BMP4 resets mouse epiblast stem cells to naive pluripotency through ZBTB7A/B-mediated chromatin remodelling
| Autor: | Bo Wang, Baomei Cai, Shengyong Yu, Xingnan Huang, Chunhua Zhou, Lizhan Xiao, Shilong Chu, Junqi Kuang, Wei Pang, Wenxiu Xie, Jing Ye, Duanqing Pei, Rongping Luo, Linlin Wu, Yue Qin, Mengying Zeng, Chen Li, Jing Guo, Xiaoshan Wang, Shuyang Xu, He Liu, Kaixin Wu, Guoqing Zhao, Jiekai Chen, Lin Guo, Jiangping He, Shangtao Cao, Jing Liu |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
Regulation of gene expression
0303 health sciences animal structures Cellular differentiation Cell Biology Biology Chromatin Cell biology 03 medical and health sciences 0302 clinical medicine Epiblast 030220 oncology & carcinogenesis embryonic structures Gene expression Stem cell Signal transduction Gene 030304 developmental biology |
| Zdroj: | Nature Cell Biology. 22:651-662 |
| ISSN: | 1476-4679 1465-7392 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full text from SpringerLink