Identification of a protein mediating respiratory supercomplex stability.

Identification of a protein mediating respiratory supercomplex stability.
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DOI:
10.1016/j.cmet.2012.02.006
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发表时间:
2012-03-07
期刊:
影响因子:
29
通讯作者:
Rutter J
Rutter J
中科院分区:
生物学1区
文献类型:
--
作者:
Chen YC;Taylor EB;Dephoure N;Heo JM;Tonhato A;Papandreou I;Nath N;Denko NC;Gygi SP;Rutter J

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电子传递链的复合物结合成大的大分子组装体,这被认为有助于有效的电子流动。我们已经确定了一个保守的线粒体蛋白,命名为呼吸超复合体因子1(Rcf 1-Yml 030 w),这是所需的呼吸超复合体的正常组装。我们证明,Rcf 1稳定和独立地与复合物III和复合物IV的电子传递链。RCF 1基因的缺失导致呼吸受损,可能是由于呼吸超复合物的不稳定。与这些呼吸组件的假设功能一致,RCF 1的丢失引起线粒体氧化应激和损伤升高。最后,我们表明,RCF 1的哺乳动物同源物,HIG 2A的敲低,导致受损的超复合物的形成。我们认为Rcf 1是一个进化上保守的蛋白质家族的成员,其作用是促进呼吸超复合物的组装和活性。
The complexes of the electron transport chain associate into large macromolecular assemblies, which are believed to facilitate efficient electron flow. We have identified a conserved mitochondrial protein, named Respiratory superComplex Factor 1 (Rcf1—Yml030w), that is required for the normal assembly of respiratory supercomplexes. We demonstrate that Rcf1 stably and independently associates with both Complex III and Complex IV of the electron transport chain. Deletion of the RCF1 gene caused impaired respiration, probably as a result of destabilization of respiratory supercomplexes. Consistent with the hypothetical function of these respiratory assemblies, loss of RCF1 caused elevated mitochondrial oxidative stress and damage. Finally, we show that knockdown of HIG2A, a mammalian homolog of RCF1, causes impaired supercomplex formation. We suggest that Rcf1 is a member of an evolutionarily conserved protein family that acts to promote respiratory supercomplex assembly and activity.
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