Cell fate decision by a morphogen-transcription factor-chromatin modifier axis

Jin Ming, Lihui Lin, Jiajun Li, Linlin Wu, Shicai Fang, Tao Huang, Yu Fu, Dong Liu, Wenhui Zhang, Chen Li, Yongzheng Yang, Yi Huang, Yue Qin, Junqi Kuang, Xingnan Huang, Liman Guo, Xiaofei Zhang, Jing Liu, Jiekai Chen, Chengchen Zhao (), Bo Wang () and Duanqing Pei ()
Additional contact information
Jin Ming: Westlake University
Lihui Lin: Chinese Academy of Sciences
Jiajun Li: Westlake University
Linlin Wu: Westlake University
Shicai Fang: Chinese Academy of Sciences
Tao Huang: Westlake University
Yu Fu: Westlake University
Dong Liu: Westlake University
Wenhui Zhang: Westlake University
Chen Li: Chinese Academy of Sciences
Yongzheng Yang: Chinese Academy of Sciences
Yi Huang: Chinese Academy of Sciences
Yue Qin: Westlake University
Junqi Kuang: Westlake University
Xingnan Huang: Westlake University
Liman Guo: Chinese Academy of Sciences
Xiaofei Zhang: Chinese Academy of Sciences
Jing Liu: Chinese Academy of Sciences
Jiekai Chen: Chinese Academy of Sciences
Chengchen Zhao: Westlake University
Bo Wang: Westlake University
Duanqing Pei: Westlake University

Nature Communications, 2024, vol. 15, issue 1, 1-13

Abstract: Abstract Cell fate decisions remain poorly understood at the molecular level. Embryogenesis provides a unique opportunity to analyze molecular details associated with cell fate decisions. Works based on model organisms have provided a conceptual framework of genes that specify cell fate control, for example, transcription factors (TFs) controlling processes from pluripotency to immunity1. How TFs specify cell fate remains poorly understood. Here we report that SALL4 relies on NuRD (nucleosome-remodeling and deacetylase complex) to interpret BMP4 signal and decide cell fate in a well-controlled in vitro system. While NuRD complex cooperates with SALL4 to convert mouse embryonic fibroblasts or MEFs to pluripotency, BMP4 diverts the same process to an alternative fate, PrE (primitive endoderm). Mechanistically, BMP4 signals the dissociation of SALL4 from NuRD physically to establish a gene regulatory network for PrE. Our results provide a conceptual framework to explore the rich landscapes of cell fate choices intrinsic to development in higher organisms involving morphogen-TF-chromatin modifier pathways.

Date: 2024
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DOI: 10.1038/s41467-024-50144-z

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