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Science. 1996 Jun 14;272(5268):1641-3.

Compensatory ahpC gene expression in isoniazid-resistant Mycobacterium tuberculosis.

Author information

1
Laboratory of Tuberculosis and Molecular Microbiology, PathoGenesis Corporation, Seattle, Washington 98119, USA.

Abstract

Mutations that eliminate KatG catalase-peroxidase activity prevent activation of isoniazid and are a major mechanism of resistance to this principal drug for the treatment of Mycobacterium tuberculosis infections. However, the loss of KatG activity in clinical isolates seemed paradoxical because KatG is considered an important factor for the survival of the organism. Expression of either KatG or the recently identified alkyl hydroperoxidase AhpC was sufficient to protect bacilli against the toxic effects of organic peroxides. To survive during infection, isoniazid-resistant KatG mutants have apparently compensated for the loss of KatG catalase-peroxidase activity by a second mutation, resulting in hyperexpression of AhpC.

PMID:
8658136
DOI:
10.1126/science.272.5268.1641
[Indexed for MEDLINE]

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