Abstract
The qnrA1 gene was cloned into a plasmid vector and transformed into Escherichia coli strains carrying chromosomal mutations in the acrAB drug efflux system. In acrAB-deleted strains, and in strains overexpressing acrAB, viable qnrA conferred higher MIC levels (at least a 32-fold increase) for fluoroquinolones than were observed in the parent strains.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Anti-Bacterial Agents / pharmacology
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Drug Resistance, Bacterial*
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Escherichia coli / drug effects*
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Escherichia coli / genetics*
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Escherichia coli Proteins / genetics*
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Fluoroquinolones / pharmacology
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Gene Deletion
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Gene Dosage
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Lipoproteins / genetics*
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Membrane Transport Proteins / genetics*
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Microbial Sensitivity Tests
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Multidrug Resistance-Associated Proteins / genetics*
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Plasmids
Substances
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AcrA protein, E coli
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AcrB protein, E coli
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Anti-Bacterial Agents
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Escherichia coli Proteins
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Fluoroquinolones
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Lipoproteins
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Membrane Transport Proteins
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Multidrug Resistance-Associated Proteins
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Qnr protein, E coli