Evidence map›Paper›PMID 27926872›Full record

ArticleCell reports2016

Deletion of the Polycomb-Group Protein EZH2 Leads to Compromised Self-Renewal and Differentiation Defects in Human Embryonic Stem Cells.

Adam Collinson, Amanda J Collier, Natasha P Morgan, Arnold R Sienerth, Tamir Chandra, Simon Andrews, Peter J Rugg-Gunn

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
6.8field-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

88 citing papers in PubMed, 135 citations in OpenAlex.

  1. Article
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  12. Histone bivalency in CNS development.Genes & development · 2025
    Review
  13. Review
  14. Thymus Ontogeny and Development.Advances in experimental medicine and biology · 2025
    Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

28 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

7 authors at 2 institutions in 1 country.

Adam CollinsonEpigenetics Programme, The Babraham Institute, Cambridge CB22 3AT, UK.
Amanda J CollierEpigenetics Programme, The Babraham Institute, Cambridge CB22 3AT, UK; Wellcome Trust - Medical Research Council Stem Cell Institute, University of Cambridge, Cambridge CB2 1QR, UK.
Natasha P MorganEpigenetics Programme, The Babraham Institute, Cambridge CB22 3AT, UK.
Arnold R SienerthEpigenetics Programme, The Babraham Institute, Cambridge CB22 3AT, UK.
Tamir ChandraEpigenetics Programme, The Babraham Institute, Cambridge CB22 3AT, UK.
Simon AndrewsBioinformatics Group, The Babraham Institute, Cambridge CB22 3AT, UK.
Peter J Rugg-GunnEpigenetics Programme, The Babraham Institute, Cambridge CB22 3AT, UK; Wellcome Trust - Medical Research Council Stem Cell Institute, University of Cambridge, Cambridge CB2 1QR, UK; Centre for Trophoblast Research, University of Cambridge, Cambridge CB2 3EG, UK. Electronic address: peter.rugg-gunn@babraham.ac.uk.
Babraham Institute · GBUniversity of Cambridge · GB

Funding

Biotechnology and Biological Sciences Research Council BBS/E/B/000C0402Medical Research Council MC_PC_12009Medical Research Council MR/J003808/1Wellcome Trust WT093736
6 · The paper itself

Abstract

Through the histone methyltransferase EZH2, the Polycomb complex PRC2 mediates H3K27me3 and is associated with transcriptional repression. PRC2 regulates cell-fate decisions in model organisms; however, its role in regulating cell differentiation during human embryogenesis is unknown. Here, we report the characterization of EZH2-deficient human embryonic stem cells (hESCs). H3K27me3 was lost upon EZH2 deletion, identifying an essential requirement for EZH2 in methylating H3K27 in hESCs, in contrast to its non-essential role in mouse ESCs. Developmental regulators were derepressed in EZH2-deficient hESCs, and single-cell analysis revealed an unexpected acquisition of lineage-restricted transcriptional programs. EZH2-deficient hESCs show strongly reduced self-renewal and proliferation, thereby identifying a more severe phenotype compared to mouse ESCs. EZH2-deficient hESCs can initiate differentiation toward developmental lineages; however, they cannot fully differentiate into mature specialized tissues. Thus, EZH2 is required for stable ESC self-renewal, regulation of transcriptional programs, and for late-stage differentiation in this model of early human development.

Indexed as

AnimalsCell DifferentiationCell ProliferationCell Self RenewalEnhancer of Zeste Homolog 2 ProteinHuman Embryonic Stem CellsHumansJumonji Domain-Containing Histone DemethylasesMicePolycomb-Group ProteinsPolycomb Repressive Complex 2Sequence DeletionSingle-Cell AnalysisEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanJumonji Domain-Containing Histone DemethylasesKdm6b protein, mousePolycomb-Group ProteinsPolycomb Repressive Complex 2differentiationepigeneticshistone methylationpluripotency

Identifiers

PMID27926872
PMCPMC5177603
OpenAlexW2560558522

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.