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TRIP6通过YAP介导的Sonic Hedgehog激活促进神经干细胞的维持

Ming-Yang Li¹, Xiu-Li Yang¹, Chia-Chi Chung¹

¹Department of Life Science, National Taiwan Normal University, Taipei, Taiwan.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

|February 27, 2024

概括

YAP蛋白对于维持神经干细胞 (NSC) 和调节成年大脑神经生成至关重要. 它的耗尽导致神经元过早分化,突出显示了TRIP6-YAP-SHH通路.

科学领域:

神经科学是一个神经科学.
细胞生物学细胞生物学
发展生物学发展生物学

背景情况:

成年哺乳动物的大脑从子室下区域 (SVZ) -嗅球 (OB) 路径中的神经干细胞 (NSC) 产生新的神经元.
作为Hippo通路的协同激活剂,YAP会影响胚胎神经前体的增殖和分化,但其在产后NSC中的作用尚不清楚.

研究的目的:

调查SVZ-OB神经性利基内的产后神经干细胞中YAP的功能.
阐明YAP神经发生的调节背后的分子机制.

主要方法:

利用RNA干扰和条件淘汰模式在产后小鼠SVZ中耗尽YAP.
采用技术来评估NSC维持,增殖和神经元分化.
研究了涉及TRIP6,PP1A,LATS1/2,YAP和Sonic Hedgehog (SHH) 途径的分子相互作用.

主要成果:

在产后小鼠SVZ NSC中存在YAP.
强迫YAP表达维持了NSC种群,并抑制了分化.
YAP的耗尽导致NSC维护减少,神经元分化过早,神经发生障碍.
TRIP6招募PP1A去化LATS1/2,促进YAP的核定位和激活.
通过YAP,TRIP6增强了NSC的维持和扩散,同时抑制了分化.
YAP调节SHH通路效应器Gli1/2,它们调节YAP对NSC维护的影响.

结论:

一个新的TRIP6-YAP-SHH信号轴被确定为SVZ-OB通路中调节产后神经发生的关键.
YAP在维持神经干细胞池和控制成年大脑的神经发生过程中发挥着至关重要的作用.
了解这种途径为神经发育和神经退行性疾病提供了潜在的治疗点.

关键词:

河马的路径河马的路径这就是SHH SHH.在TRIPS6中,我们使用的是TRIP6.哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈成年人的神经发生.神经干细胞的神经干细胞

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