Wnt信号通路
生物
神经发生
祖细胞
细胞生物学
爪蟾
神经干细胞
神经发育
转录因子
基因剔除小鼠
大脑皮层
细胞生长
异位表达
细胞周期
祖细胞
基因
信号转导
干细胞
神经科学
遗传学
作者
Jingpeng Wang,Baihui Chai,Yanlang Yang,Chengyan Chen,Yaoxin Ren,Yan Li,Zhao‐Qi Wang,Tangliang Li
标识
DOI:10.1016/j.bbrc.2023.149421
摘要
In mammalian brain development, WNT signaling balances proliferation and differentiation of neural progenitor cells, and is essential for the maintenance of regular brain development. JADE1 is a candidate transcription co-factor essential for DNA replication, cell division, and cell cycle regulation. In 293T cells, JADE1 is stabilized by von Hippel–Lindau protein pVHL, promotes the β-catenin ubiquitination and thus blunts canonical WNT signaling. Furthermore, JADE1 inhibits β-catenin-induced ectopic axis formation in Xenopus embryos. However, JADE1's role in mammalian brain development remains unknown. Here, we generated a new Jade1 knockout mouse line using CRISPR-Cas9 technology. We found that JADE1 null resulted in decreased survival rate, reduced body weight and brain weight in mice. However, histological analysis revealed a normal brain development. Furthermore, Jade1 null neural progenitor cells proliferated normally in vivo and in vitro. RNA-seq analysis further showed that JADE1 loss did not affect the cerebral cortex gene expression. Our findings indicate that JADE1 is dispensable for developing the cerebral cortex in mice.
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