MICU1 缺失改变线粒体形态和细胞色素 C 的释放。

MICU1 deficiency alters mitochondrial morphology and cytochrome C release.

机构信息

Gottfried Schatz Research Center: Molecular Biology and Biochemistry, Medical University of Graz, Neue Stiftingtalstraße 6/4, Graz, 8010 Austria.

Gottfried Schatz Research Center: Molecular Biology and Biochemistry, Medical University of Graz, Neue Stiftingtalstraße 6/4, Graz, 8010 Austria; BioTechMed, Graz, Austria.

出版信息

Cell Calcium. 2023 Jul;113:102765. doi: 10.1016/j.ceca.2023.102765. Epub 2023 Jun 2.

DOI:10.1016/j.ceca.2023.102765

PMID:37290367

Abstract

The mitochondrial inner boundary membrane harbors a protein called MICU1, which is sensitive to Ca and binds to the MICOS components Mic60 and CHCHD2. Changes in the mitochondrial cristae junction structure and organization in MICU1 cells lead to increased cytochrome c release, membrane potential rearrangement, and changes in mitochondrial Ca uptake dynamics. These findings shed new light on the multifaceted role of MICU1, highlighting its involvement not only as an interaction partner and regulator of the MCU complex but also as a crucial determinant of mitochondrial ultrastructure and, thus, an essential player in processes initiating apoptosis.

摘要

线粒体的内界膜含有一种叫做 MICU1 的蛋白质，它对 Ca 敏感，并与 MICOS 组件 Mic60 和 CHCHD2 结合。MICU1 细胞中线粒体嵴连接结构和组织的变化导致细胞色素 c 释放增加、膜电位重排以及线粒体 Ca 摄取动力学的变化。这些发现为 MICU1 的多方面作用提供了新的认识，强调了它不仅作为 MCU 复合物的相互作用伙伴和调节剂，而且作为线粒体超微结构的关键决定因素的作用，因此是启动细胞凋亡过程的重要参与者。