Deletion of mitochondrial genetic markers in yeast by ethidium and the photoaffinity probe, ethidium azide.
Induction of petite (cytoplasmic-respiration-deficient, rho-,rho-) mutations in yeast and deletion of mitochondrial drug-resistance genetic markers were compared after after treatment with ethidium and the corresponding photoaffinity probe, ethidium azide. Deletion of mitochondrial drug-resistance markers for chloramphenicol, erythromycin and oligomycin in these petite mutants was observed during prolonged treatment times with ethidium and with ethidium azide in the dark. A similar loss of drug-resistance markers was also observed in petites produced by photolytic treatment with the azide analogue, although the rate of loss appeared to be somewhat less. These results confirmed the usefulness of photoaffinity labeling with ethidium monoazide for studies of mitochondrial mutations.
D001386:Azides / Q000494:pharmacology; D002701:Chloramphenicol / Q000494:pharmacology; D004272:DNA, Mitochondrial / Q000235:genetics*; D004352:Drug Resistance, Microbial / Q000187:drug effects; D004917:Erythromycin / Q000494:pharmacology; D004996:Ethidium / Q000031:analogs & derivatives* / Q000494:pharmacology*; D008027:Light; D009154:Mutation; D009840:Oligomycins / Q000494:pharmacology; D012441:Saccharomyces cerevisiae / Q000235:genetics*
D001386:Azides; D004272:DNA, Mitochondrial; D009840:Oligomycins; D004917:Erythromycin; D002701:Chloramphenicol; C014535:8-azidoethidium; D004996:Ethidium