Berger-Bächi B
Institute of Medical Microbiology, University of Zürich, Postfach, Switzerland.
Cell Mol Life Sci. 1999 Nov 30;56(9-10):764-70. doi: 10.1007/s000180050023.
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-lactams that otherwise inhibit the endogenous PBPs. The production of PBP2' is under dual control by its own mecR1-mecI- and the penicillinase blaR1-blaI-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.
葡萄球菌对甲氧西林耐药是由于获得了mecA基因，该基因编码一种新的青霉素结合蛋白（PBP2'，PBP2a），其对甲氧西林的亲和力低于内源性青霉素结合蛋白。在高浓度β-内酰胺存在的情况下，PBP2'参与细胞壁肽聚糖的组装，否则β-内酰胺会抑制内源性青霉素结合蛋白。PBP2'的产生受其自身的mecR1-mecI以及青霉素酶blaR1-blaI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耐药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肽聚糖前体化学组成的突变都会导致耐药性降低。
