Evidence map›Paper›PMID 29769529›Full record

ArticleNature communications2018

Methionine metabolism influences genomic architecture and gene expression through H3K4me3 peak width.

Ziwei Dai, Samantha J Mentch, Xia Gao, Sailendra N Nichenametla, Jason W Locasale

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
6.0field-weighted citation impact, top 3% of its field
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

80 citing papers in PubMed, 130 citations in OpenAlex.

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  7. Epigenetic crosstalk in neuroblastoma development and progression.Frontiers in cell and developmental biology · 2026
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  14. Mechanisms and rationales of SAM homeostasis.Trends in biochemical sciences · 2025
    Review
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20 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

Ziwei DaiDepartment of Pharmacology and Cancer Biology, Duke Molecular Physiology Institute, Duke Cancer Institute, Duke University School of Medicine, Durham, NC, 27710, USA.
Samantha J MentchDepartment of Pharmacology and Cancer Biology, Duke Molecular Physiology Institute, Duke Cancer Institute, Duke University School of Medicine, Durham, NC, 27710, USA.
Xia GaoDepartment of Pharmacology and Cancer Biology, Duke Molecular Physiology Institute, Duke Cancer Institute, Duke University School of Medicine, Durham, NC, 27710, USA.
Sailendra N NichenametlaOrentreich Foundation for the Advancement of Science, Cold Spring, NY, 10516, USA.
Jason W LocasaleDepartment of Pharmacology and Cancer Biology, Duke Molecular Physiology Institute, Duke Cancer Institute, Duke University School of Medicine, Durham, NC, 27710, USA. jason.locasale@duke.edu.ORCID http://orcid.org/0000-0002-7766-3502
Duke University · USOrentreich Foundation for the Advancement of Science · US

Funding

Women's Cancer Research ProgramP30CA014236 · NCI · DUKE UNIVERSITY · PI DONNA NIEDZWIECKI · 1985 to 2026
$174.8M
Dietary methionine and cancerR01CA193256 · NCI · DUKE UNIVERSITY · PI LOCASALE, JASON W. · 2015 to 2023
$3.1M
Understanding metabolic flux and the control of mammalian cell growthR00CA168997 · NCI · DUKE UNIVERSITY · PI LOCASALE, JASON W. · 2013 to 2015
$695k
Data commons for 'omic, microscopy and analysis core facilitiesS10OD018164 · OD · DUKE UNIVERSITY · PI WRAY, GREGORY A. · 2014 to 2014
$598k
NCI NIH HHS P30 CA014236NCI NIH HHS R00 CA168997NCI NIH HHS R01 CA193256NIH HHS S10 OD018164
6 · The paper itself

Abstract

Nutrition and metabolism are known to influence chromatin biology and epigenetics through post-translational modifications, yet how this interaction influences genomic architecture and connects to gene expression is unknown. Here we consider, as a model, the metabolically-driven dynamics of H3K4me3, a histone methylation mark that is known to encode information about active transcription, cell identity, and tumor suppression. We analyze the genome-wide changes in H3K4me3 and gene expression in response to alterations in methionine availability in both normal mouse physiology and human cancer cells. Surprisingly, we find that the location of H3K4me3 peaks is largely preserved under methionine restriction, while the response of H3K4me3 peak width encodes almost all aspects of H3K4me3 biology including changes in expression levels, and the presence of cell identity and cancer-associated genes. These findings may reveal general principles for how nutrient availability modulates specific aspects of chromatin dynamics to mediate biological function.

Indexed as

Gene Expression ProfilingAnimalsGenomicsHCT116 CellsHistone CodeHistonesHumansLiverLysineMaleMethionineMethylationMice, Inbred C57BLNeoplasmsHistonesLysineMethionine

Identifiers

PMID29769529
PMCPMC5955993
OpenAlexW2803104516

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.