Suzuki E, Kuwahara-Arai K, Richardson J F, Hiramatsu K
Department of Bacteriology, Juntendo University, Tokyo, Japan.
Antimicrob Agents Chemother. 1993 Jun;37(6):1219-26. doi: 10.1128/AAC.37.6.1219.
The distributions of the mec regulator genes mecI and mecR1, which were identified on the chromosome of mecA-carrying Staphylococcus aureus N315, in methicillin-resistant staphylococci isolated in Japan and various countries were studied. Screening by dot blot hybridization by using polymerase chain reaction (PCR)-amplified probes revealed that at least the 5'-end region of the mecR1 gene was present in all strains tested, whereas about 40% of the strains were negative for the mecI gene. The data suggested that these regulator genes were the original components of the additional mec region DNA of methicillin-resistant S. aureus as well as methicillin-resistant, coagulase-negative staphylococci of seven staphylococcal species (S. epidermidis, S. haemolyticus, S. hominis, S. sciuri, S. capitis, S. caprae, and S. warneri). The mecI gene, which presumably codes for the repressor protein of the mecA gene, was found to harbor a point mutation in all six mecI-positive methicillin-resistant S. aureus strains, and their basal level of mecA gene transcription was elevated compared with that of strain N315, which harbors a presumably intact counterpart of the mecI gene. The data suggested that the mecI gene encodes for a strong repressor function on mecA gene transcription and is deleted or mutated in clinical methicillin-resistant S. aureus strains with high levels of resistance to methicillin.
对携带mecA的金黄色葡萄球菌N315染色体上鉴定出的mec调控基因mecI和mecR1,在日本及其他各国分离出的耐甲氧西林葡萄球菌中的分布情况进行了研究。使用聚合酶链反应(PCR)扩增探针通过斑点杂交进行筛选,结果显示,在所有测试菌株中至少都存在mecR1基因的5'-端区域,而约40%的菌株mecI基因呈阴性。数据表明,这些调控基因是耐甲氧西林金黄色葡萄球菌以及7种葡萄球菌属(表皮葡萄球菌、溶血葡萄球菌、人葡萄球菌、松鼠葡萄球菌、头葡萄球菌、山羊葡萄球菌和沃氏葡萄球菌)的耐甲氧西林、凝固酶阴性葡萄球菌额外mec区域DNA的原始组成部分。推测编码mecA基因阻遏蛋白的mecI基因,在所有6株mecI阳性的耐甲氧西林金黄色葡萄球菌菌株中都存在一个点突变,与携带推测完整mecI基因对应物的N315菌株相比,它们mecA基因的基础转录水平有所升高。数据表明,mecI基因对mecA基因转录具有强大的阻遏功能,在对甲氧西林具有高抗性的临床耐甲氧西林金黄色葡萄球菌菌株中缺失或发生了突变。