Abstract:
:Cell fate determination requires the cooperation between extrinsic signals and intrinsic molecules including transcription factors as well as epigenetic regulators. Nevertheless, how neural fate commitment is regulated by epigenetic modifications remains largely unclear. Here we show that transient histone deacetylation at epiblast stage promotes neural differentiation of mouse embryonic stem cells (mESCs). Histone deacetylase 1 (HDAC1) deficiency in mESCs partially phenocopies the inhibition of histone deacetylation in vitro, and displays reduced incorporation into neural tissues in chimeric mouse embryos in vivo. Mechanistic studies show that Nodal, which is repressed by histone deacetylation, is a direct target of HDAC1. Furthermore, the inhibition of histone deacetylation in the anterior explant of mouse embryos at E7.0 leads to Nodal activation and neural development repression. Thus, our study reveals an intrinsic mechanism that epigenetic histone deacetylation ensures neural fate commitment by restricting Nodal signalling in murine anterior epiblast ex vivo and mESC in vitro.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Liu P,Dou X,Liu C,Wang L,Xing C,Peng G,Chen J,Yu F,Qiao Y,Song L,Wu Y,Yue C,Li J,Han JD,Tang K,Jing Ndoi
10.1038/ncomms7830subject
Has Abstractpub_date
2015-04-23 00:00:00pages
6830issn
2041-1723pii
ncomms7830journal_volume
6pub_type
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