Analysis of ahpC gene mutations in isoniazid-resistant clinical isolates of Mycobacterium tuberculosis.
The ahpC genes of 57 clinical isolates and one in vitro mutant of Mycobacterium tuberculosis were evaluated by nucleotide sequence analyses. Although compensatory ahpC promoter mutations were identified in 8 catalase-negative, katG-defective strains, the ahpC genes of 25 catalase-positive, isoniazid-resistant isolates and 25 drug-sensitive strains were not altered.
Kelley
C L
CL
Laboratory of Mycobacteria, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, Maryland 20892, USA.
Rouse
D A
DA
Morris
S L
SL
D000995:Antitubercular Agents / Q000494:pharmacology*; D001483:Base Sequence; D002374:Catalase / Q000378:metabolism; D004352:Drug Resistance, Microbial; D007538:Isoniazid / Q000494:pharmacology*; D009154:Mutation; D009169:Mycobacterium tuberculosis / Q000187:drug effects* / Q000201:enzymology / Q000235:genetics*; D010088:Oxidoreductases / Q000235:genetics*; D010544:Peroxidases; D054464:Peroxiredoxins; D010641:Phenotype
D000995:Antitubercular Agents; D010088:Oxidoreductases; D010544:Peroxidases; D054464:Peroxiredoxins; D002374:Catalase; D007538:Isoniazid