ArticleDevelopment (Cambridge, England)2014
Trithorax monomethylates histone H3K4 and interacts directly with CBP to promote H3K27 acetylation and antagonize Polycomb silencing.
Article in Development (Cambridge, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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Who cites it
69 citing papers in PubMed, 111 citations in OpenAlex.
- Broad Epigenetic Shifts in the Aging Drosophila Retina Contribute to Its Altered Diurnal Rhythmic Transcriptome.Aging cell · 2026Article
- KMT2A-rearranged leukemia: from mechanism to drug development.Experimental hematology · 2025Review
- PARP1 and PARG Are the Draft Horses for Polycomb-Trithorax Chromatin Regulator Machinery.Biomolecules · 2025Article
- Epigenetic reprogramming induced by key metabolite depletion is an evolutionarily ancient path to tumorigenesis.Disease models & mechanisms · 2025Article
- Insights into pubertal development: a narrative review on the role of epigenetics.Journal of endocrinological investigation · 2025Review
- Dopaminergic REST is implicated in the tamoxifen-induced neuroprotection against manganese toxicity in female mice.Frontiers in pharmacology · 2025Article
- Evidence for dual roles of histone H3 lysine 4 in antagonizing Polycomb group function and promoting target gene expression.Genes & development · 2024Article
- Epigenetic inheritance and gene expression regulation in early Drosophila embryos.EMBO reports · 2024Review
- The RPD3L deacetylation complex is required for facultative heterochromatin repression inProceedings of the National Academy of Sciences of the United States of America · 2024Article
- The TELOMERE REPEAT BINDING proteins TRB4 and TRB5 function as transcriptional activators of PRC2-controlled genes to regulate plant development.Plant communications · 2024Article
- Chromatin profiling and state predictions reveal insights into epigenetic regulation during early porcine development.Epigenetics & chromatin · 2024Article
- Kdm1a safeguards the topological boundaries of PRC2-repressed genes and prevents aging-related euchromatinization in neurons.Nature communications · 2024Article
- Review
- Epigenetic control of pancreatic cancer metastasis.Cancer metastasis reviews · 2023Review
- Polycomb Recruiters Inside and Outside of the Repressed Domains.International journal of molecular sciences · 2023Review
- Diverse and dynamic forms of gene regulation by the S. cerevisiae histone methyltransferase Set1.Current genetics · 2023Review
- Stress-induced reversible cell-cycle arrest requires PRC2/PRC1-mediated control of mitophagy in Drosophila germline stem cells and human iPSCs.Stem cell reports · 2023Article
- The role of histone methyltransferases in neurocognitive disorders associated with brain size abnormalities.Frontiers in neuroscience · 2023Review
- Mechanisms of Polycomb group protein function in cancer.Cell research · 2022Review
- TRITHORAX-dependent arginine methylation of HSP68 mediates circadian repression by PERIOD in the monarch butterfly.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
9 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 1 country.
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Abstract
Trithorax (TRX) antagonizes epigenetic silencing by Polycomb group (PcG) proteins, stimulates enhancer-dependent transcription, and establishes a 'cellular memory' of active transcription of PcG-regulated genes. The mechanisms underlying these TRX functions remain largely unknown, but are presumed to involve its histone H3K4 methyltransferase activity. We report that the SET domains of TRX and TRX-related (TRR) have robust histone H3K4 monomethyltransferase activity in vitro and that Tyr3701 of TRX and Tyr2404 of TRR prevent them from being trimethyltransferases. The trx(Z11) missense mutation (G3601S), which abolishes H3K4 methyltransferase activity in vitro, reduces the H3K4me1 but not the H3K4me3 level in vivo. trx(Z11) also suppresses the impaired silencing phenotypes of the Pc(3) mutant, suggesting that H3K4me1 is involved in antagonizing Polycomb silencing. Polycomb silencing is also antagonized by TRX-dependent H3K27 acetylation by CREB-binding protein (CBP). We show that perturbation of Polycomb silencing by TRX overexpression requires CBP. We also show that TRX and TRR are each physically associated with CBP in vivo, that TRX binds directly to the CBP KIX domain, and that the chromatin binding patterns of TRX and TRR are highly correlated with CBP and H3K4me1 genome-wide. In vitro acetylation of H3K27 by CBP is enhanced on K4me1-containing H3 substrates, and independently altering the H3K4me1 level in vivo, via the H3K4 demethylase LSD1, produces concordant changes in H3K27ac. These data indicate that the catalytic activities of TRX and CBP are physically coupled and suggest that both activities play roles in antagonizing Polycomb silencing, stimulating enhancer activity and cellular memory.
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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.