Evidence map›Paper›PMID 28366589›Full record

ArticleCell stem cell2017

H3K4 Methylation-Dependent Memory of Somatic Cell Identity Inhibits Reprogramming and Development of Nuclear Transfer Embryos.

Eva Hörmanseder, Angela Simeone, George E Allen, Charles R Bradshaw, Magdalena Figlmüller, John Gurdon, Jerome Jullien

Abstract read
In one paragraph

Article in Cell stem cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing 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

65 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
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  8. Article
  9. Article
  10. Review
  11. Cell reprogramming: methods, mechanisms and applications.Cell regeneration (London, England) · 2025
    Review
  12. Article
  13. Review
  14. DNA methylation regulates RNA mCell proliferation · 2024
    Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Somatic Cell Nuclear Transfer in Pigs.Methods in molecular biology (Clifton, N.J.) · 2023
    Article

5 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.

Eva HörmansederWellcome Trust/Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge CB2 1QN, UK. Electronic address: e.hoermanseder@gurdon.cam.ac.uk.
Angela SimeoneWellcome Trust/Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge CB2 1QN, UK.
George E AllenWellcome Trust/Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge CB2 1QN, UK.
Charles R BradshawWellcome Trust/Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge CB2 1QN, UK.
Magdalena FiglmüllerWellcome Trust/Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge CB2 1QN, UK.
John GurdonWellcome Trust/Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge CB2 1QN, UK; Department of Zoology, University of Cambridge, Cambridge CB2 1QN, UK.
Jerome JullienWellcome Trust/Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge CB2 1QN, UK. Electronic address: j.jullien@gurdon.cam.ac.uk.

Funding

Biotechnology and Biological Sciences Research Council BBS/B/14647Cancer Research UK C6946/A14492Medical Research Council G1001690Medical Research Council MR/K011022/1Medical Research Council MR/P000479/1Wellcome Trust
6 · The paper itself

Abstract

Vertebrate eggs can induce the nuclear reprogramming of somatic cells to enable production of cloned animals. Nuclear reprogramming is relatively inefficient, and the development of the resultant embryos is frequently compromised, in part due to the inappropriate expression of genes previously active in the donor nucleus. Here, we identify H3K4 methylation as a major epigenetic roadblock that limits transcriptional reprogramming and efficient nuclear transfer (NT). Widespread expression of donor-cell-specific genes was observed in inappropriate cell types in NT embryos, limiting their developmental capacity. The expression of these genes in reprogrammed embryos arises from epigenetic memories of a previously active transcriptional state in donor cells that is characterized by high H3K4 methylation. Reducing H3K4 methylation had little effect on gene expression in donor cells, but it substantially improved transcriptional reprogramming and development of NT embryos. These results show that H3K4 methylation imposes a barrier to efficient nuclear reprogramming and suggest approaches for improving reprogramming strategies.

Indexed as

Cellular ReprogrammingEpigenesis, GeneticNuclear Transfer TechniquesAnimalsFemaleHistonesMaleMethylationMiceXenopus laevisXenopus ProteinsHistonesXenopus Proteinscell-fate stabilityendodermepigenetic memoryH3K4me3Kdm5bnuclear transferreprogramming

Identifiers

PMID28366589
PMCPMC5505866

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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.