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

被引:179
作者
McMurry, LM
McDermott, PF
Levy, SB
机构
[1] Tufts Univ, Sch Med, Ctr Adapt Genet & Drug Resistance, Boston, MA 02111 USA
[2] Tufts Univ, Sch Med, Dept Mol Biol & Microbiol, Boston, MA 02111 USA
[3] Tufts Univ, Sch Med, Dept Med, Boston, MA 02111 USA
关键词
D O I
10.1128/AAC.43.3.711
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
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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页码:711 / 713
页数:3
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