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首页> 外文期刊>PLoS Biology >A Conserved Endoplasmic Reticulum Membrane Protein Complex (EMC) Facilitates Phospholipid Transfer from the ER to Mitochondria
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A Conserved Endoplasmic Reticulum Membrane Protein Complex (EMC) Facilitates Phospholipid Transfer from the ER to Mitochondria

机译：保守的内质网膜蛋白复合物（EMC）促进磷脂从内质网转移到线粒体

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Mitochondrial membrane biogenesis and lipid metabolism require phospholipid transfer from the endoplasmic reticulum (ER) to mitochondria. Transfer is thought to occur at regions of close contact of these organelles and to be nonvesicular, but the mechanism is not known. Here we used a novel genetic screen in S. cerevisiae to identify mutants with defects in lipid exchange between the ER and mitochondria. We show that a strain missing multiple components of the conserved ER membrane protein complex (EMC) has decreased phosphatidylserine (PS) transfer from the ER to mitochondria. Mitochondria from this strain have significantly reduced levels of PS and its derivative phosphatidylethanolamine (PE). Cells lacking EMC proteins and the ER–mitochondria tethering complex called ERMES (the ER–mitochondria encounter structure) are inviable, suggesting that the EMC also functions as a tether. These defects are corrected by expression of an engineered ER–mitochondrial tethering protein that artificially tethers the ER to mitochondria. EMC mutants have a significant reduction in the amount of ER tethered to mitochondria even though ERMES remained intact in these mutants, suggesting that the EMC performs an additional tethering function to ERMES. We find that all Emc proteins interact with the mitochondrial translocase of the outer membrane (TOM) complex protein Tom5 and this interaction is important for PS transfer and cell growth, suggesting that the EMC forms a tether by associating with the TOM complex. Together, our findings support that the EMC tethers ER to mitochondria, which is required for phospholipid synthesis and cell growth.
机译：线粒体膜的生物发生和脂质代谢需要磷脂从内质网（ER）转移到线粒体。认为转移发生在这些细胞器的紧密接触区域，并且是非囊泡性的，但机理尚不清楚。在这里，我们在酿酒酵母中使用了一种新型的遗传筛选，以鉴定具有内质网和线粒体之间脂质交换缺陷的突变体。我们显示，缺少一个保守的ER膜蛋白复合物（EMC）的多个组件的菌株已减少了从ER到线粒体的磷脂酰丝氨酸（PS）转移。来自该菌株的线粒体具有显着降低的PS及其衍生物磷脂酰乙醇胺（PE）水平。缺少EMC蛋白的细胞和称为ERMES的ER-线粒体束缚复合物（ER-线粒体相遇结构）是不可行的，这表明EMC也可作为系绳。通过工程化的ER线粒体束缚蛋白的表达可以纠正这些缺陷，该蛋白将ER束缚到线粒体。即使这些突变体中的ERMES保持完好无损，EMC突变体的拴在线粒体上的ER数量也显着减少，这表明EMC对ERMES具有附加的拴系功能。我们发现，所有Emc蛋白都与外膜（TOM）复杂蛋白Tom5的线粒体转位酶相互作用，并且这种相互作用对于PS转移和细胞生长很重要，这表明EMC通过与TOM复杂相关形成系绳。总之，我们的发现支持EMC将ER束缚于线粒体，这是磷脂合成和细胞生长所必需的。

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