Evidence map›Paper›PMID 23637628›Full record

ArticlePLoS genetics2013

SNF5 is an essential executor of epigenetic regulation during differentiation.

Jueng Soo You, Daniel D De Carvalho, Chao Dai, Minmin Liu, Kurinji Pandiyan, Xianghong J Zhou, Gangning Liang, Peter A Jones

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

27 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. High Frequency of Ovarian Cyst Development in VhlThe American journal of pathology · 2018
    Article
  16. Alteration of Epigenetic Regulation by Long Noncoding RNAs in Cancer.International journal of molecular sciences · 2018
    Review
  17. Article
  18. Article
  19. Article
  20. Review
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

8 authors at 3 institutions in 2 countries.

Jueng Soo YouDepartments of Urology and Biochemistry and Molecular Biology, USC Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angles, California, United States of America.
Daniel D De Carvalho
Chao Dai
Minmin Liu
Kurinji Pandiyan
Xianghong J Zhou
Gangning Liang
Peter A Jones
University of Southern California · USJohns Hopkins Medicine · USKonkuk University · KR

Funding

Mechanisms of De Novo Methylation in CancerR37CA082422 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI JONES, PETER A · 2009 to 2013
$2.2M
NCI NIH HHS NIH R37 CA-082422-12NCI NIH HHS R37 CA082422
6 · The paper itself

Abstract

Nucleosome occupancy controls the accessibility of the transcription machinery to DNA regulatory regions and serves an instructive role for gene expression. Chromatin remodelers, such as the BAF complexes, are responsible for establishing nucleosome occupancy patterns, which are key to epigenetic regulation along with DNA methylation and histone modifications. Some reports have assessed the roles of the BAF complex subunits and stemness in murine embryonic stem cells. However, the details of the relationships between remodelers and transcription factors in altering chromatin configuration, which ultimately affects gene expression during cell differentiation, remain unclear. Here for the first time we demonstrate that SNF5, a core subunit of the BAF complex, negatively regulates OCT4 levels in pluripotent cells and is essential for cell survival during differentiation. SNF5 is responsible for generating nucleosome-depleted regions (NDRs) at the regulatory sites of OCT4 repressed target genes such as PAX6 and NEUROG1, which are crucial for cell fate determination. Concurrently, SNF5 closes the NDRs at the regulatory regions of OCT4-activated target genes such as OCT4 itself and NANOG. Furthermore, using loss- and gain-of-function experiments followed by extensive genome-wide analyses including gene expression microarrays and ChIP-sequencing, we highlight that SNF5 plays dual roles during differentiation by antagonizing the expression of genes that were either activated or repressed by OCT4, respectively. Together, we demonstrate that SNF5 executes the switch between pluripotency and differentiation.

Indexed as

Epigenesis, GeneticOctamer Transcription Factor-3AnimalsCell DifferentiationEmbryonic Stem CellsGene Expression Regulation, DevelopmentalGenome-Wide Association StudyOctamer Transcription Factor-3

Identifiers

PMID23637628
PMCPMC3636213
OpenAlexW1965630177

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.