ArticlePLoS genetics2010
Alternative epigenetic chromatin states of polycomb target genes.
Article in PLoS genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers.
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Who cites it
126 citing papers in PubMed, 201 citations in OpenAlex.
- Polycomb Group Proteins inBiology · 2026Review
- Sequential RNA polymerase II activation drives human hematopoiesis.Cell reports · 2026Article
- Genomic context-dependent histone H3K36 methylation by three Drosophila methyltransferases and implications for dedicated chromatin readers.Nucleic acids research · 2025Article
- Genomic context-dependent histone H3K36 methylation by three Drosophila methyltransferases and implications for dedicated chromatin readers.Nucleic acids research · 2024Article
- Distinct roles of COMPASS subunits to Drosophila heart development.Biology open · 2024Article
- Polycomb protein binding and looping in the ON transcriptional state.Science advances · 2024Article
- Forecasting histone methylation by Polycomb complexes with minute-scale precision.Science advances · 2023Article
- DNA elements tether canonical Polycomb Repressive Complex 1 to human genes.Nucleic acids research · 2023Article
- Polycomb protein binding and looping mediated by Polycomb Response Elements in the ON transcriptional state.bioRxiv : the preprint server for biology · 2023Article
- Chromatin in 3D distinguishes dMes-4/NSD and Hypb/dSet2 in protecting genes from H3K27me3 silencing.Life science alliance · 2023Article
- Topological screen identifies hundreds of Cp190- and CTCF-dependentScience advances · 2023Article
- Differences in temperature-sensitive expression of PcG-regulated genes among natural populations of Drosophila melanogaster.G3 (Bethesda, Md.) · 2021Article
- The Trithorax group protein ASH1 requires a combination of BAH domain and AT hooks, but not the SET domain, for mitotic chromatin binding and survival.Chromosoma · 2021Article
- MOCCA: a flexible suite for modelling DNA sequence motif occurrence combinatorics.BMC bioinformatics · 2021Article
- Polycomb RequiresFrontiers in cell and developmental biology · 2021Article
- BRDT is a novel regulator of eIF4EBP1 in renal cell carcinoma.Oncology reports · 2020Article
- A theoretical model of Polycomb/Trithorax action unites stable epigenetic memory and dynamic regulation.Nature communications · 2020Article
- Genetic Dissection Reveals the Role of Ash1 Domains in Counteracting Polycomb Repression.G3 (Bethesda, Md.) · 2019Article
- Genome-wide RNAi screen in Drosophila reveals Enok as a novel trithorax group regulator.Epigenetics & chromatin · 2019Article
- DNA sequence models of genome-wide Drosophila melanogaster Polycomb binding sites improve generalization to independent Polycomb Response Elements.Nucleic acids research · 2019Article
66 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polycomb (PcG) regulation has been thought to produce stable long-term gene silencing. Genomic analyses in Drosophila and mammals, however, have shown that it targets many genes, which can switch state during development. Genetic evidence indicates that critical for the active state of PcG target genes are the histone methyltransferases Trithorax (TRX) and ASH1. Here we analyze the repertoire of alternative states in which PcG target genes are found in different Drosophila cell lines and the role of PcG proteins TRX and ASH1 in controlling these states. Using extensive genome-wide chromatin immunoprecipitation analysis, RNAi knockdowns, and quantitative RT-PCR, we show that, in addition to the known repressed state, PcG targets can reside in a transcriptionally active state characterized by formation of an extended domain enriched in ASH1, the N-terminal, but not C-terminal moiety of TRX and H3K27ac. ASH1/TRX N-ter domains and transcription are not incompatible with repressive marks, sometimes resulting in a "balanced" state modulated by both repressors and activators. Often however, loss of PcG repression results instead in a "void" state, lacking transcription, H3K27ac, or binding of TRX or ASH1. We conclude that PcG repression is dynamic, not static, and that the propensity of a target gene to switch states depends on relative levels of PcG, TRX, and activators. N-ter TRX plays a remarkable role that antagonizes PcG repression and preempts H3K27 methylation by acetylation. This role is distinct from that usually attributed to TRX/MLL proteins at the promoter. These results have important implications for Polycomb gene regulation, the "bivalent" chromatin state of embryonic stem cells, and gene expression in development.
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