ArticleMolecular cell2011
Dot1 and histone H3K79 methylation in natural telomeric and HM silencing.
Article in Molecular cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 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
79 citing papers in PubMed, 116 citations in OpenAlex.
- Separable downmodulation of meiotic axis protein deposition and DNA break induction at chromosome ends.eLife · 2026Article
- Review
- Distinct chromatin regulators downmodulate meiotic axis formation and DNA break induction at chromosome ends.bioRxiv : the preprint server for biology · 2025Article
- Life cycle and morphogenetic differentiation in heteromorphic cell types of a cosmopolitan marine microalga.The New phytologist · 2025Article
- DOT1L protects against podocyte injury in diabetic kidney disease through phospholipase C-like 1.Cell communication and signaling : CCS · 2024Article
- N-terminal acetylation of Set1-COMPASS fine-tunes H3K4 methylation patterns.Science advances · 2024Article
- The 80Journal of microbiology and biotechnology · 2024Article
- TOF1 and RRM3 reveal a link between gene silencing and the pausing of replication forks.Current genetics · 2023Article
- Analyses of POL30 (PCNA) reveal positional effects in transient repression or bi-modal active/silent state at the sub-telomeres of S. cerevisiae.Epigenetics & chromatin · 2023Article
- A novel role of DOT1L in kidney diseases.Molecular biology reports · 2023Review
- Epigenetic drug library screening reveals targeting DOT1L abrogates NADJournal of pharmaceutical analysis · 2023Article
- H2B Lys34 Ubiquitination Induces Nucleosome Distortion to Stimulate Dot1L Activity.Nature chemical biology · 2022Article
- Spreading-dependent or independent Sir2-mediated gene silencing in budding yeast.Genes & genomics · 2022Article
- Histone Methylation Is Required for Virulence, Conidiation, and Multi-Stress Resistance ofFrontiers in microbiology · 2022Article
- Article
- Sir3 mediates long-range chromosome interactions in budding yeast.Genome research · 2021Article
- Metabolic regulation of telomere silencing by SESAME complex-catalyzed H3T11 phosphorylation.Nature communications · 2021Article
- Regulation of the Dot1 histone H3K79 methyltransferase by histone H4K16 acetylation.Science (New York, N.Y.) · 2021Article
- Maternal DOT1L is dispensable for mouse development.Scientific reports · 2020Article
- Polycomb Repression without Bristles: Facultative Heterochromatin and Genome Stability in Fungi.Genes · 2020Review
19 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
The expression of genes residing near telomeres is attenuated through telomere position-effect variegation (TPEV). By using a URA3 reporter located at TEL-VII-L of Saccharomyces cerevisiae, it was proposed that the disruptor of telomeric silencing-1 (Dot1) regulates TPEV by catalyzing H3K79 methylation. URA3 reporter assays also indicated that H3K79 methylation is required for HM silencing. Surprisingly, a genome-wide expression analysis of H3K79 methylation-defective mutants identified only a few telomeric genes, such as COS12 at TEL-VII-L, to be subject to H3K79 methylation-dependent natural silencing. Consistently, loss of Dot1 did not globally alter Sir2 or Sir3 occupancy in subtelomeric regions, but only led to some telomere-specific changes. Furthermore, H3K79 methylation by Dot1 did not play a role in the maintenance of natural HML silencing. Therefore, commonly used URA3 reporter assays may not report on natural PEV, and therefore, studies concerning the epigenetic mechanism of silencing in yeast should also employ assays reporting on natural gene expression patterns.
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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.