Goldman J D, White D G, Levy S B
Center for Adaptation Genetics and Drug Resistance, Tufts University School of Medicine, Boston, Massachusetts 02111, USA.
Antimicrob Agents Chemother. 1996 May;40(5):1266-9. doi: 10.1128/AAC.40.5.1266.
The multiple antibiotic resistance (mar) locus in Escherichia coli consists of two divergently expressed operons (marC and marRAB), both of which contribute to the Mar phenotype. Overexpression of the marRAB operon protected E. coli against rapid cell killing by fluoroquinolones. Inactivation of the operon in mar mutants restored a wild-type bactericidal susceptibility. Both operons of the locus were required for protection from the quinolone-mediated bactericidal activity in mar locus deletion mutants. The effect was lost at high concentrations of fluoroquinolones, unlike the case for the previously described genes hipA and hipQ. The inducible mar locus appears to specify a novel antibactericidal mechanism which may play a role in the emergence of fluoroquinolone-resistant clinical E. coli isolates.
大肠杆菌中的多重抗生素耐药性（mar）位点由两个反向表达的操纵子（marC和marRAB）组成，这两个操纵子都对Mar表型有贡献。marRAB操纵子的过表达可保护大肠杆菌免受氟喹诺酮类药物快速杀灭细胞的影响。mar突变体中该操纵子的失活恢复了野生型的杀菌敏感性。该位点的两个操纵子对于保护mar位点缺失突变体免受喹诺酮介导的杀菌活性都是必需的。与先前描述的基因hipA和hipQ不同，在高浓度氟喹诺酮类药物存在时这种作用会消失。可诱导的mar位点似乎规定了一种新的抗杀菌机制，这可能在耐氟喹诺酮临床大肠杆菌分离株的出现中起作用。
