Inhua Muijrers

Cancer Genomics Centre

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Maarten van Lohuizen

Oncode Institute

Hans Teunissen

The Netherlands Cancer Institute

Bas van Steensel

Oncode Institute

Wendy Talhout

Association of Dutch Burn Centres

Bas Tolhuis

Koninklijk Nederlands Genootschap voor Fysiotherapie

Elzo de Wit

The Netherlands Cancer Institute

Petra van der Stoop

Amsterdam UMC Location VUmc

Barbara Panning

University of California, San Francisco

Inmaculada Hernández‐Muñoz

Hospital Del Mar

York Marahrens

University of Minnesota

Cooperative Institutions

The Netherlands Cancer Institute

Cancer Genomics Centre

Oncode Institute

University of California, Los Angeles

University of California, San Francisco

Hubrecht Institute for Developmental Biology and Stem Cell Research

University Medical Center Utrecht

Erasmus University Rotterdam

Rockefeller University

Amsterdam UMC Location VUmc

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Erratum: Corrigendum: Genome-wide profiling of PRC1 and PRC2 Polycomb chromatin binding in Drosophila melanogaster

Nature Genetics (2006)

Bas Tolhuis Inhua Muijrers Elzo de Wit Hans Teunissen Wendy Talhout

PRC2

10.1038/ng0706-850a

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Genome-wide profiling of PRC1 and PRC2 Polycomb chromatin binding in Drosophila melanogaster

Nature Genetics (2006)

Bas Tolhuis Inhua Muijrers Elzo de Wit Hans Teunissen Wendy Talhout

PRC2

Polycomb-group proteins

10.1038/ng1792

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Citations (374)

Stable X chromosome inactivation involves the PRC1 Polycomb complex and requires histone MACROH2A1 and the CULLIN3/SPOP ubiquitin E3 ligase

Proceedings of the National Academy of Sciences (2005)

Inmaculada Hernández‐Muñoz Anders H. Lund Petra van der Stoop Erwin Boutsma Inhua Muijrers

X inactivation involves the stable silencing of one of the two X chromosomes in XX female mammals. Initiation of this process occurs during early development and involves Xist (X-inactive-specific transcript) RNA coating and the recruitment of Polycomb repressive complex (PRC) 2 and PRC1 proteins. This recruitment results in an inactive state that is initially labile but is further locked in by epigenetic marks such as DNA methylation, histone hypoacetylation, and MACROH2A deposition. Here, we report that the E3 ubiquitin ligase consisting of SPOP and CULLIN3 is able to ubiquitinate the Polycomb group protein BMI1 and the variant histone MACROH2A. We find that in addition to MACROH2A, PRC1 is recruited to the inactivated X chromosome in somatic cells in a highly dynamic, cell cycle-regulated manner. Importantly, RNAi-mediated knock-down of CULLIN3 or SPOP results in loss of MACROH2A1 from the inactivated X chromosome (Xi), leading to reactivation of the Xi in the presence of inhibitors of DNA methylation and histone deacetylation. Likewise, Xi reactivation is also seen on MacroH2A1 RNAi under these conditions. Hence, we propose that the PRC1 complex is involved in the maintenance of X chromosome inactivation in somatic cells. We further demonstrate that MACROH2A1 deposition is regulated by the CULLIN3/SPOP ligase complex and is actively involved in stable X inactivation, likely through the formation of an additional layer of epigenetic silencing.

XIST

Dosage compensation

10.1073/pnas.0408918102

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Citations (310)