ArticleEpigenetics & chromatin2011
Dot1 binding induces chromatin rearrangements by histone methylation-dependent and -independent mechanisms.
Article in Epigenetics & chromatin, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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Who cites it
20 citing papers in PubMed, 38 citations in OpenAlex.
- Separable downmodulation of meiotic axis protein deposition and DNA break induction at chromosome ends.eLife · 2026Article
- Histone methyltransferase DOT1L differentially affects the development of dendritic cell subsets.Life science alliance · 2026Article
- Chromatin structure in totipotent mouse early preimplantation embryos.The Journal of reproduction and development · 2024Review
- Article
- Signals for antigen-independent differentiation of memory CD8Cellular and molecular life sciences : CMLS · 2021Review
- AF10 (MLLT10) prevents somatic cell reprogramming through regulation of DOT1L-mediated H3K79 methylation.Epigenetics & chromatin · 2021Article
- Metabolic regulation of telomere silencing by SESAME complex-catalyzed H3T11 phosphorylation.Nature communications · 2021Article
- Conserved crosstalk between histone deacetylation and H3K79 methylation generates DOT1L-dose dependency in HDAC1-deficient thymic lymphoma.The EMBO journal · 2019Article
- Dot1 promotes H2B ubiquitination by a methyltransferase-independent mechanism.Nucleic acids research · 2018Article
- Transcriptional activator DOT1L putatively regulates human embryonic stem cell differentiation into the cardiac lineage.Stem cell research & therapy · 2018Article
- TERRA and the histone methyltransferase Dot1 cooperate to regulate senescence in budding yeast.PloS one · 2018Article
- Normally lethal amino acid substitutions suppress an ultramutator DNA Polymerase δ variant.Scientific reports · 2017Article
- Review
- Getting down to the core of histone modifications.Chromosoma · 2014Review
- The histone methyltransferase Dot1/DOT1L as a critical regulator of the cell cycle.Cell cycle (Georgetown, Tex.) · 2014Review
- Epigenetics in Saccharomyces cerevisiae.Cold Spring Harbor perspectives in biology · 2013Review
- Emergence of DNA polymerase ε antimutators that escape error-induced extinction in yeast.Genetics · 2013Article
- The role of multiple marks in epigenetic silencing and the emergence of a stable bivalent chromatin state.PLoS computational biology · 2013Article
- Epigenetic Editing: targeted rewriting of epigenetic marks to modulate expression of selected target genes.Nucleic acids research · 2012Review
- Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMethylation of histone H3 lysine 79 (H3K79) by Dot1 is highly conserved among species and has been associated with both gene repression and activation. To eliminate indirect effects and examine the direct consequences of Dot1 binding and H3K79 methylation, we investigated the effects of targeting Dot1 to different positions in the yeast genome.
resultsTargeting Dot1 did not activate transcription at a euchromatic locus. However, chromatin-bound Dot1 derepressed heterochromatin-mediated gene silencing over a considerable distance. Unexpectedly, Dot1-mediated derepression was established by both a H3K79 methylation-dependent and a methylation-independent mechanism; the latter required the histone acetyltransferase Gcn5. By monitoring the localization of a fluorescently tagged telomere in living cells, we found that the targeting of Dot1, but not its methylation activity, led to the release of a telomere from the repressive environment at the nuclear periphery. This probably contributes to the activity-independent derepression effect of Dot1.
conclusionsTargeting of Dot1 promoted gene expression by antagonizing gene repression through both histone methylation and chromatin relocalization. Our findings show that binding of Dot1 to chromatin can positively affect local gene expression by chromatin rearrangements over a considerable distance.
Identifiers
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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.