Genetic evidence that InhA of Mycobacterium smegmatis is a target for triclosan.
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.
McMurry
L M
LM
Center for Adaptation Genetics and Drug Resistance, Tufts University School of Medicine, Boston, Massachusetts 02111, USA.
McDermott
P F
PF
Levy
S B
SB
D000891:Anti-Infective Agents, Local / Q000494:pharmacology*; D001426:Bacterial Proteins / Q000235:genetics*; D006801:Humans; D007538:Isoniazid / Q000494:pharmacology; D009154:Mutation; D020102:Mycobacterium smegmatis / Q000187:drug effects* / Q000235:genetics* / Q000302:isolation & purification; D010088:Oxidoreductases / Q000235:genetics*; D014260:Triclosan / Q000494:pharmacology*
D000891:Anti-Infective Agents, Local; D001426:Bacterial Proteins; D014260:Triclosan; D010088:Oxidoreductases; C085257:InhA protein, Mycobacterium; D007538:Isoniazid