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GDPP 蛋白功能丧失导致金黄色葡萄球菌对β-内酰胺/糖肽类药物的联合耐受。

Loss of function of the gdpP protein leads to joint β-lactam/glycopeptide tolerance in Staphylococcus aureus.

机构信息

Antimicrobial Research Centre and Institute of Molecular and Cellular Biology, University of Leeds, Leeds, United Kingdom.

出版信息

Antimicrob Agents Chemother. 2012 Jan;56(1):579-81. doi: 10.1128/AAC.05148-11. Epub 2011 Oct 10.

DOI:10.1128/AAC.05148-11
PMID:21986827
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3256080/
Abstract

The genetic basis of tolerance to inhibitors of peptidoglycan biosynthesis in Staphylococcus aureus was investigated by generating tolerant mutants in vitro and characterizing them by comparative genome sequencing. Two independently selected tolerant mutants harbored nonsynonymous mutations in gdpP, a gene encoding a putative membrane-located signaling protein. Insertional inactivation of gdpP also conferred tolerance. Our findings further implicate altered signal transduction as a route to antibiotic tolerance in S. aureus.

摘要

通过在体外生成耐受突变体并通过比较基因组测序对其进行表征,研究了金黄色葡萄球菌对肽聚糖生物合成抑制剂的耐受的遗传基础。两种独立选择的耐受突变体在 gdpP 中具有非同义突变,该基因编码一种假定的膜定位信号蛋白。gdpP 的插入失活也赋予了耐受能力。我们的发现进一步表明,改变信号转导是金黄色葡萄球菌产生抗生素耐受的一种途径。

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