Department of Neurobiology, Stanford University School of Medicine, Laboratory of Thomas Clandinin, Fairchild Building, D217, 299 Campus Drive West, Stanford, CA 94305, USA.
Curr Opin Cell Biol. 2016 Feb;38:90-9. doi: 10.1016/j.ceb.2016.02.022. Epub 2016 Mar 15.
A properly organized, healthy mitochondrial network is critical for preserving neuronal form and function. Large, elaborately branched neuronal morphologies, energetic demands that fluctuate in time and space, and long neuronal lifespans make the distribution of mitochondria in neurons a particularly complex problem. Moreover, mitochondrial networks are dynamic systems in which mitochondria grow, divide and fuse, move along cytoskeletal filaments, and are degraded in an active fashion. Although the molecular mechanisms that govern mitochondrial motility, in particular, are increasingly well-characterized, the manner in which these mechanisms are coordinated to give rise to the global mitochondrial distribution in neurons is less well understood. Here I review several molecular mechanisms for mitochondrial motility in the context of a general mechanical framework. In this framework, molecular pathways that control mitochondrial movement can be reduced to their effects on the balance of forces that act on mitochondria, driving and opposing movement.
一个组织良好、健康的线粒体网络对于维持神经元的形态和功能至关重要。大型、分支复杂的神经元形态、随时间和空间变化的能量需求以及较长的神经元寿命,使得线粒体在神经元中的分布成为一个特别复杂的问题。此外,线粒体网络是一个动态系统,其中线粒体生长、分裂和融合,沿细胞骨架丝移动,并以活跃的方式被降解。尽管控制线粒体运动的分子机制,特别是越来越多地被描述,但这些机制如何协调以产生神经元中全局线粒体分布的方式还不太清楚。在这里,我将在一个通用的力学框架内,回顾线粒体运动的几种分子机制。在这个框架中,控制线粒体运动的分子途径可以简化为它们对作用于线粒体的力的平衡的影响,推动和对抗运动。