Hegde Sneha, Modi Souvik, Deihl Ennis W, Glomb Oliver Vinzenz, Yogev Shaul, Hoerndli Frederic J, Koushika Sandhya P
Tata Institute of Fundamental Research, Homi Bhabha Road, Navy Nagar, Colaba, Mumbai-400005, India.
Colorado State University, Anatomy and Zoology W309, 1617 Campus Delivery, Fort Collins, 80523 Colorado.
bioRxiv. 2024 Aug 13:2024.08.13.607780. doi: 10.1101/2024.08.13.607780.
Actin in neuronal processes is both stable and dynamic. The origin & functional roles of the different pools of actin is not well understood. We find that mutants that lack mitochondria, and , in neuronal processes also lack dynamic actin. Mitochondria can regulate actin dynamics upto a distance ~80 μm along the neuronal process. Absence of axonal mitochondria and dynamic actin does not markedly alter the Spectrin Membrane Periodic Skeleton (MPS) in touch receptor neurons (TRNs). Restoring mitochondria inTRNs cell autonomously restores dynamic actin in a dependent manner. We find that dynamic actin is necessary and sufficient for the localization of gap junction proteins in the TRNs and for the gentle touch response. We identify an mechanism by which axonal mitochondria locally facilitate actin dynamics through reactive oxygen species that we show is necessary for electrical synapses & behaviour.
神经元突起中的肌动蛋白既稳定又具有动态性。不同肌动蛋白池的起源和功能作用尚未得到很好的理解。我们发现，在神经元突起中缺乏线粒体的突变体也缺乏动态肌动蛋白。线粒体可沿神经元突起在约80微米的距离内调节肌动蛋白动力学。轴突线粒体和动态肌动蛋白的缺失不会显著改变触觉受体神经元（TRN）中的血影蛋白膜周期性骨架（MPS）。在TRN中自主恢复线粒体以一种依赖于……的方式恢复动态肌动蛋白。我们发现，动态肌动蛋白对于TRN中缝隙连接蛋白的定位以及轻柔触觉反应是必要且充分的。我们确定了一种机制，通过该机制轴突线粒体通过活性氧在局部促进肌动蛋白动力学，我们证明这对于电突触和行为是必要的。 （注：原文中存在一些不完整或表述不太清晰的地方，翻译可能会存在一定局限性。）
