Evidence map›Paper›PMID 30472189›Full record

SynthesisMolecular cell2019

Nucleosome Turnover Regulates Histone Methylation Patterns over the Genome.

Emma J Chory, Joseph P Calarco, Nathaniel A Hathaway, Oliver Bell, Dana S Neel, Gerald R Crabtree

Abstract readMeta-AnalysisVideo-Audio Media
In one paragraph

Synthesis in Molecular cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

58 citing papers in PubMed.

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  17. Two-way feedback between chromatin compaction and histone modification state explainsProceedings of the National Academy of Sciences of the United States of America · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Emma J ChoryDepartment of Chemical Engineering, Stanford University, Stanford, CA 94305, USA; Departments of Pathology and Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Joseph P CalarcoDepartments of Pathology and Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Nathaniel A HathawayDivision of Chemical Biology and Medicinal Chemistry, Center for Integrative Chemical Biology and Drug Discovery, UNC Eshelman School of Pharmacy, Chapel Hill, NC 27599, USA.
Oliver BellInstitute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna Biocenter (VBC), 1030 Vienna, Austria; Department of Biochemistry and Molecular Medicine and the Norris Comprehensive Cancer Center, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90089-9601, USA.
Dana S NeelDepartments of Pathology and Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Gerald R CrabtreeDepartments of Pathology and Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305, USA; Howard Hughes Medical Institute, Chevy Chase, MD, USA. Electronic address: crabtree@stanford.edu.

Funding

ATP-Dependent Chromatin Remodeling in Human MalignancyR01CA163915 · NCI · STANFORD UNIVERSITY · PI Gerald R. Crabtree · 2012 to 2026
$5.4M
ATP-Dependent Chromatin Regulation in Neurodevelopment and Human DiseaseR37NS046789 · NINDS · STANFORD UNIVERSITY · PI CRABTREE, GERALD R. · 2013 to 2019
$2.7M
HIJACKING OF SUPER-ENHANCERS FOR CANCER-SPECIFIC THERAPEUTICSF31CA203228 · NCI · STANFORD UNIVERSITY · PI CHORY, EMMA J · 2016 to 2018
$92k
NCI NIH HHS F31 CA203228NCI NIH HHS R01 CA163915NINDS NIH HHS R37 NS046789
6 · The paper itself

Abstract

Recent studies have indicated that nucleosome turnover is rapid, occurring several times per cell cycle. To access the effect of nucleosome turnover on the epigenetic landscape, we investigated H3K79 methylation, which is produced by a single methyltransferase (Dot1l) with no known demethylase. Using chemical-induced proximity (CIP), we find that the valency of H3K79 methylation (mono-, di-, and tri-) is determined by nucleosome turnover rates. Furthermore, propagation of this mark is predicted by nucleosome turnover simulations over the genome and accounts for the asymmetric distribution of H3K79me toward the transcriptional unit. More broadly, a meta-analysis of other conserved histone modifications demonstrates that nucleosome turnover models predict both valency and chromosomal propagation of methylation marks. Based on data from worms, flies, and mice, we propose that the turnover of modified nucleosomes is a general means of propagation of epigenetic marks and a determinant of methylation valence.

Indexed as

DNA MethylationEpigenesis, GeneticGenomeAnimalsCaenorhabditis elegansChromatin Assembly and DisassemblyComputer SimulationDrosophila melanogasterHEK293 CellsHistone-Lysine N-MethyltransferaseHistonesHumansJurkat CellsKineticsMethyltransferasesMiceDOT1L protein, humanDot1l protein, mouseHistone-Lysine N-MethyltransferaseHistonesMethyltransferasesNucleosomesDOT1L/KMT4epigenome modelinghistone demethylationhistone methyltransferasemixed lineage leukemianucleosome turnover

Identifiers

PMID30472189
PMCPMC6510544

What OpenQuestion holds

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Registered trials

None linked

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.