ArticleNucleic acids research2021
A conserved BAH module within mammalian BAHD1 connects H3K27me3 to Polycomb gene silencing.
Article in Nucleic acids research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 29 citations in OpenAlex.
- DNA Methylation and Transcriptomic Profiles of Wilms Tumour Reveal New Deregulated Genes and Epigenetic Processes Relevant for Tumour Stratification and Management.International journal of cancer · 2026Article
- Extensive binding of poorly characterized human transcription factors to genomic dark matter.Nature communications · 2026Article
- Integrative Transcriptomic Analysis Identifies Shared Immune-Fibrotic Transcriptional Programs Across Crohn's Disease and Idiopathic Pulmonary Fibrosis.International journal of molecular sciences · 2026Article
- Structural landscape of H3K27me3 recognition by protein domains and their potential for inhibition.The Journal of biological chemistry · 2026Review
- A H3K27me3 reader complex couples H3K27me3 accumulation to nascent transcription of transposable elements in Paramecium.Genome biology · 2026Article
- H3K27me3-dependent imprinting and transcriptional regulation in early mouse embryos requires EZHIP-mediated restriction of PRC2 activity.Nature communications · 2026Article
- A de novo missense variant in MIDEAS results in increased deacetylase activity of the MiDAC HDAC complex causing a neurodevelopmental syndrome.Nature communications · 2025Article
- BAHCC1 binds H4K20me1 to facilitate the MCM complex loading and DNA replication.Nature communications · 2025Article
- Transcriptional silencing in Saccharomyces cerevisiae: known unknowns.Epigenetics & chromatin · 2024Review
- A repressive H3K36me2 reader mediates Polycomb silencing.Nature communications · 2024Article
- H3K27me3-mediated epigenetic regulation in pluripotency maintenance and lineage differentiation.Cell insight · 2024Review
- Structure-guided functional suppression of AML-associated DNMT3A hotspot mutations.Nature communications · 2024Article
- Reader-Effectors as Actuators of Epigenome Editing.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Article
- A potential histone-chaperone activity for the MIER1 histone deacetylase complex.Nucleic acids research · 2023Article
- Chromatin structure and context-dependent sequence features control prime editing efficiency.bioRxiv : the preprint server for biology · 2023Article
- Targeting Menin disrupts the KMT2A/B and polycomb balance to paradoxically activate bivalent genes.Nature cell biology · 2023Article
- Polycomb Repressive Complex 2 in Oncology.Cancer treatment and research · 2023Article
- Chromatin structure and context-dependent sequence features control prime editing efficiency.Frontiers in genetics · 2023Article
- Hypoxic condition induced H3K27me3 modification of the LncRNA Tmem235 promoter thus supporting apoptosis of BMSCs.Apoptosis : an international journal on programmed cell death · 2022Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
Trimethylation of histone H3 lysine 27 (H3K27me3) is important for gene silencing and imprinting, (epi)genome organization and organismal development. In a prevalent model, the functional readout of H3K27me3 in mammalian cells is achieved through the H3K27me3-recognizing chromodomain harbored within the chromobox (CBX) component of canonical Polycomb repressive complex 1 (cPRC1), which induces chromatin compaction and gene repression. Here, we report that binding of H3K27me3 by a Bromo Adjacent Homology (BAH) domain harbored within BAH domain-containing protein 1 (BAHD1) is required for overall BAHD1 targeting to chromatin and for optimal repression of the H3K27me3-demarcated genes in mammalian cells. Disruption of direct interaction between BAHD1BAH and H3K27me3 by point mutagenesis leads to chromatin remodeling, notably, increased histone acetylation, at its Polycomb gene targets. Mice carrying an H3K27me3-interaction-defective mutation of Bahd1BAH causes marked embryonic lethality, showing a requirement of this pathway for normal development. Altogether, this work demonstrates an H3K27me3-initiated signaling cascade that operates through a conserved BAH 'reader' module within BAHD1 in mammals.
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