Evidence map›Paper›PMID 28740264›Full record

ArticleNature genetics2017

PRDM15 safeguards naive pluripotency by transcriptionally regulating WNT and MAPK-ERK signaling.

Slim Mzoughi, Jingxian Zhang, Delphine Hequet, Shun Xie Teo, Haitong Fang, Qiao Rui Xing, Marco Bezzi, Michelle Kay Yi Seah, Sheena L M Ong, Eun Myoung Shin and 9 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

39 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
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  3. Review
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  5. Review
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  8. Review
  9. Article
  10. BRD8 Guards the Pluripotent State by Sensing and Maintaining Histone Acetylation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  11. Article
  12. Prdm15 acts upstream of Wnt4 signaling in anterior neural development ofFrontiers in cell and developmental biology · 2024
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
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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

19 authors at 5 institutions in 4 countries.

Slim MzoughiMethyltransferases in Development and Disease Group, Institute of Molecular and Cell Biology, Agency for Science, Technology and Research (A*STAR), Singapore.
Jingxian ZhangMethyltransferases in Development and Disease Group, Institute of Molecular and Cell Biology, Agency for Science, Technology and Research (A*STAR), Singapore.
Delphine HequetMethyltransferases in Development and Disease Group, Institute of Molecular and Cell Biology, Agency for Science, Technology and Research (A*STAR), Singapore.
Shun Xie TeoMethyltransferases in Development and Disease Group, Institute of Molecular and Cell Biology, Agency for Science, Technology and Research (A*STAR), Singapore.
Haitong FangEpigenetics and Cell Fates Group, Institute of Molecular and Cell Biology, Agency for Science, Technology and Research (A*STAR), Singapore.
Qiao Rui XingEpigenetics and Cell Fates Group, Institute of Molecular and Cell Biology, Agency for Science, Technology and Research (A*STAR), Singapore.
Marco BezziMethyltransferases in Development and Disease Group, Institute of Molecular and Cell Biology, Agency for Science, Technology and Research (A*STAR), Singapore.
Michelle Kay Yi SeahDevelopmental Epigenetics and Disease Group, Institute of Molecular and Cell Biology, Agency for Science, Technology and Research (A*STAR), Singapore.
Sheena L M OngInstitute of Medical Biology (IMB), Agency for Science, Technology and Research (A*STAR), Singapore.
Eun Myoung ShinCancer Science Institute of Singapore (CSI), National University of Singapore, Singapore.
Heike WollmannDNA Sequencing Facility NGS Unit, Institute of Molecular and Cell Biology, Agency for Science, Technology and Research (A*STAR), Singapore.
Esther S M WongInstitute of Medical Biology (IMB), Agency for Science, Technology and Research (A*STAR), Singapore.
Muthafar Al-HaddawiAdvanced Molecular Pathology Laboratory, IMCB, Singapore.
Colin L StewartInstitute of Medical Biology (IMB), Agency for Science, Technology and Research (A*STAR), Singapore.
Vinay TergaonkarDepartment of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
Yuin-Han LohEpigenetics and Cell Fates Group, Institute of Molecular and Cell Biology, Agency for Science, Technology and Research (A*STAR), Singapore.
N Ray DunnInstitute of Medical Biology (IMB), Agency for Science, Technology and Research (A*STAR), Singapore.
Daniel M MesserschmidtDepartment of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
Ernesto GuccioneMethyltransferases in Development and Disease Group, Institute of Molecular and Cell Biology, Agency for Science, Technology and Research (A*STAR), Singapore.
Agency for Science, Technology and Research · SGInstitute of Molecular and Cell Biology · SGInstitute of Medical Biology · SGNational University of Singapore · SGUniversity of South Australia · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transcriptional network acting downstream of LIF, WNT and MAPK-ERK to stabilize mouse embryonic stem cells (ESCs) in their naive state has been extensively characterized. However, the upstream factors regulating these three signaling pathways remain largely uncharted. PR-domain-containing proteins (PRDMs) are zinc-finger sequence-specific chromatin factors that have essential roles in embryonic development and cell fate decisions. Here we characterize the transcriptional regulator PRDM15, which acts independently of PRDM14 to regulate the naive state of mouse ESCs. Mechanistically, PRDM15 modulates WNT and MAPK-ERK signaling by directly promoting the expression of Rspo1 (R-spondin1) and Spry1 (Sprouty1). Consistent with these findings, CRISPR-Cas9-mediated disruption of PRDM15-binding sites in the Rspo1 and Spry1 promoters recapitulates PRDM15 depletion, both in terms of local chromatin organization and the transcriptional modulation of these genes. Collectively, our findings uncover an essential role for PRDM15 as a chromatin factor that modulates the transcription of upstream regulators of WNT and MAPK-ERK signaling to safeguard naive pluripotency.

Indexed as

Gene Expression RegulationAnimalsBlotting, WesternCell LineCells, CulturedCell Self RenewalCellular ReprogrammingDNA-Binding ProteinsEmbryonic Stem CellsFluorescent Antibody TechniqueGene Expression ProfilingHumansInduced Pluripotent Stem CellsMAP Kinase Signaling SystemMice, KnockoutMice, NudeDNA-Binding ProteinsPRDM15 protein, humanPRDM15 protein, mouseTranscription Factors

Identifiers

PMID28740264
OpenAlexW2739283654

What OpenQuestion holds

Textmetadata
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.