The PR-DUB complex is responsible for erasing the repressive histone modification, H2AK119ub1. ASXL1-3 proteins are mutually exclusive catalytic partners of BAP1 in the PR-DUB complex. Somatic heteroz...

Niekamp et al. show that biomolecular condensates formed by Polycomb repressive complexes can physically restrict access of the activating remodeler SWI/SNF to chromatin. Establishing this barrier dep...

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Some proteins mimic the repressive mark H3K27me3, but the physiological relevance of this phenomenon was unclear. Agius et al. show that the PRC2 subunits JARID2 and PALI1 mimic H3K27me3 to antagonize PRC2-mediated H3K27me3 deposition, limit Polycomb domain spreading, and enable timely activation of developmental genes in vivo.

Some proteins mimic the repressive mark H3K27me3, but the physiological relevance of this phenomenon was unclear. Agius et al. show that the PRC2 subunits JARID2 and PALI1 mimic H3K27me3 to antagonize PRC2-mediated H3K27me3 deposition, limit Polycomb domain spreading, and enable timely activation of developmental genes in vivo.

Some proteins mimic the repressive mark H3K27me3, but the physiological relevance of this phenomenon was unclear. Agius et al. show that the PRC2 subunits JARID2 and PALI1 mimic H3K27me3 to antagonize...

Neville, Ferguson et al. show that non-canonical Polycomb repressive complex 1.1-mediated gene silencing is antagonized by DOT1L and is required for the therapeutic efficacy of Menin and DOT1L inhibit...

Borges, González-Blanco, Arigela, et al. report new missense mutations in the PRC1 genes RNF2 and RING1 in individuals with neurodevelopmental disorders. Functional dissection of a deleterious variant...

Neville, Ferguson et al. show that non-canonical Polycomb repressive complex 1.1-mediated gene silencing is antagonized by DOT1L and is required for the therapeutic efficacy of Menin and DOT1L inhibit...

Neville, Ferguson et al. show that non-canonical Polycomb repressive complex 1.1-mediated gene silencing is antagonized by DOT1L and is required for the therapeutic efficacy of Menin and DOT1L inhibit...

The Nobel laureate and CU Boulder professor, recently ranked #1 globally for RNA research, will speak at the World Economic Forum annual meeting in Davos,

The Polycomb Repressive Complex 2 (PRC2) is an ancient, conserved chromatin-interacting complex that controls gene expression, facilitating differentiation and cellular identity during development. It...

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imageimageAEBP2 is an accessory subunit of the PRC2 complex previously implicated both in promoting and antagonizing Polycomb repressive activity. This study reveals that its alternative isoforms, AEB...

The catalytic subunit of Polycomb Repressive Complex 2 (PRC2), EZH2, is recurrently mutated in 25% of diffuse large B-cell lymphomas (DLBCL), causing increased H3K27me3 and decreased H3K27me2 levels. ...

Chromatin structure plays a central role in regulating transcription, genome stability, and epigenetic inheritance in eukaryotes. Much of our understanding of chromatin architecture and histone post-t...

In mammals, repression of germline-specific gene expression is essential for preserving somatic cell identity and preventing disease. Germline gene silencing is often dependent on the presence of prom...

Schulten et al. show that VEL polymerization domains produce higher-order protein assemblies to maintain chromatin association of Polycomb proteins, enabling a stable epigenetic switch at the floral r...

The Polycomb repressive complex 2 (PRC2) is an essential modulator of gene repression. We previously reported that, in mouse embryonic stem cells, PRC…

The nuclear periphery is a key site for heterochromatin organization in eukaryotic cells, where lamina-associated domains (LADs) promote transcriptional repression and genome stability. Despite their ...

Much et al. reveal that the PRC2 subcomplexes PRC2.1 and PRC2.2 play distinct roles in the epigenetic repression of developmental genes in human stem cells. Interactions between the PRC2 core and its ...

October 20-22, 2025

Cis-regulatory elements (CREs) have a major effect on phenotypes including disease. They are identified in a genome-wide manner by analyzing the binding of transcription factors (TFs), various co-fact...