H3K27me3 spreading organizes canonical PRC1 chromatin architecture to regulate developmental programs.
Brian KrugBo HuHaifen ChenAdam PtackXiao ChenKristjan H GretarssonShriya DeshmukhNisha KabirAugusto Faria AndradeElias JabbourAshot S HarutyunyanJohn J Y LeeMaud HulswitDamien FauryCaterina RussoXinjing XuMichael J JohnstonAudrey BaguetteNathan A DahlAlexander G WeilBenjamin EllezamRola DaliMathieu BlanchetteKhadija WilsonBenjamin A GarciaRajesh Kumar SoniMarco GalloMichael D TaylorClaudia L KleinmanJacek MajewskiNada JabadoChao LuPublished in: bioRxiv : the preprint server for biology (2023)
The confinement of H3K27me3 at PRC2 nucleation sites without its spreading correlates with increased 3D chromatin interactions.The H3K27M oncohistone concentrates canonical PRC1 that anchors chromatin loop interactions in gliomas, silencing developmental programs.Stem and progenitor cells require factors promoting H3K27me3 confinement, including H3K36me2, to maintain cPRC1 loop architecture.The cPRC1-H3K27me3 interaction is a targetable driver of aberrant self-renewal in tumor cells.