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


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.

SUBMITTER: McMurry LM 

PROVIDER: S-EPMC89191 | biostudies-literature | 1999 Mar

REPOSITORIES: biostudies-literature

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

McMurry L M LM   McDermott P F PF   Levy S B SB  

Antimicrobial agents and chemotherapy 19990301 3


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 Escherichi  ...[more]

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