Stp1 Loss of Function Promotes β-Lactam Resistance in Staphylococcus aureus That Is Independent of Classical Genes | Zendy

Aditi Chatterjee | Zendy; Raymond Poon | Zendy; Som S. Chatterjee | Zendy

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Stp1 Loss of Function Promotes β-Lactam Resistance in Staphylococcus aureus That Is Independent of Classical Genes

Author(s) -

Aditi Chatterjee,

Raymond Poon,

Som S. Chatterjee

Publication year - 2020

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.02222-19

Subject(s) - staphylococcus aureus , serine , threonine , microbiology and biotechnology , biology , phosphatase , gene , point mutation , bacteria , genetics , phosphorylation , mutation

β-Lactam resistance in Staphylococcus aureus limits treatment options. Stp1 and Stk1, a serine-threonine phosphatase and kinase, respectively, mediate serine-threonine kinase (STK) signaling. Loss-of-function point mutations in stp1 were detected among laboratory-passaged β-lactam-resistant S. aureus strains lacking mecA and blaZ , the major determinants of β-lactam resistance in the bacteria. Loss of Stp1 function facilitates β-lactam resistance of the bacteria.

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