The NuRD complex cooperates with SALL4 to orchestrate reprogramming.
Journal
Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555
Informations de publication
Date de publication:
18 05 2023
18 05 2023
Historique:
received:
20
04
2022
accepted:
08
05
2023
medline:
22
5
2023
pubmed:
20
5
2023
entrez:
19
5
2023
Statut:
epublish
Résumé
Cell fate decision involves rewiring of the genome, but remains poorly understood at the chromatin level. Here, we report that chromatin remodeling complex NuRD participates in closing open chromatin in the early phase of somatic reprogramming. Sall4, Jdp2, Glis1 and Esrrb can reprogram MEFs to iPSCs efficiently, but only Sall4 is indispensable capable of recruiting endogenous components of NuRD. Yet knocking down NuRD components only reduces reprogramming modestly, in contrast to disrupting the known Sall4-NuRD interaction by mutating or deleting the NuRD interacting motif at its N-terminus that renders Sall4 inept to reprogram. Remarkably, these defects can be partially rescured by grafting NuRD interacting motif onto Jdp2. Further analysis of chromatin accessibility dynamics demonstrates that the Sall4-NuRD axis plays a critical role in closing the open chromatin in the early phase of reprogramming. Among the chromatin loci closed by Sall4-NuRD encode genes resistant to reprogramming. These results identify a previously unrecognized role of NuRD in reprogramming, and may further illuminate chromatin closing as a critical step in cell fate control.
Identifiants
pubmed: 37208322
doi: 10.1038/s41467-023-38543-0
pii: 10.1038/s41467-023-38543-0
pmc: PMC10199099
doi:
Substances chimiques
Mi-2 Nucleosome Remodeling and Deacetylase Complex
EC 3.5.1.98
Transcription Factors
0
Histone Deacetylases
EC 3.5.1.98
Chromatin
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
2846Informations de copyright
© 2023. The Author(s).
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