| Literature DB >> 32393886 |
Shengyong Yu1,2,3,4, Chunhua Zhou1,2,3,4, Shangtao Cao1,2,4, Jiangping He1,2,3,4, Baomei Cai1,2,3,4, Kaixin Wu1,2,3, Yue Qin1,2,3,4, Xingnan Huang1,5, Lizhan Xiao1,2,3, Jing Ye1,2,4, Shuyang Xu1,2,3,4, Wenxiu Xie1,2,4, Junqi Kuang1,2,3,4, Shilong Chu1,2,4, Jing Guo1,2,4, He Liu1,2,4, Wei Pang1,2,4, Lin Guo1,2,4, Mengying Zeng1,2,4, Xiaoshan Wang1,2,4,5, Rongping Luo1,2,4, Chen Li1,2,4, Guoqing Zhao1,3,4,6, Bo Wang1,2,4, Linlin Wu1,2,4, Jiekai Chen1,2,4,5,6, Jing Liu7,8,9,10,11, Duanqing Pei12,13,14,15,16.
Abstract
BMP4 regulates a plethora of developmental processes, including the dorsal-ventral axis and neural patterning. Here, we report that BMP4 reconfigures the nuclear architecture during the primed-to-naive transition (PNT). We first established a BMP4-driven PNT and show that BMP4 orchestrates the chromatin accessibility dynamics during PNT. Among the loci opened early by BMP4, we identified Zbtb7a and Zbtb7b (Zbtb7a/b) as targets that drive PNT. ZBTB7A/B in turn facilitate the opening of naive pluripotent chromatin loci and the activation of nearby genes. Mechanistically, ZBTB7A not only binds to chromatin loci near to the genes that are activated, but also strategically occupies those that are silenced, consistent with a role of BMP4 in both activating and suppressing gene expression during PNT at the chromatin level. Our results reveal a previously unknown function of BMP4 in regulating nuclear architecture and link its targets ZBTB7A/B to chromatin remodelling and pluripotent fate control.Entities:
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Year: 2020 PMID： 32393886 DOI： 10.1038/s41556-020-0516-x
Source DB: PubMed Journal: Nat Cell Biol ISSN： 1465-7392 Impact factor: 28.824