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Cardiolipin remodeling enables protein crowding in the inner mitochondrial membrane
The EMBO Journal ( IF 11.4 ) Pub Date : 2021-10-18 , DOI: 10.15252/embj.2021108428
Yang Xu 1 , Hediye Erdjument-Bromage 2, 3 , Colin K L Phoon 4 , Thomas A Neubert 2, 3 , Mindong Ren 1, 3 , Michael Schlame 1, 3
Affiliation  

Mitochondrial cristae are extraordinarily crowded with proteins, which puts stress on the bilayer organization of lipids. We tested the hypothesis that the high concentration of proteins drives the tafazzin-catalyzed remodeling of fatty acids in cardiolipin, thereby reducing bilayer stress in the membrane. Specifically, we tested whether protein crowding induces cardiolipin remodeling and whether the lack of cardiolipin remodeling prevents the membrane from accumulating proteins. In vitro, the incorporation of large amounts of proteins into liposomes altered the outcome of the remodeling reaction. In yeast, the concentration of proteins involved in oxidative phosphorylation (OXPHOS) correlated with the cardiolipin composition. Genetic ablation of either remodeling or biosynthesis of cardiolipin caused a substantial drop in the surface density of OXPHOS proteins in the inner membrane of the mouse heart and Drosophila flight muscle mitochondria. Our data suggest that OXPHOS protein crowding induces cardiolipin remodelling and that remodeled cardiolipin supports the high concentration of these proteins in the inner mitochondrial membrane.

中文翻译:

心磷脂重塑使蛋白质在线粒体内膜中拥挤

线粒体嵴中挤满了蛋白质,这给脂质的双层组织带来了压力。我们测试了这样一个假设,即高浓度蛋白质会驱动心磷脂中 tafazzin 催化的脂肪酸重塑,从而减少膜中的双层应力。具体来说,我们测试了蛋白质拥挤是否会诱导心磷脂重塑,以及心磷脂重塑的缺乏是否会阻止膜积累蛋白质。体外,将大量蛋白质掺入脂质体改变了重塑反应的结果。在酵母中,参与氧化磷酸化 (OXPHOS) 的蛋白质浓度与心磷脂成分相关。心磷脂重塑或生物合成的基因消融导致小鼠心脏内膜和果蝇飞行肌线粒体中 OXPHOS 蛋白的表面密度显着下降。我们的数据表明,OXPHOS 蛋白拥挤诱导心磷脂重塑,重塑的心磷脂支持线粒体内膜中这些蛋白质的高浓度。
更新日期:2021-12-01
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