Mitochondrial movement and distribution are fundamental to their function. Here we report a mechanism that regulates mitochondrial movement by anchoring mitochondria to the F-actin cytoskeleton. This mechanism is activated by an increase in glucose influx and the consequent O-GlcNAcylation of TRAK (Milton), a component of the mitochondrial motor-adaptor complex. The protein four and a half LIM domains protein 2 (FHL2) serves as the anchor. FHL2 associates with O-GlcNAcylated TRAK and is both necessary and sufficient to drive the accumulation of F-actin around mitochondria and to arrest mitochondrial movement by anchoring to F-actin. Disruption of F-actin restores mitochondrial movement that had been arrested by either TRAK O-GlcNAcylation or forced direction of FHL2 to mitochondria. This pathway for mitochondrial immobilization is present in both neurons and non-neuronal cells and can thereby adapt mitochondrial dynamics to changes in glucose availability.

中文翻译：

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FHL2 将线粒体锚定在肌动蛋白上，并使线粒体动力学适应葡萄糖供应

线粒体的运动和分布是其功能的基础。在这里，我们报告了一种通过将线粒体锚定到 F-肌动蛋白细胞骨架来调节线粒体运动的机制。该机制是通过葡萄糖流入的增加以及随后 TRAK (Milton) 的 O-GlcNAc 酰化激活的，TRAK (Milton) 是线粒体运动适配器复合物的一个组成部分。四个半 LIM 结构域蛋白 2 (FHL2) 充当锚定点。FHL2 与 O-GlcNAcylated TRAK 结合，对于驱动 F-肌动蛋白在线粒体周围的积累以及通过锚定到 F-肌动蛋白来阻止线粒体运动来说是必要且充分的。F-肌动蛋白的破坏可恢复因 TRAK O-GlcNAcylation 或 FHL2 强制定向至线粒体而抑制的线粒体运动。这种线粒体固定途径存在于神经元和非神经元细胞中，从而可以使线粒体动力学适应葡萄糖可用性的变化。