Pernas Lena, Scorrano Luca
Dulbecco-Telethon Institute, Venetian Institute of Molecular Medicine, 35129 Padova, Italy; email:
Annu Rev Physiol. 2016;78:505-31. doi: 10.1146/annurev-physiol-021115-105011. Epub 2015 Nov 19.
Permanent residency in the eukaryotic cell pressured the prokaryotic mitochondrial ancestor to strategize for intracellular living. Mitochondria are able to autonomously integrate and respond to cellular cues and demands by remodeling their morphology. These processes define mitochondrial dynamics and inextricably link the fate of the mitochondrion and that of the host eukaryote, as exemplified by the human diseases that result from mutations in mitochondrial dynamics proteins. In this review, we delineate the architecture of mitochondria and define the mechanisms by which they modify their shape. Key players in these mechanisms are discussed, along with their role in manipulating mitochondrial morphology during cellular action and development. Throughout, we highlight the evolutionary context in which mitochondrial dynamics emerged and consider unanswered questions whose dissection might lead to mitochondrial morphology-based therapies.
在真核细胞中的永久居留迫使原核生物的线粒体祖先制定细胞内生存策略。线粒体能够通过重塑其形态自主整合并响应细胞信号和需求。这些过程定义了线粒体动力学,并将线粒体的命运与宿主真核生物的命运紧密相连,线粒体动力学蛋白突变导致的人类疾病就是例证。在本综述中,我们描绘了线粒体的结构,并确定了它们改变形状的机制。讨论了这些机制中的关键参与者,以及它们在细胞活动和发育过程中操纵线粒体形态的作用。在整个过程中,我们强调了线粒体动力学出现的进化背景,并思考了一些尚未解答的问题,对这些问题的剖析可能会带来基于线粒体形态的治疗方法。