ArticleThe Journal of biological chemistry2011
Evidence that the histone methyltransferase Dot1 mediates global genomic repair by methylating histone H3 on lysine 79.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 61 citations in OpenAlex.
- DOT1L as a Therapeutic Target: Insights into Epigenetic Regulation and Cancer Treatment.Biomolecules & therapeutics · 2025Review
- Life cycle and morphogenetic differentiation in heteromorphic cell types of a cosmopolitan marine microalga.The New phytologist · 2025Article
- DNA Repair in Nucleosomes: Insights from Histone Modifications and Mutants.International journal of molecular sciences · 2024Review
- Set2 histone methyltransferase regulates transcription coupled-nucleotide excision repair in yeast.PLoS genetics · 2022Article
- Epigenetic Regulation of Nucleotide Excision Repair.Frontiers in cell and developmental biology · 2022Review
- Nucleotide excision repair leaves a mark on chromatin: DNA damage detection in nucleosomes.Cellular and molecular life sciences : CMLS · 2021Review
- Ready, SET, Go: Post-translational regulation of the histone lysine methylation network in budding yeast.The Journal of biological chemistry · 2021Review
- The Ubiquitin Ligase TRAIP: Double-Edged Sword at the Replisome.Trends in cell biology · 2021Review
- CAF-1 and Rtt101p function within the replication-coupled chromatin assembly network to promote H4 K16ac, preventing ectopic silencing.PLoS genetics · 2020Article
- Maternal DOT1L is dispensable for mouse development.Scientific reports · 2020Article
- Regulation of UV damage repair in quiescent yeast cells.DNA repair · 2020Article
- A chromatin scaffold for DNA damage recognition: how histone methyltransferases prime nucleosomes for repair of ultraviolet light-induced lesions.Nucleic acids research · 2020Article
- Methyltransferase Inhibitors: Competing with, or Exploiting the Bound Cofactor.Molecules (Basel, Switzerland) · 2019Review
- DOT1L complex suppresses transcription from enhancer elements and ectopic RNAi inRNA (New York, N.Y.) · 2019Article
- Histone H4 H75E mutation attenuates global genomic and Rad26-independent transcription-coupled nucleotide excision repair.Nucleic acids research · 2019Article
- The protective role of DOT1L in UV-induced melanomagenesis.Nature communications · 2018Article
- Reduced mutation rate in exons due to differential mismatch repair.Nature genetics · 2017Article
- A Novel Histone Crosstalk Pathway Important for Regulation of UV-Induced DNA Damage Repair inGenetics · 2017Article
- 2D-DIGE proteomic analysis of vastus lateralis from COPD patients with low and normal fat free mass index and healthy controls.Respiratory research · 2017Article
- Epigenetic therapy with inhibitors of histone methylation suppresses DNA damage signaling and increases glioma cell radiosensitivity.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Global genomic repair (GGR) and transcription coupled repair (TCR) are two pathways of nucleotide excision repair (NER) that differ in the damage recognition step. How NER factors, especially GGR factors, access DNA damage in the chromatin of eukaryotic cells has been poorly understood. Dot1, a histone methyltransferase required for methylation of histone H3 lysine 79 (H3K79), has been shown to confer yeast cells with resistance to DNA-damaging agents and play a role in activation of DNA damage checkpoints. Here, we show that Dot1 and H3K79 methylation are required for GGR in both nucleosomal core regions and internucleosomal linker DNA, but play no role in TCR. H3K79 trimethylation contributes to but is not absolutely required for GGR, and lower levels of H3K79 methylation (mono- and dimethylation) also promote GGR. Our results also indicate that the roles of Dot1 and H3K79 methylation in GGR are not achieved by either activating DNA damage checkpoints or regulating the expression of the GGR-specific factor Rad16. Rather, the methylated H3K79 may serve as a docking site for the GGR machinery on the chromatin. Our studies identified a novel GGR-specific NER factor and unveiled the critical link between a covalent histone modification and GGR.
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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.