Genetic evidence that InhA of Mycobacterium smegmatis is a target for triclosan |
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Authors: | McMurry L M McDermott P F Levy S B |
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Affiliation: | Center for Adaptation Genetics and Drug Resistance, Tufts University School of Medicine, Boston, Massachusetts 02111, USA. |
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Abstract: | ![]() Three Mycobacterium smegmatis mutants selected for resistance to triclosan each had a different mutation in InhA, an enoyl reductase involved in fatty acid synthesis. Two expressed some isoniazid resistance. A mutation originally selected on isoniazid also mediated triclosan resistance, as did the wild-type inhA gene on a multicopy plasmid. Replacement of the mutant chromosomal inhA genes with wild-type inhA eliminated resistance. These results suggest that M. smegmatis InhA, like its Escherichia coli homolog FabI, is a target for triclosan. |
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