Restoration of electron transport without proton pumping in mammalian mitochondria
Restoration of electron transport without proton pumping in mammalian mitochondria
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DOI：
10.1073/pnas.0810518105
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发表时间：
2008-12-02
影响因子：
11.1
通讯作者：
Antonio Enriquez, Jose
中科院分区：
文献类型：
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作者：
Perales-Clemente, Ester;Pilar Bayona-Bafaluy, Maria;Antonio Enriquez, Jose
我们已经恢复了辅酶Q氧化能力的小鼠线粒体DNA少细胞（p细胞）转化他们的替代氧化酶Aox的Emericella nidulans。用酿酒酵母的NADH脱氢酶、Ndi 1和Aox共转化p细胞，恢复了NADH DH/CoQ还原酶和CoQ氧化酶的活性。AOX氧化辅酶Q可降低rho degree细胞对丙酮酸和尿苷的依赖性。AOX和NDI 1的共表达进一步改善了NAD（+）的再循环。因此，2种单蛋白酶恢复哺乳动物线粒体中的电子传递，取代了>80种核DNA编码的蛋白和11种mtDNA编码的蛋白。由于这些酶不泵质子，我们能够分裂电子传递和质子泵（ATP合成），并询问与氧化磷酸化损失相关的代谢缺陷应归因于这两个过程中的每一个。
We have restored the CoQ oxidative capacity of mouse mtDNA-less cells (p cells) by transforming them with the alternative oxidase Aox of Emericella nidulans. Cotransforming p cells with the NADH dehydrogenase of Saccharomyces cerevisiae, Ndi1 and Aox recovered the NADH DH/CoQ reductase and the CoQ oxidase activities. CoQ oxidation by AOX reduces the dependence of rho degrees cells on pyruvate and uridine. Coexpression of AOX and NDI1 further improves the recycling of NAD(+). Therefore, 2 single-protein enzymes restore the electron transport in mammalian mitochondria substituting >80 nuclear DNA-encoded and 11 mtDNA-encoded proteins. Because those enzymes do not pump protons, we were able to split electron transport and proton pumping (ATP synthesis) and inquire which of the metabolic deficiencies associated with the loss of oxidative phosphorylation should be attributed to each of the 2 processes.