ArticleGenetics2012
DNA replication origin function is promoted by H3K4 di-methylation in Saccharomyces cerevisiae.
Article in Genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
26 citing papers in PubMed, 43 citations in OpenAlex.
- A systematic interactome ofeLife · 2026Article
- Insights into the recruitment of the H3K4me3 reader Spp1 by the meiotic double-strand break protein Mer2.Nucleic acids research · 2026Article
- Functional dissection of H3K4 methyltransferases reveals distinct catalytic and non-catalytic roles in C. elegans development.Development (Cambridge, England) · 2025Article
- Review
- Where and when to start: Regulating DNA replication origin activity in eukaryotic genomes.Nucleus (Austin, Tex.) · 2023Review
- Diverse and dynamic forms of gene regulation by the S. cerevisiae histone methyltransferase Set1.Current genetics · 2023Review
- LSD1 is required for euchromatic origin firing and replication timing.Signal transduction and targeted therapy · 2022Article
- Loss of SET1/COMPASS methyltransferase activity reduces lifespan and fertility inLife science alliance · 2022Article
- The genetic architecture of DNA replication timing in human pluripotent stem cells.Nature communications · 2021Observational
- Methylation of histone H3 at lysine 37 by Set1 and Set2 prevents spurious DNA replication.Molecular cell · 2021Article
- H3K4 Methylation in Aging and Metabolism.Epigenomes · 2021Review
- H3K4 methylation at active genes mitigates transcription-replication conflicts during replication stress.Nature communications · 2020Article
- Article
- A systematic assessment of chemical, genetic, and epigenetic factors influencing the activity of anticancer drug KP1019 (FFC14A).Oncotarget · 2017Article
- E3 ubiquitin ligase Bre1 couples sister chromatid cohesion establishment to DNA replication ineLife · 2017Article
- Cell cycle-dependent degradation of the methyltransferase SETD3 attenuates cell proliferation and liver tumorigenesis.The Journal of biological chemistry · 2017Article
- Nup100 regulatesRNA (New York, N.Y.) · 2017Article
- The plant cell cycle: Pre-Replication complex formation and controls.Genetics and molecular biology · 2017Article
- Selectivity of ORC binding sites and the relation to replication timing, fragile sites, and deletions in cancers.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Histone modifications as regulators of life and death inMicrobial cell (Graz, Austria) · 2015Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
DNA replication is a highly regulated process that is initiated from replication origins, but the elements of chromatin structure that contribute to origin activity have not been fully elucidated. To identify histone post-translational modifications important for DNA replication, we initiated a genetic screen to identify interactions between genes encoding chromatin-modifying enzymes and those encoding proteins required for origin function in the budding yeast Saccharomyces cerevisiae. We found that enzymes required for histone H3K4 methylation, both the histone methyltransferase Set1 and the E3 ubiquitin ligase Bre1, are required for robust growth of several hypomorphic replication mutants, including cdc6-1. Consistent with a role for these enzymes in DNA replication, we found that both Set1 and Bre1 are required for efficient minichromosome maintenance. These phenotypes are recapitulated in yeast strains bearing mutations in the histone substrates (H3K4 and H2BK123). Set1 functions as part of the COMPASS complex to mono-, di-, and tri-methylate H3K4. By analyzing strains lacking specific COMPASS complex members or containing H2B mutations that differentially affect H3K4 methylation states, we determined that these replication defects were due to loss of H3K4 di-methylation. Furthermore, histone H3K4 di-methylation is enriched at chromosomal origins. These data suggest that H3K4 di-methylation is necessary and sufficient for normal origin function. We propose that histone H3K4 di-methylation functions in concert with other histone post-translational modifications to support robust genome duplication.
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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.