Functional redundancy among Polycomb complexes in maintaining the pluripotent state of embryonic stem cells.
PCGF
PRC1
Polycomb
RING1A/B
cPRC1
embryonic stem cells
germ layer lineages
ncPRC1
pluripotency
redundancy
Journal
Stem cell reports
ISSN: 2213-6711
Titre abrégé: Stem Cell Reports
Pays: United States
ID NLM: 101611300
Informations de publication
Date de publication:
10 05 2022
10 05 2022
Historique:
received:
22
09
2021
revised:
27
02
2022
accepted:
28
02
2022
pubmed:
2
4
2022
medline:
18
5
2022
entrez:
1
4
2022
Statut:
ppublish
Résumé
Polycomb group proteins assemble into multi-protein complexes, known as Polycomb repressive complexes 1 and 2 (PRC1 and PRC2), that guide cell fate decisions during embryonic development. PRC1 forms an array of biochemically distinct canonical PRC1 (cPRC1) or non-canonical PRC1 (ncPRC1) complexes characterized by the mutually exclusive presence of PCGF (PCGF1-PCGF6) paralog subunit; however, whether each one of these subcomplexes fulfills a distinct role remains largely controversial. Here, by performing a CRISPR-based loss-of-function screen in embryonic stem cells (ESCs), we uncovered a previously unappreciated functional redundancy among PRC1 subcomplexes. Disruption of ncPRC1, but not cPRC1, displayed severe defects in ESC pluripotency. Remarkably, coablation of non-canonical and canonical PRC1 in ESCs resulted in exacerbation of the phenotype observed in the non-canonical PRC1-null ESCs, highlighting the importance of functional redundancy among PRC1 subcomplexes. Together, our studies demonstrate that PRC1 subcomplexes act redundantly to silence lineage-specific genes and ensure robust maintenance of ESC identity.
Identifiants
pubmed: 35364009
pii: S2213-6711(22)00133-3
doi: 10.1016/j.stemcr.2022.02.020
pmc: PMC9120860
pii:
doi:
Substances chimiques
Drosophila Proteins
0
Polycomb-Group Proteins
0
Polycomb Repressive Complex 2
EC 2.1.1.43
Polycomb Repressive Complex 1
EC 2.3.2.27
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1198-1214Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.
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