BAP1 complex promotes transcription by opposing PRC1-mediated H2A ubiquitylation

Antoine Campagne, Ming-Kang Lee, Dina Zielinski, Audrey Michaud, Stéphanie Corre, Florent Dingli, Hong Chen, Lara Z. Shahidian, Ivaylo Vassilev, Nicolas Servant, Damarys Loew, Eric Pasmant, Sophie Postel-Vinay, Michel Wassef () and Raphaël Margueron ()
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Antoine Campagne: Paris Sciences et Lettres Research University, Sorbonne University
Ming-Kang Lee: Paris Sciences et Lettres Research University, Sorbonne University
Dina Zielinski: Paris Sciences et Lettres Research University, Sorbonne University
Audrey Michaud: Paris Sciences et Lettres Research University, Sorbonne University
Stéphanie Corre: Paris Sciences et Lettres Research University, Sorbonne University
Florent Dingli: Paris Sciences et Lettres Research University, Sorbonne University
Hong Chen: Paris Sciences et Lettres Research University, Sorbonne University
Lara Z. Shahidian: Helmholtz Zentrum München
Ivaylo Vassilev: Paris Sciences et Lettres Research University, Sorbonne University
Nicolas Servant: Paris Sciences et Lettres Research University, Sorbonne University
Damarys Loew: Paris Sciences et Lettres Research University, Sorbonne University
Eric Pasmant: University of Paris Descartes
Sophie Postel-Vinay: Université Paris-Saclay
Michel Wassef: Paris Sciences et Lettres Research University, Sorbonne University
Raphaël Margueron: Paris Sciences et Lettres Research University, Sorbonne University

Nature Communications, 2019, vol. 10, issue 1, 1-15

Abstract: Abstract 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.

Date: 2019
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DOI: 10.1038/s41467-018-08255-x

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