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

被引：6
作者：
Chatterjee, Aditi [1 ,2 ]
Poon, Raymond [1 ,2 ]
Chatterjee, Som S. [1 ,2 ]
机构：
[1] Univ Maryland, Sch Dent, Dept Microbial Pathogenesis, Baltimore, MD 21201 USA
[2] Inst Marine & Environm Technol, Baltimore, MD 21202 USA
来源：
ANTIMICROBIAL AGENTS AND CHEMOTHERAPY | 2020年 / 64卷 / 06期
关键词：
Stp1; beta-lactam resistance; Staphylococcus aureus; ANTIBIOTIC-RESISTANCE; SERINE/THREONINE KINASE; VIRULENCE REGULATION; PHOSPHORYLATION; SUSCEPTIBILITY; FAMILY; STRAIN;
D O I：
10.1128/AAC.02222-19
中图分类号：
Q93 [微生物学];
学科分类号：
071005 ; 100705 ;
摘要：
beta-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 beta-lactam-resistant S. aureus strains lacking mecA and blaZ, the major determinants of beta-lactam resistance in the bacteria. Loss of Stp1 function facilitates beta-lactam resistance of the bacteria.
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页数：4
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