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Nuclear Suppression of Mitochondrial Defects in Cells without the ND6 Subunit

机译：没有ND6亚基的细胞中线粒体缺陷的核抑制

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Previously, we characterized a mouse cell line, 4A, carrying a mitochondrial DNA mutation in the subunit for respiratory complex I, NADH dehydrogenase, in the ND6 gene. This mutation abolished the complex I assembly and disrupted the respiratory function of complex I. We now report here that a galactose-resistant clone, 4AR, was isolated from the cells carrying the ND6 mutation. 4AR still contained the homoplasmic mutation, and apparently there was no ND6 protein synthesis, whereas the assembly of other complex I subunits into complex I was recovered. Furthermore, the respiratory activity and mitochondrial membrane potential were fully recovered. To investigate the genetic origin of this compensation, the mitochondrial DNA (mtDNA) from 4AR was transferred to a new nuclear background. The transmitochondrial lines failed to grow in galactose medium. We further transferred mtDNA with a nonsense mutation at the ND5 gene to the 4AR nuclear background, and a suppression for mitochondrial deficiency was observed. Our results suggest that change(s) in the expression of a certain nucleus-encoded factor(s) can compensate for the absence of the ND6 or ND5 subunit.
机译：以前，我们表征了小鼠细胞系4A，该细胞系在ND6基因的呼吸道复合体I NADH脱氢酶的亚基中携带线粒体DNA突变。此突变废除了复合体I的装配，并破坏了复合体I的呼吸功能。我们现在在此报告，从带有ND6突变的细胞中分离出了半乳糖抗性克隆4AR。 4AR仍然包含同质突变，并且显然没有ND6蛋白合成，而其他复合物I亚基组装成复合物I被回收。此外，呼吸活动和线粒体膜电位已完全恢复。为了研究这种补偿的遗传起源，将来自4AR的线粒体DNA（mtDNA）转移到了新的核背景中。线粒体系不能在半乳糖培养基中生长。我们进一步将在ND5基因无意义突变的mtDNA转移至4AR核背景，并观察到线粒体缺乏的抑制。我们的结果表明，某些核编码因子表达的变化可以弥补ND6或ND5亚基的缺失。

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