Genetic evidence that InhA of Mycobacterium smegmatis is a target for triclosan.

Published on Mar 1, 1999in Antimicrobial Agents and Chemotherapy4.71
· DOI :10.1128/AAC.43.3.711
Laura M. McMurry24
Estimated H-index: 24
Patrick F. McDermott52
Estimated H-index: 52
Stuart B. Levy77
Estimated H-index: 77
(Tufts University)
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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