Song Wenjun, Cho Yongcheol, Watt Dana, Cavalli Valeria
From the Department of Anatomy and Neurobiology, Washington University in St. Louis, School of Medicine, St. Louis, Missouri 63110.
From the Department of Anatomy and Neurobiology, Washington University in St. Louis, School of Medicine, St. Louis, Missouri 63110
J Biol Chem. 2015 Jun 5;290(23):14765-75. doi: 10.1074/jbc.M114.622753. Epub 2015 Apr 24.
Injured peripheral neurons successfully activate a pro-regenerative program to enable axon regeneration and functional recovery. The microtubule-dependent retrograde transport of injury signals from the lesion site in the axon back to the cell soma stimulates the increased growth capacity of injured neurons. However, the mechanisms initiating this retrograde transport remain poorly understood. Here we show that tubulin-tyrosine ligase (TTL) is required to increase the levels of tyrosinated α-tubulin at the axon injury site and plays an important role in injury signaling. Preventing the injury-induced increase in tyrosinated α-tubulin by knocking down TTL impairs retrograde organelle transport and delays activation of the pro-regenerative transcription factor c-Jun. In the absence of TTL, axon regeneration is reduced severely. We propose a model in which TTL increases the levels of tyrosinated α-tubulin locally at the injury site to facilitate the retrograde transport of injury signals that are required to activate a pro-regenerative program.
受损的外周神经元成功激活一个促再生程序,以实现轴突再生和功能恢复。损伤信号从轴突中的损伤部位通过微管依赖性逆行运输回到细胞体,刺激受损神经元生长能力增强。然而,启动这种逆行运输的机制仍知之甚少。在这里,我们表明微管蛋白酪氨酸连接酶(TTL)是轴突损伤部位酪氨酸化α-微管蛋白水平升高所必需的,并且在损伤信号传导中起重要作用。通过敲低TTL来阻止损伤诱导的酪氨酸化α-微管蛋白增加,会损害逆行细胞器运输,并延迟促再生转录因子c-Jun的激活。在没有TTL的情况下,轴突再生会严重减少。我们提出了一个模型,其中TTL在损伤部位局部增加酪氨酸化α-微管蛋白的水平,以促进激活促再生程序所需的损伤信号的逆行运输。