Contributions of MexAB-OprM and an EmrE homolog to intrinsic resistance of Pseudomonas aeruginosa to aminoglycosides and dyes.

Antimicrob Agents Chemother

Department of Molecular and Cell Biology, University of California, Berkeley, California 94720-3206, USA.

Published: January 2003

Of the six putative small multidrug resistance (SMR) family proteins of Pseudomonas aeruginosa, a protein encoded by the PA4990 gene (emrE(Pae)) shows the highest identity to the well-characterized EmrE efflux transporter of Escherichia coli. Reverse transcription-PCR confirmed the expression of emrE(Pae) in the wild-type strain of P. aeruginosa. Using isogenic emrE(Pae), mexAB-oprM, and/or mexB deletion mutants, the contributions of the EmrE protein and the MexAB-OprM efflux system to drug resistance in P. aeruginosa were assessed by a drug susceptibility test carried out in a low-ionic-strength medium, Difco nutrient broth. We found that EmrE(Pae) contributed to intrinsic resistance not only to ethidium bromide and acriflavine but also to aminoglycosides. In this low-ionic-strength medium, MexAB-OprM was also shown to contribute to aminoglycoside resistance, presumably via active efflux. Aminoglycoside resistance caused by these two pumps could not be demonstrated in high-ionic-strength media, such as Luria broth or Mueller-Hinton broth. The EmrE-dependent efflux of ethidium bromide was confirmed by a continuous fluorescence assay.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC149025PMC
http://dx.doi.org/10.1128/AAC.47.1.27-33.2003DOI Listing

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