Abstract:
:The transcriptional repressors Polycomb repressive complex 1 (PRC1) and PRC2 are required to maintain cell fate during embryonic development. PRC1 and PRC2 catalyze distinct histone modifications, establishing repressive chromatin at shared targets. How PRC1, which consists of canonical PRC1 (cPRC1) and variant PRC1 (vPRC1) complexes, and PRC2 cooperate to silence genes and support mouse embryonic stem cell (mESC) self-renewal is unclear. Using combinatorial genetic perturbations, we show that independent pathways of cPRC1 and vPRC1 are responsible for maintenance of H2A monoubiquitylation and silencing of shared target genes. Individual loss of PRC2-dependent cPRC1 or PRC2-independent vPRC1 disrupts only one pathway and does not impair mESC self-renewal capacity. However, loss of both pathways leads to mESC differentiation and activation of a subset of lineage-specific genes co-occupied by relatively high levels of PRC1/PRC2. Thus, parallel pathways explain the differential requirements for PRC1 and PRC2 and provide robust silencing of lineage-specific genes.
journal_name
Sci Advjournal_title
Science advancesauthors
Zepeda-Martinez JA,Pribitzer C,Wang J,Bsteh D,Golumbeanu S,Zhao Q,Burkard TR,Reichholf B,Rhie SK,Jude J,Moussa HF,Zuber J,Bell Odoi
10.1126/sciadv.aax5692subject
Has Abstractpub_date
2020-04-01 00:00:00pages
eaax5692issue
14issn
2375-2548pii
aax5692journal_volume
6pub_type
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