ThemsaABCROperon Regulates Resistance in Vancomycin-Intermediate Staphylococcus aureus Strains

Abstract

ABSTRACTVancomycin-intermediateStaphylococcus 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 themsaABCRoperon in vancomycin resistance in three clinical VISA strains, i.e., Mu50, HIP6297, and LIM2. Deletion of themsaABCRoperon 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 themsaABCRoperon also reduced the binding capacity for vancomycin. We conclude that themsaABCRoperon contributes to resistance to vancomycin and cell wall synthesis inS. aureus.