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首页> 外文期刊>Cell metabolism >CCDC90A (MCUR1) Is a Cytochrome c Oxidase Assembly Factor and Not a Regulator of the Mitochondrial Calcium Uniporter
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CCDC90A (MCUR1) Is a Cytochrome c Oxidase Assembly Factor and Not a Regulator of the Mitochondrial Calcium Uniporter

机译：CCDC90A（MCUR1）是细胞色素c氧化酶装配因子，而不是线粒体钙单向转运蛋白的调节剂

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摘要

Mitochondrial calcium is an important modulator of cellular metabolism. CCDC90A was reported to be a regulator of the mitochondrial calcium uniporter (MCU) complex, a selective channel that controls mitochondrial calcium uptake, and hence was renamed MCUR1. Here we show that suppression of CCDC90A in human fibroblasts produces a specific cytochrome c oxidase (COX) assembly defect, resulting in decreased mitochondrial membrane potential and reduced mitochondrial calcium uptake capacity. Fibroblasts from patients with COX assembly defects due to mutations in TACO1 or COX10 also showed reduced mitochondrial membrane potential and impaired calcium uptake capacity, both of which were rescued by expression of the respective wild-type cDNAs. Deletion of fmp32, a homolog of CCDC90A in Saccharomyces cerevisiae, an organism that lacks an MCU, also produces a COX deficiency, demonstrating that the function of CCDC90A is evolutionarily conserved. We conclude that CCDC90A plays a role in COX assembly and does not directly regulate MCU.
机译：线粒体钙是细胞代谢的重要调节剂。据报道，CCDC90A是线粒体钙单向转运蛋白（MCU）复合物的调节剂，该复合物是控制线粒体钙摄取的选择性通道，因此被更名为MCUR1。在这里，我们表明抑制人类成纤维细胞中的CCDC90A会产生特定的细胞色素C氧化酶（COX）组装缺陷，从而导致线粒体膜电位降低和线粒体钙摄取能力降低。来自因TACO1或COX10突变而导致COX装配缺陷的患者的成纤维细胞还显示线粒体膜电位降低和钙摄取能力受损，这两者均通过各自野生型cDNA的表达得以挽救。缺失酿酒酵母（一种缺乏MCU的生物体）中CCDC90A的同系物fmp32也会产生COX缺乏症，这表明CCDC90A的功能在进化上是保守的。我们得出的结论是CCDC90A在COX组装中起作用，并且不直接调节MCU。

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