Evidence map›Paper›PMID 28100686›Full record

ArticleThe Journal of cell biology2017

Noncanonical function of DGCR8 controls mESC exit from pluripotency.

Daniel Cirera-Salinas, Jian Yu, Maxime Bodak, Richard P Ngondo, Kristina M Herbert, Constance Ciaudo

Open access · hybridAbstract read
In one paragraph

Article in The Journal of cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

31 citing papers in PubMed, 61 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Regulation of the microprocessor by post-translational modifications.Frontiers in cell and developmental biology · 2025
    Review
  5. Article
  6. Review
  7. Article
  8. International journal of molecular sciences · 2023
    Article
  9. Article
  10. Review
  11. Splice site mPeerJ · 2023
    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

6 authors at 3 institutions in 2 countries.

Daniel Cirera-SalinasDepartment of Biology, Institute of Molecular Health Sciences, RNAi and Genome Integrity, Swiss Federal Institute of Technology Zurich, Zurich 8093, Switzerland.ORCID 0000-0003-2171-5032
Jian YuDepartment of Biology, Institute of Molecular Health Sciences, RNAi and Genome Integrity, Swiss Federal Institute of Technology Zurich, Zurich 8093, Switzerland.
Maxime BodakDepartment of Biology, Institute of Molecular Health Sciences, RNAi and Genome Integrity, Swiss Federal Institute of Technology Zurich, Zurich 8093, Switzerland.ORCID 0000-0003-0500-4767
Richard P NgondoDepartment of Biology, Institute of Molecular Health Sciences, RNAi and Genome Integrity, Swiss Federal Institute of Technology Zurich, Zurich 8093, Switzerland.ORCID 0000-0003-4847-9375
Kristina M HerbertSanford Burnham Prebys Medical Discovery Institute, La Jolla, San Diego, CA 92037.ORCID 0000-0002-5288-3381
Constance CiaudoDepartment of Biology, Institute of Molecular Health Sciences, RNAi and Genome Integrity, Swiss Federal Institute of Technology Zurich, Zurich 8093, Switzerland cciaudo@ethz.ch.ORCID 0000-0002-0857-4506
École Polytechnique Fédérale de Lausanne · CHUniversity of Zurich · CHSanford Burnham Prebys Medical Discovery Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mouse embryonic stem cells (mESCs) deficient for DGCR8, a key component of the microprocessor complex, present strong differentiation defects. However, the exact reasons impairing their commitment remain elusive. The analysis of newly generated mutant mESCs revealed that DGCR8 is essential for the exit from the pluripotency state. To dissociate canonical versus noncanonical functions of DGCR8, we complemented the mutant mESCs with a phosphomutant DGCR8, which restored microRNA levels but did not rescue the exit from pluripotency defect. Integration of omics data and RNA immunoprecipitation experiments established DGCR8 as a direct interactor of Tcf7l1 mRNA, a core component of the pluripotency network. Finally, we found that DGCR8 facilitated the splicing of Tcf7l1, an event necessary for the differentiation of mESCs. Our data reveal a new noncanonical function of DGCR8 in the modulation of the alternative splicing of Tcf7l1 mRNA in addition to its established function in microRNA biogenesis.

Indexed as

Cell DifferentiationAlternative SplicingAnimalsCell CycleCell LineCell ProliferationEmbryonic Stem CellsGene Knockdown TechniquesGenotypeMiceMicroRNAsMutationPhenotypePhosphorylationPluripotent Stem CellsProtein BindingDgcr8 protein, mouseMicroRNAsRNA-Binding ProteinsRNA, MessengerRNA PrecursorsTcf7l1 protein, mouseTranscription Factor 7-Like 1 Protein

Identifiers

PMID28100686
PMCPMC5294780
OpenAlexW2573897599

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.