ArticlePloS one2014
Dot1-dependent histone H3K79 methylation promotes the formation of meiotic double-strand breaks in the absence of histone H3K4 methylation in budding yeast.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- Separable downmodulation of meiotic axis protein deposition and DNA break induction at chromosome ends.eLife · 2026Article
- Insights into the recruitment of the H3K4me3 reader Spp1 by the meiotic double-strand break protein Mer2.Nucleic acids research · 2026Article
- Histone H3 N-Terminal Tail Residues Important for Meiosis inBiomolecules · 2025Article
- Distinct chromatin regulators downmodulate meiotic axis formation and DNA break induction at chromosome ends.bioRxiv : the preprint server for biology · 2025Article
- Replication protein-A, RPA, plays a pivotal role in the maintenance of recombination checkpoint in yeast meiosis.Scientific reports · 2024Article
- Meiosis in budding yeast.Genetics · 2023Article
- Diverse and dynamic forms of gene regulation by the S. cerevisiae histone methyltransferase Set1.Current genetics · 2023Review
- The Msh5 complex shows homeostatic localization in response to DNA double-strand breaks in yeast meiosis.Frontiers in cell and developmental biology · 2023Article
- Ready, SET, Go: Post-translational regulation of the histone lysine methylation network in budding yeast.The Journal of biological chemistry · 2021Review
- SCFLife science alliance · 2021Article
- Rad9, a 53BP1 Ortholog of Budding Yeast, Is Insensitive to Spo11-Induced Double-Strand Breaks During Meiosis.Frontiers in cell and developmental biology · 2021Article
- DOT-1.1-dependent H3K79 methylation promotes normal meiotic progression and meiotic checkpoint function in C. elegans.PLoS genetics · 2020Article
- Genetic Interactions of Histone Modification Machinery Set1 and PAF1C with the Recombination Complex Rec114-Mer2-Mei4 in the Formation of Meiotic DNA Double-Strand Breaks.International journal of molecular sciences · 2020Article
- The Putative Histone Methyltransferase DOT1 Regulates Aflatoxin and Pathogenicity Attributes in Aspergillus flavus.Toxins · 2017Article
- Correlation of Meiotic DSB Formation and Transcription Initiation Around Fission Yeast Recombination Hotspots.Genetics · 2017Article
- Budding Yeast SLX4 Contributes to the Appropriate Distribution of Crossovers and Meiotic Double-Strand Break Formation on Bivalents During Meiosis.G3 (Bethesda, Md.) · 2016Article
- Rad61/Wpl1 (Wapl), a cohesin regulator, controls chromosome compaction during meiosis.Nucleic acids research · 2016Article
- Article
- Dot1 histone methyltransferases share a distributive mechanism but have highly diverged catalytic properties.Scientific reports · 2015Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epigenetic marks such as histone modifications play roles in various chromosome dynamics in mitosis and meiosis. Methylation of histones H3 at positions K4 and K79 is involved in the initiation of recombination and the recombination checkpoint, respectively, during meiosis in the budding yeast. Set1 promotes H3K4 methylation while Dot1 promotes H3K79 methylation. In this study, we carried out detailed analyses of meiosis in mutants of the SET1 and DOT1 genes as well as methylation-defective mutants of histone H3. We confirmed the role of Set1-dependent H3K4 methylation in the formation of double-strand breaks (DSBs) in meiosis for the initiation of meiotic recombination, and we showed the involvement of Dot1 (H3K79 methylation) in DSB formation in the absence of Set1-dependent H3K4 methylation. In addition, we showed that the histone H3K4 methylation-defective mutants are defective in SC elongation, although they seem to have moderate reduction of DSBs. This suggests that high levels of DSBs mediated by histone H3K4 methylation promote SC elongation.
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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.