Mechanism of Reduced Vancomycin Susceptibility Conferred by walK Mutation in Community-Acquired Methicillin-Resistant Staphylococcus aureus Strain MW2 | Zendy

Jinfeng Hu | Zendy; Xu Zhang | Zendy; Xiaoyu Liu | Zendy; Chuan Chen | Zendy; Baolin Sun | Zendy

Open Access

Mechanism of Reduced Vancomycin Susceptibility Conferred by walK Mutation in Community-Acquired Methicillin-Resistant Staphylococcus aureus Strain MW2

Author(s) -

Jinfeng Hu,

Xu Zhang,

Xiaoyu Liu,

Chuan Chen,

Baolin Sun

Publication year - 2014

Publication title -

antimicrobial agents and chemotherapy

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.07

H-Index - 259

eISSN - 1070-6283

pISSN - 0066-4804

DOI - 10.1128/aac.04290-14

Subject(s) - vancomycin , staphylococcus aureus , microbiology and biotechnology , mutation , point mutation , phosphorylation , autophosphorylation , strain (injury) , biology , gene , chemistry , bacteria , genetics , protein kinase a , anatomy

Point mutations with unclear molecular mechanisms are often associated with vancomycin resistance in Staphylococcus aureus. Here, we observed that the walK (G223D) mutation caused decreased expression of genes associated with cell wall metabolism, decreased autolytic activity, thickened cell walls, and reduced vancomycin susceptibility. A phosphorylation assay showed that WalK (G223D) exhibited reduced autophosphorylation, which led to reduced phosphorylation of WalR. An electrophoretic mobility shift assay indicated that WalK (G223D)-phosphorylated WalR had a reduced capacity to bind to the atlA promoter.

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