Open AccessStp1 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 , microbiology and biotechnology , threonine , biology , phosphatase , gene , staphylococcus , bacteria , biochemistry , genetics , phosphorylation
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.