Liu Xingguo, Hajnóczky György
Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Int J Biochem Cell Biol. 2009 Oct;41(10):1972-6. doi: 10.1016/j.biocel.2009.05.013. Epub 2009 May 27.
Calcium oscillations control mitochondrial motility along the microtubules and in turn, support on-demand distribution of mitochondria. However, the mechanism mediating the Ca(2+) effect remained a mystery. Recently, several papers reported on the Ca(2+)-dependent regulation of mitochondrial dynamics by a Miro-Milton complex linking mitochondria to kinesin motors. Both mitochondrial motility and fusion-fission dynamics seem to be sensitive to a Ca(2+)-dependent switch by this complex. Evidence is emerging that calcium signaling through Miro-Milton is central to coordination of the local oxidative metabolism with the energy demands and protection against Ca(2+)-induced cell injury.
钙振荡控制线粒体沿微管的运动,进而支持线粒体的按需分布。然而,介导Ca(2+)效应的机制仍是个谜。最近,几篇论文报道了一种将线粒体与驱动蛋白连接起来的Miro-Milton复合体对线粒体动力学的Ca(2+)依赖性调节。线粒体的运动性和融合-分裂动力学似乎都对该复合体的Ca(2+)依赖性开关敏感。越来越多的证据表明,通过Miro-Milton的钙信号传导对于局部氧化代谢与能量需求的协调以及防止Ca(2+)诱导的细胞损伤至关重要。