EmmdR, a new member of the MATE family of multidrug transporters, extrudes quinolones from Enterobacter cloacae
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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.
KeywordsMultidrug transporter Enterobacter cloacae Resistance MATE Family
This work was supported by an Internal Research Grant from the University of Massachusetts Lowell (G. HE), and an NIH Grant P20 RR016480 (M.F.V.) which is from the NM-INBRE program of the National Center for Research Resources. We truly appreciate Dr. Tomofusa Tsuchiya for providing KAM32 and plasmids. The views presented in this article do not necessarily reflect those of the Food and Drug Administration.
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