SNX10 at the crossroad of endocytosis and piecemeal mitophagy.

Laura Trachsel-Moncho, Benan John Mathai, Chiara Veroni, Anne Simonsen
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Abstract

Mitophagy targets damaged or dysfunctional mitochondria for lysosomal degradation. While canonical mitophagy pathways target the whole mitochondria for lysosomal degradation, it has become clear that selected mitochondrial components can be targeted for lysosomal degradation via other pathways, such as piecemeal mitophagy or mitochondria-derived vesicles. In a recent study, we identified the PX domain-containing endosomal protein SNX10 as a negative modulator of piecemeal mitophagy. Endosomal SNX10-positive vesicles dynamically interact with mitochondria and acquire selected mitochondrial proteins upon hypoxia. Zebrafish larvae lacking Snx10 show elevated Cox-IV degradation, increased levels of reactive oxygen species (ROS), and ROS-dependent neuronal death.

SNX10处于内吞作用和碎片有丝分裂的十字路口。
线粒体自噬以受损或功能失调的线粒体为目标进行溶酶体降解。虽然典型的线粒体自噬途径以整个线粒体为目标进行溶酶体降解,但很明显,选择的线粒体成分可以通过其他途径,如片段线粒体自噬或线粒体来源的囊泡,成为溶酶体降解的目标。在最近的一项研究中,我们发现含有PX结构域的内体蛋白SNX10是片段有丝分裂的负调节因子。内体snx10阳性囊泡与线粒体动态相互作用,并在缺氧时获得选定的线粒体蛋白。缺乏Snx10的斑马鱼幼虫表现出Cox-IV降解升高,活性氧(ROS)水平升高以及ROS依赖性神经元死亡。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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