Evidence map›Paper›PMID 28765214›Full record

ArticleDevelopment (Cambridge, England)2017

Epigenetic resetting of human pluripotency.

Ge Guo, Ferdinand von Meyenn, Maria Rostovskaya, James Clarke, Sabine Dietmann, Duncan Baker, Anna Sahakyan, Samuel Myers, Paul Bertone, Wolf Reik and 2 more

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Development (Cambridge, England), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 193 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
193citing papers in PubMed, 1 pooled it
10.1field-weighted citation impact, top 1% 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

193 citing papers in PubMed, 1 synthesis or guideline pooled it, 324 citations in OpenAlex.

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  17. Mechanisms of human germ cell development.Nature reviews. Molecular cell biology · 2026
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133 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 2 countries.

Ge GuoWellcome Trust - Medical Research Council Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 1QR, UK gg251@cam.ac.uk austin.smith@cscr.cam.ac.uk.ORCID 0000-0002-3273-9147
Ferdinand von MeyennEpigenetics Programme, Babraham Institute, Cambridge CB22 3AT, UK.
Maria RostovskayaWellcome Trust - Medical Research Council Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 1QR, UK.
James ClarkeWellcome Trust - Medical Research Council Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 1QR, UK.
Sabine DietmannWellcome Trust - Medical Research Council Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 1QR, UK.
Duncan BakerCentre for Stem Cell Biology, Department of Biomedical Science, University of Sheffield, Sheffield S10 2TN, UK.
Anna SahakyanDepartment of Biological Chemistry, University of California, Los Angeles, CA 90095, USA.
Samuel MyersWellcome Trust - Medical Research Council Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 1QR, UK.
Paul BertoneWellcome Trust - Medical Research Council Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 1QR, UK.
Wolf ReikWellcome Trust - Medical Research Council Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 1QR, UK.
Kathrin PlathDepartment of Biological Chemistry, University of California, Los Angeles, CA 90095, USA.
Austin SmithWellcome Trust - Medical Research Council Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 1QR, UK gg251@cam.ac.uk austin.smith@cscr.cam.ac.uk.ORCID 0000-0002-3029-4682
Wellcome/MRC Cambridge Stem Cell Institute · GBBabraham Institute · GBUniversity of California, Los Angeles · USUniversity of Sheffield · GB

Funding

Biotechnology and Biological Sciences Research Council BB/K010867/1Medical Research Council G1001028Medical Research Council G1100526Medical Research Council MR/L012537/1Medical Research Council MR/P00072X/1Wellcome TrustWellcome Trust 095645/Z/11/Z
6 · The paper itself

Abstract

Much attention has focussed on the conversion of human pluripotent stem cells (PSCs) to a more naïve developmental status. Here we provide a method for resetting via transient histone deacetylase inhibition. The protocol is effective across multiple PSC lines and can proceed without karyotype change. Reset cells can be expanded without feeders with a doubling time of around 24 h. WNT inhibition stabilises the resetting process. The transcriptome of reset cells diverges markedly from that of primed PSCs and shares features with human inner cell mass (ICM). Reset cells activate expression of primate-specific transposable elements. DNA methylation is globally reduced to a level equivalent to that in the ICM and is non-random, with gain of methylation at specific loci. Methylation imprints are mostly lost, however. Reset cells can be re-primed to undergo tri-lineage differentiation and germline specification. In female reset cells, appearance of biallelic X-linked gene transcription indicates reactivation of the silenced X chromosome. On reconversion to primed status,

Indexed as

AnimalsCell DifferentiationCell LineDNA MethylationDNA Transposable ElementsEmbryo, MammalianEmbryonic Stem CellsEpigenesis, GeneticFlow CytometryGenes, X-LinkedHumansIn Situ Hybridization, FluorescenceMicePluripotent Stem CellsReal-Time Polymerase Chain ReactionX Chromosome InactivationDNA Transposable ElementsDifferentiationHuman embryoMethylomePluripotent stem cellsReprogramming

Identifiers

PMID28765214
PMCPMC5560041
OpenAlexW2952949965

What OpenQuestion holds

Textmetadata
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.