BAF Complex in Embryonic Stem Cells and Early Embryonic Development.

Heyao Zhang,Ying Ye,Ronghua Shi,Xuepeng Wang,Jingsheng Li,Qiang Wu

doi:10.1155/2021/6668866

Abstract

Embryonic stem cells (ESCs) can self-renew indefinitely and maintain their pluripotency status. The pluripotency gene regulatory network is critical in controlling these properties and particularly chromatin remodeling complexes. In this review, we summarize the research progresses of the functional and mechanistic studies of BAF complex in mouse ESCs and early embryonic development. A discussion of the mechanistic bases underlying the distinct phenotypes upon the deletion of different BAF subunits in ESCs and embryos will be highlighted.

Highlights

Embryonic stem cells (ESCs) are derived from the inner cell mass of blastocysts in early embryos [1,2,3]
Numerous studies demonstrate that the identity of ESCs is controlled by a core transcriptional regulatory network composed of signaling pathways such as the Leukemia Inhibitory Factor (LIF)/STAT3 pathway [4,5,6], pluripotent transcription factors such as OCT4, SOX2, NANOG, and KLF4 [7,8,9], protein complexes [10,11,12], microRNAs [13], and chromatin remodeling complexes [12]
The binding of STAT3 to genes associated with pluripotency depends on the presence of the catalytic subunit BRG1 in the esBAF complex, which loosens the chromatin structure at the target gene of STAT3 and responds to the LIF signal [47]

Summary

Introduction

Embryonic stem cells (ESCs) are derived from the inner cell mass of blastocysts in early embryos [1,2,3]. With the remarkable abilities to indefinitely self-renew and differentiate to all types of cells in the body, ESCs become an ideal model to study cell fate determination and lineage differentiation, having broad applications in the fields of regenerative medicine and translational medicine. Numerous studies demonstrate that the identity of ESCs is controlled by a core transcriptional regulatory network composed of signaling pathways such as the LIF/STAT3 pathway [4,5,6], pluripotent transcription factors such as OCT4, SOX2, NANOG, and KLF4 [7,8,9], protein complexes [10,11,12], microRNAs [13], and chromatin remodeling complexes [12]

Chromatin Remodeling Complexes

E BD BR7

Conclusion

Conflicts of Interest