Borbolis Fivos, Kteniadaki Myrsini, Palikaras Konstantinos
Department of Physiology, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
Athens International Master's Programme in Neurosciences, Department of Biology, National and Kapodistrian University of Athens, Athens, Greece.
MicroPubl Biol. 2024 Jun 24;2024. doi: 10.17912/micropub.biology.001232. eCollection 2024.
Mitophagy, the selective removal of dysfunctional mitochondria, is pivotal for the maintenance of neuronal function and survival. MEC-12/α-tubulin contributes to neuronal physiology through the regulation of microtubule assembly, intracellular transport and mitochondrial distribution. However, its role in mitochondrial dynamics and mitophagy remains obscure. Here, we demonstrate that MEC-12 influences mitochondrial morphology under basal conditions and regulates the axonal mitochondrial population. Impairment of MEC-12 results in compromised axonal mitophagy under both basal conditions and oxidative stress. Our results uncover the critical role of MEC-12/α-tubulin for maintaining a healthy mitochondrial population in axons and highlight the complex interplay between microtubules, mitophagy and neuronal health.
线粒体自噬，即对功能失调的线粒体进行选择性清除，对于维持神经元功能和存活至关重要。MEC - 12/α - 微管蛋白通过调节微管组装、细胞内运输和线粒体分布，对神经元生理功能发挥作用。然而，其在线粒体动力学和线粒体自噬中的作用仍不清楚。在此，我们证明MEC - 12在基础条件下影响线粒体形态，并调节轴突中的线粒体数量。MEC - 12功能受损会导致基础条件下和氧化应激时轴突线粒体自噬功能受损。我们的研究结果揭示了MEC - 12/α - 微管蛋白在维持轴突中健康线粒体数量方面的关键作用，并突出了微管、线粒体自噬和神经元健康之间复杂的相互作用。
