Cytoplasmically inherited mutations of a human cell line resulting in deficient mitochondrial protein synthesis.
A large number of mutants deficient in mitochondrial protein synthesis (mtPS-) have been isolated from the human cell line VA2-B by subjecting cells partially depleted of their mtDNA to mutagenic treatments thought to be specific for mtDNA. Each of these mtPS- mutants has less than 10% of the wild-type rate of mitochondrial protein synthesis, exhibits reduced cytochrome oxidase and rutamycin sensitive ATPase activities, requires high concentrations of glucose, and grows indefinitely in the presence of 100 micrograms/ml of chloramphenicol (CAP). Fusion of cytoplasts from seven mtPS- mutants to the nucleated thioguanine-resistant VA2-B derivative TG-6 has yielded numerous cybrid clones which grow in CAP plus thioguanine, whereas almost no clones have resulted from the fusion of nucleated mtPS- cells to TG-6 cells: these results suggest that the gene(s) coding for the phenotype of mtPS- cells is localized in the cytoplasm (mtDNA?).
D002460:Cell Line; D002701:Chloramphenicol / Q000494:pharmacology; D004272:DNA, Mitochondrial / Q000235:genetics*; D004351:Drug Resistance; D005947:Glucose / Q000378:metabolism; D006801:Humans; D008928:Mitochondria / Q000378:metabolism*; D009154:Mutation; D010641:Phenotype; D011506:Proteins / Q000378:metabolism*
D004272:DNA, Mitochondrial; D011506:Proteins; D002701:Chloramphenicol; D005947:Glucose