ArticleMolecular and cellular biology2005
Role of Dot1-dependent histone H3 methylation in G1 and S phase DNA damage checkpoint functions of Rad9.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 165 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
165 citing papers in PubMed, 289 citations in OpenAlex.
- Slx4 and Fun30/SMARCAD1 coordinate S-phase checkpoint regulation and replication fork protection in response to Top1-DNA crosslinks.Nucleic acids research · 2026Article
- Article
- Unraveling gene expression: a beginner's guide from chromatin modifications to mRNA export inNucleus (Austin, Tex.) · 2025Review
- DOT1L as a Therapeutic Target: Insights into Epigenetic Regulation and Cancer Treatment.Biomolecules & therapeutics · 2025Review
- DNA Damage and Replication Stress Checkpoints.Annual review of biochemistry · 2025Review
- Multifaceted roles of H2B mono-ubiquitylation in D-loop metabolism during homologous recombination repair.Nucleic acids research · 2025Article
- Mms22-Rtt107 axis attenuates the DNA damage checkpoint and the stability of the Rad9 checkpoint mediator.Nature communications · 2025Article
- Keep calm and reboot - how cells restart transcription after DNA damage and DNA repair.FEBS letters · 2025Review
- DOT1L-mediated RAP80 methylation promotes BRCA1 recruitment to elicit DNA repair.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The Mms22-Rtt107 axis dampens the DNA damage checkpoint by reducing the stability of the Rad9 checkpoint mediator.Research square · 2024Article
- γH2A/γH2AX Mediates DNA Damage-Specific Control of Checkpoint Signaling inInternational journal of molecular sciences · 2024Article
- Transcriptional Reprogramming ofJournal of fungi (Basel, Switzerland) · 2023Article
- A novel role of DOT1L in kidney diseases.Molecular biology reports · 2023Review
- The Chromatin Landscape around DNA Double-Strand Breaks in Yeast and Its Influence on DNA Repair Pathway Choice.International journal of molecular sciences · 2023Review
- Genes and Longevity of Lifespan.International journal of molecular sciences · 2022Review
- The DNA damage checkpoint: A tale from budding yeast.Frontiers in genetics · 2022Review
- Epigenetic Regulation of Nucleotide Excision Repair.Frontiers in cell and developmental biology · 2022Review
- DNA Damage-Induced Phosphorylation of Histone H2A at Serine 15 Is Linked to DNA End Resection.Molecular and cellular biology · 2021Article
- Antagonistic relationship of NuA4 with the non-homologous end-joining machinery at DNA damage sites.PLoS genetics · 2021Article
- Dpb4 promotes resection of DNA double-strand breaks and checkpoint activation by acting in two different protein complexes.Nature communications · 2021Article
105 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
We screened radiation-sensitive yeast mutants for DNA damage checkpoint defects and identified Dot1, the conserved histone H3 Lys 79 methyltransferase. DOT1 deletion mutants (dot1Delta) are G1 and intra-S phase checkpoint defective after ionizing radiation but remain competent for G2/M arrest. Mutations that affect Dot1 function such as Rad6-Bre1/Paf1 pathway gene deletions or mutation of H2B Lys 123 or H3 Lys 79 share dot1Delta checkpoint defects. Whereas dot1Delta alone confers minimal DNA damage sensitivity, combining dot1Delta with histone methyltransferase mutations set1Delta and set2Delta markedly enhances lethality. Interestingly, set1Delta and set2Delta mutants remain G1 checkpoint competent, but set1Delta displays a mild S phase checkpoint defect. In human cells, H3 Lys 79 methylation by hDOT1L likely mediates recruitment of the signaling protein 53BP1 via its paired tudor domains to double-strand breaks (DSBs). Consistent with this paradigm, loss of Dot1 prevents activation of the yeast 53BP1 ortholog Rad9 or Chk2 homolog Rad53 and decreases binding of Rad9 to DSBs after DNA damage. Mutation of Rad9 to alter tudor domain binding to methylated Lys 79 phenocopies the dot1Delta checkpoint defect and blocks Rad53 phosphorylation. These results indicate a key role for chromatin and methylation of histone H3 Lys 79 in yeast DNA damage signaling.
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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.