Evidence map›Paper›PMID 22874919›Full record

ArticleDevelopment (Cambridge, England)2012

A Sox9/Fgf feed-forward loop maintains pancreatic organ identity.

Philip A Seymour, Hung Ping Shih, Nisha A Patel, Kristine K Freude, Ruiyu Xie, Christopher J Lim, Maike Sander

Open access · bronzeAbstract read
In one paragraph

Article in Development (Cambridge, England), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
7.9field-weighted citation impact, top 2% 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

63 citing papers in PubMed, 110 citations in OpenAlex.

  1. Article
  2. Review
  3. Integrating Prior Knowledge Using Transformer for Gene Regulatory Network Inference.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. SOX9 in organogenesis: shared and unique transcriptional functions.Cellular and molecular life sciences : CMLS · 2022
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

3 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 1 institution in 1 country.

Philip A SeymourDepartments of Pediatrics and Cellular and Molecular Medicine, University of California San Diego, La Jolla, CA 92093-0695, USA.
Hung Ping Shih
Nisha A Patel
Kristine K Freude
Ruiyu Xie
Christopher J Lim
Maike Sander
University of California, Irvine · US

Funding

Novel insights into nutrient-dependent regulation of beta cell proliferationR01DK078803 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SANDER, MAIKE · 2007 to 2022
$4.4M
NIDDK NIH HHS DK078803NIDDK NIH HHS R01 DK078803
6 · The paper itself

Abstract

All mature pancreatic cell types arise from organ-specific multipotent progenitor cells. Although previous studies have identified cell-intrinsic and -extrinsic cues for progenitor cell expansion, it is unclear how these cues are integrated within the niche of the developing organ. Here, we present genetic evidence in mice that the transcription factor Sox9 forms the centerpiece of a gene regulatory network that is crucial for proper organ growth and maintenance of organ identity. We show that pancreatic progenitor-specific ablation of Sox9 during early pancreas development causes pancreas-to-liver cell fate conversion. Sox9 deficiency results in cell-autonomous loss of the fibroblast growth factor receptor (Fgfr) 2b, which is required for transducing mesenchymal Fgf10 signals. Likewise, Fgf10 is required to maintain expression of Sox9 and Fgfr2 in epithelial progenitors, showing that Sox9, Fgfr2 and Fgf10 form a feed-forward expression loop in the early pancreatic organ niche. Mirroring Sox9 deficiency, perturbation of Fgfr signaling in pancreatic explants or genetic inactivation of Fgf10 also result in hepatic cell fate conversion. Combined with previous findings that Fgfr2b or Fgf10 are necessary for pancreatic progenitor cell proliferation, our results demonstrate that organ fate commitment and progenitor cell expansion are coordinately controlled by the activity of a Sox9/Fgf10/Fgfr2b feed-forward loop in the pancreatic niche. This self-promoting Sox9/Fgf10/Fgfr2b loop may regulate cell identity and organ size in a broad spectrum of developmental and regenerative contexts.

Indexed as

AnimalsCell DifferentiationEmbryo, MammalianFibroblast Growth Factor 10Gene Expression Regulation, DevelopmentalImmunohistochemistryLiverMicePancreasReceptor, Fibroblast Growth Factor, Type 2SOX9 Transcription FactorFgf10 protein, mouseFgfr2 protein, mouseFibroblast Growth Factor 10Receptor, Fibroblast Growth Factor, Type 2Sox9 protein, mouseSOX9 Transcription Factor

Identifiers

PMID22874919
PMCPMC3424044
OpenAlexW2055405167

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.