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首页> 外文期刊>Cell metabolism >A SIRT7-dependent acetylation switch of GABPβ1 controls mitochondrial function
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A SIRT7-dependent acetylation switch of GABPβ1 controls mitochondrial function

机译：GABPβ1的依赖SIRT7的乙酰化开关控制线粒体功能

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摘要

Mitochondrial activity is controlled by proteins encoded by both nuclear and mitochondrial DNA. Here, we identify Sirt7 as a crucial regulator of mitochondrial homeostasis. Sirt7 deficiency in mice induces multisystemic mitochondrial dysfunction, which is reflected by increased blood lactate levels, reduced exercise performance, cardiac dysfunction, hepatic microvesicular steatosis, and age-related hearing loss. This link between SIRT7 and mitochondrial function is translatable in humans, where SIRT7 overexpression rescues the mitochondrial functional defect in fibroblasts with a mutation in NDUFSI. These wide-ranging effects of SIRT7 on mitochondrial homeostasis are the consequence of the deacetylation of distinct lysine residues located in the hetero- and homodimerization domains of GABPβ1, a master regulator of nuclear-encoded mitochondrial genes. SIRT7-mediated deacetylation of GABPβ1 facilitates complex formation with GABPα and the transcriptional activation of the GABPα/GABPβ heterotetramer. Altogether, these data suggest that SIRT7 is a dynamic nuclear regulator of mitochondrial function through its impact on GABPβ1 function.
机译：线粒体活性受核和线粒体DNA编码的蛋白质控制。在这里，我们确定Sirt7是线粒体稳态的关键调节器。小鼠的Sirt7缺乏症会诱发多系统性线粒体功能障碍，这可通过血液乳酸水平升高，运动表现降低，心脏功能障碍，肝微囊脂肪变性和与年龄相关的听力损失来反映。 SIRT7和线粒体功能之间的这种联系在人类中是可翻译的，SIRT7的过表达可以挽救成纤维细胞中线粒体功能缺陷，并导致NDUFSI发生突变。 SIRT7对线粒体稳态的这些广泛影响是位于GABPβ1（核编码线粒体基因的主要调控因子）的异二聚域和同二聚域中的不同赖氨酸残基脱乙酰化的结果。 SIRT7介导的GABPβ1脱乙酰基促进了与GABPα的复合物形成以及GABPα/GABPβ异四聚体的转录激活。总而言之，这些数据表明SIRT7通过影响GABPβ1功能而成为线粒体功能的动态核调节剂。

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