Tagaya Mitsuo, Arasaki Kohei
School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Hachioji, Tokyo, 192-0392, Japan.
Adv Exp Med Biol. 2017;997:33-47. doi: 10.1007/978-981-10-4567-7_3.
Mitochondria are powerhouses and central to metabolism in cells. They are highly dynamic organelles that continuously fuse, divide, and move along the cytoskeleton to form the mitochondrial network. The fusion and fission are catalyzed by four dynamin-related GTPases in mammals that are controlled by a variety of protein-protein interactions and posttranslational modifications. Mitochondrial dynamics and metabolism are linked and regulate each other. Starvation induces mitochondrial elongation, which enables the mitochondria to produce energy more efficiently and to escape from autophagic degradation. Damaged portions of mitochondria are removed from the healthy parts by division, and subsequently degraded via a specific mode of autophagy termed mitophagy. Recent studies shed light on the contribution of the endoplasmic reticulum to mitochondrial dynamics and the cooperation of the two organelles for the progression of autophagy including mitophagy. A subdomain of the endoplasmic reticulum apposed to mitochondria is called the mitochondria-associated membrane (MAM), which comprises a unique set of proteins that interact with mitochondrial proteins. Here we review our current understanding of the molecular mechanisms of mitochondrial dynamics and mitochondria-related processes in the context of the interaction with the endoplasmic reticulum.
线粒体是细胞中的能量工厂，也是细胞新陈代谢的核心。它们是高度动态的细胞器，不断融合、分裂，并沿着细胞骨架移动以形成线粒体网络。在哺乳动物中，融合和裂变由四种与发动蛋白相关的GTP酶催化，这些酶受多种蛋白质-蛋白质相互作用和翻译后修饰的控制。线粒体动态变化与新陈代谢相互关联、相互调节。饥饿会诱导线粒体延长，使线粒体能够更有效地产生能量，并避免自噬降解。线粒体受损部分通过分裂从健康部分移除，随后通过一种称为线粒体自噬的特定自噬模式进行降解。最近的研究揭示了内质网对线粒体动态变化的作用以及这两种细胞器在包括线粒体自噬在内的自噬进程中的协同作用。内质网中与线粒体相邻的亚结构域称为线粒体相关膜（MAM），它包含一组独特的与线粒体蛋白相互作用的蛋白质。在此，我们在与内质网相互作用的背景下，综述了我们目前对线粒体动态变化和线粒体相关过程分子机制的理解。
