作者: J. A. Zepeda-Martinez , C. Pribitzer , J. Wang , D. Bsteh , S. Golumbeanu
关键词:
摘要: The transcriptional repressors Polycomb repressive complex 1 (PRC1) and PRC2 are required to maintain cell fate during embryonic development. PRC1 catalyze distinct histone modifications, establishing chromatin at shared targets. How PRC1, which consists of canonical (cPRC1) variant (vPRC1) complexes, cooperate silence genes support mouse stem (mESC) self-renewal is unclear. Using combinatorial genetic perturbations, we show that independent pathways cPRC1 vPRC1 responsible for maintenance H2A monoubiquitylation silencing target genes. Individual loss PRC2-dependent or PRC2-independent disrupts only one pathway does not impair mESC capacity. However, both leads differentiation activation a subset lineage-specific co-occupied by relatively high levels PRC1/PRC2. Thus, parallel explain the differential requirements provide robust