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Antimicrobial Agents and Chemotherapy, March 1999, p. 711-713, Vol. 43, No. 3
0066-4804/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Genetic Evidence that InhA of Mycobacterium smegmatis Is a Target for Triclosan

Laura M. McMurry,1,* Patrick F. McDermott,1,dagger and Stuart B. Levy1,2

Center for Adaptation Genetics and Drug Resistance, and Departments of Molecular Biology and Microbiology1 and Medicine,2 Tufts University School of Medicine, Boston, Massachusetts 02111

Received 14 September 1998/Returned for modification 12 November 1998/Accepted 14 December 1998

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.

* Corresponding author. Mailing address: Center for Adaptation Genetics and Drug Resistance, Tufts University School of Medicine, 136 Harrison Ave., Boston, MA 02111. Phone: (617) 636-6764. Fax: (617) 636-0458. E-mail: slevy{at}opal.tufts.edu or lmcmur01{at}tufts.edu.

dagger Present address: Department of Microbiology and Immunology, Wake Forest University School of Medicine, Winston-Salem, NC 27157.

Antimicrobial Agents and Chemotherapy, March 1999, p. 711-713, Vol. 43, No. 3
0066-4804/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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