Genetic basis of methicillin resistance in Staphylococcus aureus
Genetic basis of methicillin resistance in Staphylococcus aureus
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DOI：
10.1007/s000180050023
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发表时间：
1999-11-30
影响因子：
8
通讯作者：
Berger-Bächi, B
中科院分区：
文献类型：
--
作者：
Berger-Bächi, B
葡萄球菌中的甲氧西林耐药性是由于获得了编码新青霉素结合蛋白（PBP2、PBP2a）的 mecA 基因，该蛋白对甲氧西林的亲和力比内源性 PBP 更低。 PBP2' 在高浓度 β-内酰胺存在的情况下参与细胞壁肽聚糖的组装，否则会抑制内源性 PBP。 PBP2' 的产生受到其自身的 mecR1-mecI 和青霉素酶 blaR1-bla1 编码的调控元件的双重控制。除了 PBP2' 之外，对高水平甲氧西林的抗性还取决于参与肽聚糖合成和降解的染色体编码因子。任何减少肽聚糖前体形成或改变壁肽前体化学组成的突变都会导致耐药性降低。
Methicillin resistance in staphylococci is due to the acquisition of the mecA gene encoding a new penicillin-binding protein (PBP2, PBP2a) that has a lower affinity to methicillin than the endogenous PBPs. PBP2' is involved in the assembly of the cell wall peptidoglycan in the presence of high concentrations of beta-lactarns that otherwise inhibit the endogenous PBPs. The production of PBP2' is under dual control by its own mecR1-mecI- and the penicillinase blaR1-bla1-encoded regulatory elements. Resistance to high levels of methicillin depends, in addition to PBP2', on chromosomally encoded factors that are involved in the synthesis and degradation of the peptidoglycan. Any mutations that reduce peptidoglycan precursor formation or change the chemical composition of the muropeptide precursor result in lowered resistance.