接合作用
Wnt信号通路
细胞生物学
新皮层
连环素
神经发生
泛素
生物
祖细胞
WNT3A型
信号转导
神经科学
干细胞
遗传学
基因
泛素连接酶
作者
Lei Zhang,Hongyang Jing,Haiwen Li,Wenbing Chen,Bin Luo,Hongsheng Zhang,Zhaoqi Dong,Lei Li,Huabo Su,Wen‐Cheng Xiong,Lin Mei
标识
DOI:10.1073/pnas.2005395117
摘要
Wnt signaling plays a critical role in production and differentiation of neurons and undergoes a progressive reduction during cortical development. However, how Wnt signaling is regulated is not well understood. Here we provide evidence for an indispensable role of neddylation, a ubiquitylation-like protein modification, in inhibiting Wnt/β-catenin signaling. We show that β-catenin is neddylated; and inhibiting β-catenin neddylation increases its nuclear accumulation and Wnt/β-catenin signaling. To test this hypothesis in vivo, we mutated Nae1, an obligative subunit of the E1 for neddylation in cortical progenitors. The mutation leads to eventual reduction in radial glia progenitors (RGPs). Consequently, the production of intermediate progenitors (IPs) and neurons is reduced, and neuron migration is impaired, resulting in disorganization of the cerebral cortex. These phenotypes are similar to those of β-catenin gain-of-function mice. Finally, suppressing β-catenin expression is able to rescue deficits of Nae1 mutant mice. Together, these observations identified a mechanism to regulate Wnt/β-catenin signaling in cortical development.
科研通智能强力驱动
Strongly Powered by AbleSci AI