Evidence map›Paper›PMID 28250819›Full record

ArticleEpigenetics & chromatin2017

SMYD5 regulates H4K20me3-marked heterochromatin to safeguard ES cell self-renewal and prevent spurious differentiation.

Benjamin L Kidder, Gangqing Hu, Kairong Cui, Keji Zhao

Open access · goldAbstract read
In one paragraph

Article in Epigenetics & chromatin, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

44 citing papers in PubMed, 72 citations in OpenAlex.

  1. Lentiviral Transduction of Embryonic Stem Cells.Methods in molecular biology (Clifton, N.J.) · 2027
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  14. DNMT1 can induce primary germ layer differentiation through de novo DNA methylation.Genes to cells : devoted to molecular & cellular mechanisms · 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

4 authors at 3 institutions in 1 country.

Benjamin L KidderDepartment of Oncology, Wayne State University School of Medicine, Detroit, MI USA.
Gangqing HuSystems Biology Center, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD USA.
Kairong CuiSystems Biology Center, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD USA.
Keji ZhaoSystems Biology Center, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD USA.
National Heart Lung and Blood Institute · USNational Institutes of Health · USWayne State University · US

Funding

Epigenetic Regulation of Hematopoietic Stem CellsZIAHL006031 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI ZHAO, KEJI · 2009 to 2025
$16.6M
Regulation of chromatin and genome stability by the H4K20 methyltransferase SMYD5K22HL126842 · NHLBI · WAYNE STATE UNIVERSITY · PI KIDDER, BENJAMIN L · 2016 to 2018
$736k
NHLBI NIH HHS K22 HL126842
6 · The paper itself

Abstract

backgroundEpigenetic regulation of chromatin states is thought to control the self-renewal and differentiation of embryonic stem (ES) cells. However, the roles of repressive histone modifications such as trimethylated histone 4 lysine 20 (H4K20me3) in pluripotency and development are largely unknown.

resultsHere, we show that the histone lysine methyltransferase SMYD5 mediates H4K20me3 at heterochromatin regions. Depletion of SMYD5 leads to compromised self-renewal, including dysregulated expression of OCT4 targets, and perturbed differentiation. SMYD5-bound regions are enriched with repetitive DNA elements. Knockdown of SMYD5 results in a global decrease of H4K20me3 levels, a redistribution of heterochromatin constituents including H3K9me3/2, G9a, and HP1α, and de-repression of endogenous retroelements. A loss of SMYD5-dependent silencing of heterochromatin nearby genic regions leads to upregulated expression of lineage-specific genes, thus contributing to the decreased self-renewal and perturbed differentiation of SMYD5-depleted ES cells.

conclusionsAltogether, these findings implicate a role for SMYD5 in regulating ES cell self-renewal and H4K20me3-marked heterochromatin.

Indexed as

AnimalsCell DifferentiationCell Self RenewalChromatin ImmunoprecipitationChromobox Protein Homolog 5Chromosomal Proteins, Non-HistoneDNA MethylationEmbryoid BodiesHeterochromatinHistone-Lysine N-MethyltransferaseHistonesInterspersed Repetitive SequencesMethyltransferasesMiceMice, SCIDMicroscopy, FluorescenceChromobox Protein Homolog 5Chromosomal Proteins, Non-HistoneHeterochromatinHistone-Lysine N-MethyltransferaseHistonesMethyltransferasesRNA, Small InterferingSmyd5 protein, mouseTranscription FactorsTumor Suppressor ProteinsChIP-SeqChromatinDifferentiationEmbryoid bodyEmbryonic stem cellsEpigeneticsGene expressionGenomicsH4K20me3HeterochromatinHistone methyltransferaseLINELTRPluripotentRepetitive DNARNA-SeqSelf-renewalSMYD5

Identifiers

PMID28250819
PMCPMC5324308
OpenAlexW2589421242

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.