喹诺酮耐药突变DNA促旋酶gyrA和金黄色葡萄球菌的gyrB基因。
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吉田Ito H, H, Bogaki-Shonai M,中村Niga T,服部年宏H, S
喹诺酮耐药突变DNA促旋酶gyrA和金黄色葡萄球菌的gyrB基因。
Antimicrob代理Chemother。1994年9月,38(9):2014 - 23所示。
- PubMed ID
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7811012 (在PubMed]
- 文摘
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6.4 kb DNA片段包含DNA促旋酶gyrA和gyrB基因被克隆和测序quinolone-susceptible写明ATCC 12600株金黄色葡萄球菌类型。一种表达质粒是由将克隆的基因插入到大肠coli-S。球菌穿梭载体pAT19,只删除质粒携带功能gyrA和gyrB基因来源于这个质粒。一个有效的转换系统建立了金黄色葡萄球菌RN4220通过使用这些质粒。Quinolone-resistant突变体的金黄色葡萄球菌RN4220孤立了三步选择喹诺酮类。第一和第二次突变体被认为是运输突变体,和第三步突变体被分成五组对其阻力模式和转换结果与gyrA gyrB基因。产生的突变促旋酶基因测序分析显示,他们有以下点突变:组1,ser - 84 (TCA)在GyrA低浓缩铀(TTA);组2,ser - 84 (TCA)阿拉巴马州(GCA), ser - 85 (TCT)专业(有条件现金转移支付),或glu - 88(棉酚)赖氨酸GyrA (AAA);组3,asp - 437 (GAC)在GyrB Asn (AAC);组4参数- 458 (CGA) Gln GyrB (CAA); and group 5, Ser-85 (TCT) to Pro (CCT) in GyrA and Asp-437 (GAC) to Asn (AAC) in GyrB. When the gyrA and/or gyrB mutants were transformed with the wild-type gyrA and/or gyrB plasmids, they became quinolone susceptible, but transformants with the plasmids having the same mutations on the gyrA and/or gyrB genes did not confer susceptibility. These results indicate that mutations in both gyrA and gyrB can be responsible for quinolone resistance in S. aureus.