F.M. Kirby Neurobiology Center, Children's Hospital Boston, and Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115, USA.
Cold Spring Harb Perspect Biol. 2013 Jun 1;5(6):a011304. doi: 10.1101/cshperspect.a011304.
Neurons, perhaps more than any other cell type, depend on mitochondrial trafficking for their survival. Recent studies have elucidated a motor/adaptor complex on the mitochondrial surface that is shared between neurons and other animal cells. In addition to kinesin and dynein, this complex contains the proteins Miro (also called RhoT1/2) and milton (also called TRAK1/2) and is responsible for much, although not necessarily all, mitochondrial movement. Elucidation of the complex has permitted inroads for understanding how this movement is regulated by a variety of intracellular signals, although many mysteries remain. Regulating mitochondrial movement can match energy demand to energy supply throughout the extraordinary architecture of these cells and can control the clearance and replenishing of mitochondria in the periphery. Because the extended axons of neurons contain uniformly polarized microtubules, they have been useful for studying mitochondrial motility in conjunction with biochemical assays in many cell types.
神经元可能比其他任何类型的细胞都更依赖于线粒体的运输来维持其生存。最近的研究揭示了一种存在于神经元和其他动物细胞之间的线粒体表面的运动蛋白/衔接蛋白复合物。除了驱动蛋白和动力蛋白外,该复合物还包含蛋白 Miro(也称为 RhoT1/2)和 Milton(也称为 TRAK1/2),并且负责大部分(尽管不一定是全部)线粒体的运动。该复合物的阐明使得人们能够深入了解这种运动是如何被各种细胞内信号调节的,尽管仍有许多谜团存在。调节线粒体的运动可以使能量需求与这些细胞的特殊结构中的能量供应相匹配,并控制线粒体在周边的清除和补充。由于神经元的长轴突含有均匀极化的微管,因此它们一直被用于与许多细胞类型的生化测定结合研究线粒体的运动。