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Optical Activation of TrkB Signaling

机译：TRKB信号传导的光学激活

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Brain-derived neurotrophic factor, via activation of tropomyosin receptor kinase B (TrkB), plays a critical role in neuronal proliferation, differentiation, survival, and death. Dysregulation of TrkB signaling is implicated in neurodegenerative disorders and cancers. Precise activation of TrkB signaling with spatial and temporal resolution is greatly desired to study the dynamic nature of TrkB signaling and its role in related diseases. Here we develop different optogenetic approaches that use light to activate TrkB signaling. Utilizing the photosensitive protein Arabidopsis thaliana cryptochrome 2, the light-inducible homo-interaction of the intracellular domain of TrkB in the cytosol or on the plasma membrane is able to induce the activation of downstream MAPK/ERK and PI3K/Akt signaling as well as the neurite outgrowth of PC12 cells. Moreover, we prove that such strategies are generalizable to other optical homo-dimerizers by demonstrating the optical TrkB activation based on the light-oxygen-voltage domain of aureochrome 1 from Vaucheria frigida. The results open up new possibilities of many other optical platforms to activate TrkB signaling to fulfill customized needs. By comparing all the different strategies, we find that the cryptochrome 2-integrated approach to achieve light-induced cell membrane recruitment and homo-interaction of intracellular domain of TrkB is most efficient in activating TrkB signaling. The optogenetic strategies presented are promising tools to investigate brain-derived neurotrophic factor/TrkB signaling with tight spatial and temporal control. (C) 2020 Elsevier Ltd. All rights reserved.
机译：脑衍生的神经营养因子，通过激活原鸡受体激酶B（TRKB），在神经元增殖，分化，生存和死亡中起重要作用。 TRKB信号传导的失调涉及神经变性疾病和癌症。大大希望具有空间和时间分辨率的TRKB信号的精确激活，以研究TRKB信号传导的动态性质及其在相关疾病中的作用。在这里，我们开发了不同的光学方法，该方法使用光激活TRKB信令。利用光敏蛋白质拟南芥拟南芥2，Trkb在细胞溶胶中的细胞内结构域或血浆膜的光诱导均匀相互作用能够诱导下游MAPK / ERK和PI3K / AKT信号传导的激活以及PC12细胞的神经突生长。此外，我们证明，通过从Vaucheria frigida的荧光色谱域1的光 - 氧 - 电压域来证明光学Trkb活化，这些策略是概括的其他光学均二甲酸。结果开辟了许多其他光学平台的新可能性，以激活TRKB信令以满足定制需求。通过比较所有不同的策略，我们发现，在激活TRKB信号传导方面最有效地达到达到光诱导的细胞膜募集和HONTALLALLACLULAL的促进和同型相互作用的加密色细胞膜募集和同级相互作用。提出的致致策略是具有紧密空间和时间控制的脑衍生的神经营养因子/ TRKB信号传导的前景工具。 （c）2020 elestvier有限公司保留所有权利。

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