节点信号
SMAD公司
细胞生物学
ACVR2B型
生物
激活素2型受体
染色质
节的
爪蟾
信号转导
Smad2蛋白
R-SMAD
转录调控
细胞命运测定
原肠化
转录因子
转化生长因子β信号通路
遗传学
转化生长因子
胚胎
胚胎发生
基因
内皮糖蛋白
干细胞
川地34
作者
Tao Liang,Jianbo Bai,Wei Zhou,Hao Lin,Shixin Ma,Xinhui Zhu,Qinghua Tao,Qiaoran Xi
出处
期刊:Cell Reports
[Elsevier]
日期:2022-07-01
卷期号:40 (2): 111038-111038
被引量:1
标识
DOI:10.1016/j.celrep.2022.111038
摘要
Despite the fundamental roles of TGF-β family signaling in cell fate determination in all metazoans, the mechanism by which these signals are spatially and temporally interpreted remains elusive. The cell-context-dependent function of TGF-β signaling largely relies on transcriptional regulation by SMAD proteins. Here, we discover that the DNA repair-related protein, HMCES, contributes to early development by maintaining nodal/activin- or BMP-signaling-regulated transcriptional network. HMCES binds with R-SMAD proteins, co-localizing at active histone marks. However, HMCES chromatin occupancy is independent on nodal/activin or BMP signaling. Mechanistically, HMCES competitively binds chromatin to limit binding by R-SMAD proteins, thereby forcing their dissociation and resulting in repression of their regulatory effects. In Xenopus laevis embryo, hmces KD causes dramatic development defects with abnormal left-right axis asymmetry along with increasing expression of lefty1. These findings reveal HMCES transcriptional regulatory function in the context of TGF-β family signaling.
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