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Antimicrobial Agents and Chemotherapy, December 2001, p. 3574-3579, Vol. 45, No. 12
Department of Microbiology and Molecular
Genetics,1 Center for the Study of
Emerging and Re-emerging Pathogens,3 and
Division of Infectious Diseases,2
University of Texas Medical School, Houston, Texas 77030
Received 28 February 2001/Returned for modification 9 July
2001/Accepted 7 September 2001
We hypothesized that multidrug resistance efflux pumps (MDRs) may
be contributing to the drug resistance of enterococci. We recently
identified potential MDR-encoding genes in the Enterococcus faecalis V583 genome. Among the putative MDRs, we found a
gene that encodes a NorA homolog and have characterized this
enterococcal MDR in the present study. A mutant from which the
enterococcal NorA homolog has been deleted has reduced resistance to
several NorA substrates. Complementation of the deletion mutant with
the wild-type gene verified the involvement of this enterococcal gene in resistance to ethidium bromide (EtBr) and norfloxacin. Known MDR
inhibitors (reserpine, lansoprazole, and verapamil) inhibit the efflux
of EtBr and norfloxacin in wild-type strain OG1RF. A fluorescence assay
with EtBr allowed us to quantitate the efflux capability of the
enterococcal NorA pump. On the basis of these results, we have named
this enterococcal gene emeA (enterococcal multidrug
resistance efflux).
0066-4804/01/$04.00+0 DOI: 10.1128/AAC.45.12.3574-3579.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Characterization of emeA, a
norA Homolog and Multidrug Resistance Efflux Pump, in
Enterococcus faecalis
*
Corresponding author. Mailing address: Human Genome
Sequencing Center, Baylor College of Medicine, One Baylor Plaza, Alkek N1519, Houston, TX 77030. Phone: (713) 798-6539. Fax: (713) 798-5741. E-mail: gwstock{at}bcm.tmc.edu.
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