Lichtor T, Tung B, Getz G S
Biochemistry. 1979 Jun 12;18(12):2582-90. doi: 10.1021/bi00579a023.
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.
分离出对药物鲁塔霉素具有抗性的小鼠成纤维细胞,发现它们也存在呼吸缺陷。这些细胞产生大量乳酸,耗氧数据表明电子传递链的第一个复合物NADH - 辅酶Q还原酶存在缺陷。突变细胞中鱼藤酮敏感的NADH - 细胞色素c还原酶和丙酮酸脱氢酶复合物的丙酮酸脱羧酶水平明显降低。电子传递链的其他成分似乎功能正常。将突变细胞去核并与另一种细胞系融合,得到的胞质杂种表现出与原始突变体相似的呼吸缺陷模式。这些结果表明,这种呼吸缺陷是该细胞系中细胞质遗传的特征。