Lee Hakjoo, Yoon Yisang
Department of Physiology, Medical College of Georgia, Augusta University, Augusta, GA 30912, USA.
Antioxidants (Basel). 2018 Dec 8;7(12):186. doi: 10.3390/antiox7120186.
The maintenance of mitochondrial energetics requires the proper regulation of mitochondrial morphology, and vice versa. Mitochondrial dynamins control mitochondrial morphology by mediating fission and fusion. One of them, optic atrophy 1 (OPA1), is the mitochondrial inner membrane remodeling protein. OPA1 has a dual role in maintaining mitochondrial morphology and energetics through mediating inner membrane fusion and maintaining the cristae structure. OPA1 is expressed in multiple variant forms through alternative splicing and post-translational proteolytic cleavage, but the functional differences between these variants have not been completely understood. Recent studies generated new information regarding the role of OPA1 cleavage. In this review, we will first provide a brief overview of mitochondrial membrane dynamics by describing fission and fusion that are mediated by mitochondrial dynamins. The second part describes OPA1-mediated fusion and energetic maintenance, the role of OPA1 cleavage, and a new development in OPA1 function, in which we will provide new insight for what OPA1 does and what proteolytic cleavage of OPA1 is for.
线粒体能量代谢的维持需要对线粒体形态进行适当调控,反之亦然。线粒体动力蛋白通过介导分裂和融合来控制线粒体形态。其中之一,视神经萎缩蛋白1(OPA1),是线粒体内膜重塑蛋白。OPA1在维持线粒体形态和能量代谢方面具有双重作用,即通过介导内膜融合和维持嵴结构来实现。OPA1通过可变剪接和翻译后蛋白水解切割以多种变体形式表达,但这些变体之间的功能差异尚未完全明确。最近的研究产生了关于OPA1切割作用的新信息。在本综述中,我们将首先通过描述由线粒体动力蛋白介导的分裂和融合来简要概述线粒体膜动力学。第二部分描述OPA1介导的融合和能量维持、OPA1切割的作用以及OPA1功能的新进展,我们将为OPA1的作用以及OPA1的蛋白水解切割目的提供新的见解。