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线粒体基质 Ca2+ 作为一种内在信号调节轴突中线粒体的运动。

Mitochondrial matrix Ca2+ as an intrinsic signal regulating mitochondrial motility in axons.

机构信息

Zilkha Neurogenetic Institute and Department of Cell and Neurobiology, University of Southern California, Los Angeles, CA 90033, USA.

出版信息

Proc Natl Acad Sci U S A. 2011 Sep 13;108(37):15456-61. doi: 10.1073/pnas.1106862108. Epub 2011 Aug 29.

Abstract

The proper distribution of mitochondria is particularly vital for neurons because of their polarized structure and high energy demand. Mitochondria in axons constantly move in response to physiological needs, but signals that regulate mitochondrial movement are not well understood. Aside from producing ATP, Ca(2+) buffering is another main function of mitochondria. Activities of many enzymes in mitochondria are also Ca(2+)-dependent, suggesting that intramitochondrial Ca(2+) concentration is important for mitochondrial functions. Here, we report that mitochondrial motility in axons is actively regulated by mitochondrial matrix Ca(2+). Ca(2+) entry through the mitochondrial Ca(2+) uniporter modulates mitochondrial transport, and mitochondrial Ca(2+) content correlates inversely with the speed of mitochondrial movement. Furthermore, the miro1 protein plays a role in Ca(2+) uptake into the mitochondria, which subsequently affects mitochondrial movement.

摘要

线粒体的适当分布对神经元尤为重要,因为它们具有极化结构和高能量需求。轴突中的线粒体不断根据生理需求移动,但调节线粒体运动的信号尚未得到很好的理解。除了产生 ATP 外,Ca(2+)缓冲也是线粒体的另一个主要功能。线粒体中许多酶的活性也依赖于 Ca(2+),这表明线粒体内 Ca(2+)浓度对线粒体功能很重要。在这里,我们报告说,轴突中的线粒体运动是由线粒体基质 Ca(2+)主动调节的。通过线粒体 Ca(2+)单向转运体进入 Ca(2+)调节线粒体运输,线粒体 Ca(2+)含量与线粒体运动速度呈反比。此外,miro1 蛋白在 Ca(2+)摄取到线粒体中发挥作用,进而影响线粒体运动。

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