Department of Clinical Laboratory and Nutritional Sciences, University of Massachusetts Lowell, Lowell, MA 01854, USA.
Arch Microbiol. 2011 Oct;193(10):759-65. doi: 10.1007/s00203-011-0738-1. Epub 2011 Aug 7.
We cloned a gene, ECL_03329, from the chromosome of Enterobacter cloacae ATCC13047, using a drug-hypersensitive Escherichia coli KAM32 cell as the host. We show here that this gene, designated as emmdR, is responsible for multidrug resistance in E. cloacae. E. coli KAM32 host cells containing the cloned emmdR gene (KAM32/pEMMDR28) showed decreased susceptibilities to benzalkonium chloride, norfloxacin, ciprofloxacin, levofloxacin, ethidium bromide, acriflavine, rhodamine6G, and trimethoprim. emmdR-deficient E. cloacae cells (EcΔemmdR) showed increased susceptibilities to several of the antimicrobial agents tested. EmmdR has twelve predicted transmembrane segments and some shared identity with members of the multidrug and toxic compound extrusion (MATE) family of transporters. Study of the antimicrobial agent efflux activities revealed that EmmdR is an H+-drug antiporter but not a Na+ driven efflux pump. These results indicate that EmmdR is responsible for multidrug resistance and pumps out quinolones from E. cloacae.
我们使用对药物敏感的大肠杆菌 KAM32 细胞作为宿主，从阴沟肠杆菌 ATCC13047 的染色体中克隆了一个基因 ECL_03329。我们在这里表明，该基因被命名为 emmdR，负责阴沟肠杆菌的多药耐药性。含有克隆的 emmdR 基因的大肠杆菌 KAM32 宿主细胞（KAM32/pEMMDR28）对苯扎氯铵、诺氟沙星、环丙沙星、左氧氟沙星、溴化乙锭、吖啶黄、罗丹明 6G 和甲氧苄啶的敏感性降低。缺乏 emmdR 的阴沟肠杆菌细胞（EcΔemmdR）对测试的几种抗菌剂的敏感性增加。EmmdR 有十二个预测的跨膜片段，与多药和毒性化合物外排（MATE）家族的转运蛋白的一些成员具有一些共同的身份。对抗菌剂外排活性的研究表明，EmmdR 是一种 H+-药物反向转运体，但不是 Na+驱动的外排泵。这些结果表明，EmmdR 负责多药耐药性，并将喹诺酮类药物从阴沟肠杆菌中泵出。
