Cytoplasmically inherited respiratory deficiency of a mouse fibroblast line which is resistant to rutamycin

Mouse fibroblasts resistant to the drug rutamycin were isolated and found also to be respiratory deficient. These cells produce large amounts of lactic acid, and oxygen consumption data indicate that the first complex of the electron transport chain, NADH-coenzyme Q reductase, is defective. Levels of rotenone-sensitive NADH-cytochrome c reductase and pyruvate decarboxylase of the pyruvate dehydrogenase complex are markedly depressed in the mutant cells. Other components of the electron transport chain appear to be fully functional. The mutant cells were enucleated and fused with another cell line, and the resulting cybrid demonstrated a similar pattern of respiratory deficiency as did the original mutant. These results indicate that this defect in respiration is a cytoplasmically inherited characteristic in this cell line.