The msaABCR Operon Regulates Resistance in Vancomycin-Intermediate Staphylococcus aureus Strains

Document Type

Article

Publication Date

11-1-2014

Department

Biological Sciences

School

Biological, Environmental, and Earth Sciences

Abstract

Vancomycin-intermediate Staphylococcus aureus (VISA) strains present an increasingly difficult problem in terms of public health. However, the molecular mechanism for this resistance is not yet understood. In this study, we define the role of the msaABCR operon in vancomycin resistance in three clinical VISA strains, i.e., Mu50, HIP6297, and LIM2. Deletion of the msaABCR operon resulted in significant decreases in the vancomycin MIC (from 6.25 to 1.56 μg/ml) and significant reductions of cell wall thickness in strains Mu50 and HIP6297. Growth of the mutants in medium containing vancomycin at concentrations greater than 2 μg/ml resulted in decreases in the growth rate, compared with the wild-type strains. Mutation of the msaABCR operon also reduced the binding capacity for vancomycin. We conclude that the msaABCR operon contributes to resistance to vancomycin and cell wall synthesis in S. aureus.

Publication Title

Antimicrobial Agents and Chemotherapy

Volume

58

Issue

11

First Page

6685

Last Page

6695

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