ArticleThe EMBO journal2010
UTX mediates demethylation of H3K27me3 at muscle-specific genes during myogenesis.
Article in The EMBO journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers.
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136 citing papers in PubMed, 224 citations in OpenAlex.
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- Parp3 assists muscle function and skeletal muscle differentiation by selectively adjusting H3K27me3 enrichment.iScience · 2025Article
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- Lysine methylation signaling in skeletal muscle biology: from myogenesis to clinical insights.The Biochemical journal · 2023Review
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- Context-Dependent Functions of KDM6 Lysine Demethylases in Physiology and Disease.Advances in experimental medicine and biology · 2023Article
- SET domain containing 2 (SETD2) influences metabolism and alternative splicing during myogenesis.The FEBS journal · 2022Article
- Sex-biased and parental allele-specific gene regulation by KDM6A.Biology of sex differences · 2022Article
- Sex-Related Effects on Cardiac Development and Disease.Journal of cardiovascular development and disease · 2022Review
- Chromatin Reorganization during Myoblast Differentiation Involves the Caspase-Dependent Removal of SATB2.Cells · 2022Article
76 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
Polycomb (PcG) and Trithorax (TrxG) group proteins act antagonistically to establish tissue-specific patterns of gene expression. The PcG protein Ezh2 facilitates repression by catalysing histone H3-Lys27 trimethylation (H3K27me3). For expression, H3K27me3 marks are removed and replaced by TrxG protein catalysed histone H3-Lys4 trimethylation (H3K4me3). Although H3K27 demethylases have been identified, the mechanism by which these enzymes are targeted to specific genomic regions to remove H3K27me3 marks has not been established. Here, we demonstrate a two-step mechanism for UTX-mediated demethylation at muscle-specific genes during myogenesis. Although the transactivator Six4 initially recruits UTX to the regulatory region of muscle genes, the resulting loss of H3K27me3 marks is limited to the region upstream of the transcriptional start site. Removal of the repressive H3K27me3 mark within the coding region then requires RNA Polymerase II (Pol II) elongation. Interestingly, blocking Pol II elongation on transcribed genes leads to increased H3K27me3 within the coding region, and formation of bivalent (H3K27me3/H3K4me3) chromatin domains. Thus, removal of repressive H3K27me3 marks by UTX occurs through targeted recruitment followed by spreading across the gene.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.