Abstract
Mutations in genes mexR and nalC have previously been shown to drive overexpression of the MexAB-OprM multidrug efflux system in Pseudomonas aeruginosa. A transposon insertion multidrug-resistant mutant of P. aeruginosa overproducing MexAB-OprM was disrupted in yet a third gene, PA3574, encoding a probable repressor of the TetR/AcrR family that we have dubbed NalD. Clinical strains overexpressing MexAB-OprM but lacking mutations in mexR or nalC were also shown to carry mutations in nalD. Moreover, the cloned nalD gene reduced the multidrug resistance and MexAB-OprM expression of the transposon mutant and clinical isolates, highlighting the significance of the nalD mutations vis-a-vis MexAB-OprM overexpression in these isolates.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Bacterial Outer Membrane Proteins / biosynthesis*
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Bacterial Outer Membrane Proteins / genetics*
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Cloning, Molecular
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DNA Transposable Elements / genetics
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DNA, Bacterial / genetics
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Drug Resistance, Multiple, Bacterial
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Electrophoresis, Polyacrylamide Gel
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Immunoblotting
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Membrane Transport Proteins / biosynthesis*
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Membrane Transport Proteins / genetics*
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Microbial Sensitivity Tests
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Mutagenesis
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Mutation / genetics*
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Mutation / physiology
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Phenotype
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Plasmids / genetics
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Pseudomonas Infections / microbiology*
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Pseudomonas aeruginosa / drug effects*
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Pseudomonas aeruginosa / genetics*
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Reverse Transcriptase Polymerase Chain Reaction
Substances
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Bacterial Outer Membrane Proteins
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DNA Transposable Elements
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DNA, Bacterial
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Membrane Transport Proteins
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OprM protein, Pseudomonas aeruginosa