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Campagne, A.* ; Lee, M.K.* ; Zielinski, D.* ; Michaud, A.* ; Le Corre, S.* ; Dingli, F.* ; Chen, H.* ; Shahidian, L.Z. ; Vassilev, I.* ; Servant, N.* ; Loew, D.* ; Pasmant, E.* ; Postel-Vinay, S.* ; Wassef, M.* ; Margueron, R.*

BAP1 complex promotes transcription by opposing PRC1-mediated H2A ubiquitylation.

Nat. Commun. 10:348 (2019)
Verlagsversion Forschungsdaten DOI PMC
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In Drosophila, a complex consisting of Calypso and ASX catalyzes H2A deubiquitination and has been reported to act as part of the Polycomb machinery in transcriptional silencing. The mammalian homologs of these proteins (BAP1 and ASXL1/2/3, respectively), are frequently mutated in various cancer types, yet their precise functions remain unclear. Using an integrative approach based on isogenic cell lines generated with CRISPR/Cas9, we uncover an unanticipated role for BAP1 in gene activation. This function requires the assembly of an enzymatically active BAP1-associated core complex (BAP1. com) containing one of the redundant ASXL proteins. We investigate the mechanism underlying BAP1. com-mediated transcriptional regulation and show that it does not participate in Polycomb-mediated silencing. Instead, our results establish that the function of BAP1. com is to safeguard transcriptionally active genes against silencing by the Polycomb Repressive Complex 1.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Brca1-associated Protein-1; Ubiquitin Hydrolase; Asxl1 Mutations; Polycomb; Cells; Prc2; Methylation; Recruitment; Regulator; Versatile
Sprache englisch
Veröffentlichungsjahr 2019
HGF-Berichtsjahr 2019
ISSN (print) / ISBN 2041-1723
e-ISSN 2041-1723
Zeitschrift Nature Communications
Quellenangaben Band: 10, Heft: 1, Seiten: , Artikelnummer: 348 Supplement: ,
Verlag Nature Publishing Group
Verlagsort London
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Functional Epigenetics (IFE)
POF Topic(s) 30203 - Molecular Targets and Therapies
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-502800-001
DOI 10.1038/s41467-018-08255-x
WOS ID WOS:000456164800005
Scopus ID 85060237126
PubMed ID 30664650
Erfassungsdatum 2019-03-01
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