Stp1 Loss of Function Promotes β-Lactam Resistance in Staphylococcus aureus That Is Independent of Classical Genes
Stp1 Loss of Function Promotes β-Lactam Resistance in Staphylococcus aureus That Is Independent of Classical Genes
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DOI：
10.1128/aac.02222-19
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发表时间：
2020-06-01
影响因子：
4.9
通讯作者：
Chatterjee, Som S.
中科院分区：
文献类型：
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作者：
Chatterjee, Aditi;Poon, Raymond;Chatterjee, Som S.
金黄色葡萄球菌的β-内酰胺耐药性限制了治疗选择。Stp 1和Stk 1分别是丝氨酸-苏氨酸磷酸酶和激酶，介导丝氨酸-苏氨酸激酶（STK）信号传导。在实验室传代的β-内酰胺类耐药链球菌中检测到stp 1的功能缺失点突变。金黄色葡萄球菌菌株缺乏mecA和blaZ，这是细菌中β-内酰胺耐药性的主要决定因素。Stp 1功能的丧失促进细菌的β-内酰胺抗性。
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.