Evidence map›Paper›PMID 26116666›Full record

ArticleDevelopment (Cambridge, England)2015

Fat4/Dchs1 signaling between stromal and cap mesenchyme cells influences nephrogenesis and ureteric bud branching.

Yaopan Mao, Philippa Francis-West, Kenneth D Irvine

Open access · bronzeAbstract read
In one paragraph

Article in Development (Cambridge, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

45 citing papers in PubMed, 67 citations in OpenAlex.

  1. Innate immunity · 2020
    Trial
  2. The kidney stroma in development and disease.Nature reviews. Nephrology · 2025
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
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  12. Principles of human and mouse nephron development.Nature reviews. Nephrology · 2022
    Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Metabolic programming of nephron progenitor cell fate.Pediatric nephrology (Berlin, Germany) · 2021
    Review
  18. Review
  19. Review
  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

3 authors at 3 institutions in 2 countries.

Yaopan MaoHoward Hughes Medical Institute, Waksman Institute and Department of Molecular Biology and Biochemistry, Rutgers University, Piscataway, NJ 08854, USA.
Philippa Francis-WestDepartment of Craniofacial Development and Stem Cell Biology, King's College London, Floor 27, Guy's Tower, London SE1 9RT, UK.
Kenneth D IrvineHoward Hughes Medical Institute, Waksman Institute and Department of Molecular Biology and Biochemistry, Rutgers University, Piscataway, NJ 08854, USA irvine@waksman.rutgers.edu.
Howard Hughes Medical Institute · USKing's College London · GBRutgers, The State University of New Jersey · US

Funding

Biotechnology and Biological Sciences Research Council BB/K001671/1Howard Hughes Medical Institute
6 · The paper itself

Abstract

Formation of the kidney requires reciprocal signaling among the ureteric tubules, cap mesenchyme and surrounding stromal mesenchyme to orchestrate complex morphogenetic events. The protocadherin Fat4 influences signaling from stromal to cap mesenchyme cells to regulate their differentiation into nephrons. Here, we characterize the role of a putative binding partner of Fat4, the protocadherin Dchs1. Mutation of Dchs1 in mice leads to increased numbers of cap mesenchyme cells, which are abnormally arranged around the ureteric bud tips, and impairment of nephron morphogenesis. Mutation of Dchs1 also reduces branching of the ureteric bud and impairs differentiation of ureteric bud tip cells into trunk cells. Genetically, Dchs1 is required specifically within cap mesenchyme cells. The similarity of Dchs1 phenotypes to stromal-less kidneys and to those of Fat4 mutants implicates Dchs1 in Fat4-dependent stroma-to-cap mesenchyme signaling. Antibody staining of genetic mosaics reveals that Dchs1 protein localization is polarized within cap mesenchyme cells, where it accumulates at the interface with stromal cells, implying that it interacts directly with a stromal protein. Our observations identify a role for Fat4 and Dchs1 in signaling between cell layers, implicate Dchs1 as a Fat4 receptor for stromal signaling that is essential for kidney development, and establish that vertebrate Dchs1 can be molecularly polarized in vivo.

Indexed as

AnimalsCadherinsGalactosidesHistological TechniquesImage Processing, Computer-AssistedIndolesKidneyMesenchymal Stem CellsMiceMicroscopy, ConfocalMorphogenesisMutationNephronsSignal TransductionUreter5-bromo-4-chloro-3-indolyl beta-galactosideCadherinsDchs1 protein, mouseFat4 protein, mouseGalactosidesIndolesDachsousFatKidneyNephron

Identifiers

PMID26116666
PMCPMC4529033
OpenAlexW2166423354

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.