann Meier, Patricia. Institute of Medical Microbiology, University of Zürich, Zürich, Switzerland
    Type de document
    • Postprint
    Identifiant OAI-PMH
    • oai:doc.rero.ch:304122
    Summary
    MsrR, a factor contributing to methicillin resistance in Staphylococcus aureus, belongs to the LytR-CpsA-Psr family of cell envelope-associated proteins. Deletion of msrR increased cell size and aggregation, and altered envelope properties, leading to a temporary reduction in cell surface hydrophobicity, diminished colony-spreading ability, and an increased susceptibility to Congo red. The reduced phosphorus content of purified cell walls of the msrR mutant suggested a reduction in wall teichoic acids, which may explain some of the observed phenotypes. Microarray analysis of the msrR deletion mutant revealed only minor changes in the global transcriptome, suggesting that MsrR has structural rather than regulatory functions. Importantly, virulence of the msrR mutant was decreased in a nematode-killing assay as well as in rat experimental endocarditis. MsrR is therefore likely to play a role in cell envelope maintenance, cell separation, and pathogenicity of S. aureus