Harbauer Angelika B
F.M. Kirby Center for Neurobiology, Children's Hospital Boston, Boston, MA 02115, U.S.A.
Department of Neurobiology, Harvard Medical School, Cambridge, MA, U.S.A.
Biochem Soc Trans. 2017 Oct 15;45(5):1045-1052. doi: 10.1042/BST20170023. Epub 2017 Aug 4.
Neurons are post-mitotic cells that must function throughout the life of an organism. The high energetic requirements and Ca spikes of synaptic transmission place a burden on neuronal mitochondria. The removal of older mitochondria and the replenishment of the functional mitochondrial pool in axons with freshly synthesized components are therefore important parts of neuronal maintenance. Although the mechanism of mitochondrial protein import and dynamics is studied in great detail, the length of neurons poses additional challenges to those processes. In this mini-review, I briefly cover the basics of mitochondrial biogenesis and proceed to explain the interdependence of mitochondrial transport and mitochondrial health. I then extrapolate recent findings in yeast and mammalian cultured cells to neurons, making a case for axonal translation as a contributor to mitochondrial biogenesis in neurons.
神经元是终末分化细胞,必须在生物体的整个生命过程中发挥作用。突触传递对能量的高需求以及钙信号峰值给神经元线粒体带来了负担。因此,清除老化的线粒体并用新合成的成分补充轴突中功能性线粒体池是神经元维持的重要组成部分。尽管线粒体蛋白质导入和动态变化的机制已得到详细研究,但神经元的长度给这些过程带来了额外的挑战。在这篇小型综述中,我简要介绍了线粒体生物发生的基础知识,并进而解释线粒体运输与线粒体健康之间的相互依存关系。然后,我将酵母和哺乳动物培养细胞中的最新发现外推至神经元,提出轴突翻译是神经元线粒体生物发生的一个促成因素。