Evidence map›Paper›PMID 12502739›Full record

ArticleGenes & development2002

FGF4, a direct target of LEF1 and Wnt signaling, can rescue the arrest of tooth organogenesis in Lef1(-/-) mice.

Klaus Kratochwil, Juan Galceran, Sabine Tontsch, Wera Roth, Rudolf Grosschedl

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed
–field-weighted citation impact
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

106 citing papers in PubMed, 268 citations in OpenAlex.

  1. Review
  2. Review
  3. FGF family in health and disease.Molecular biomedicine · 2026
    Review
  4. Review
  5. International journal of molecular sciences · 2025
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. wnt10a is required for zebrafish median fin fold maintenance and adult unpaired fin metamorphosis.Developmental dynamics : an official publication of the American Association of Anatomists · 2024
    Article
  11. Article
  12. Review
  13. A shark-inspired general model of tooth morphogenesis unveils developmental asymmetries in phenotype transitions.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  14. Tooth number abnormality: from bench to bedside.International journal of oral science · 2023
    Review
  15. Selection signature analysis revealsArchives animal breeding · 2023
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Primary Cilia Formation Does Not Rely on WNT/β-Catenin Signaling.Frontiers in cell and developmental biology · 2021
    Article

46 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

5 authors at 1 institution in 1 country.

Klaus KratochwilInstitute of Molecular Biology, Austrian Academy of Sciences, 5020 Salzburg, Austria.
Juan Galceran
Sabine Tontsch
Wera Roth
Rudolf Grosschedl
Austrian Academy of Sciences · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lymphoid enhancer factor (LEF1), a nuclear mediator of Wnt signaling, is required for the formation of organs that depend on inductive interactions between epithelial and mesenchymal tissues. In previous tissue recombination experiments with normal and Lef1(-/-) tooth germs, we found that the effect of LEF1 expression in the epithelium is tissue nonautonomous and transferred to the subjacent mesenchyme. Here we examine the molecular basis for LEF1 function and find that the epithelium of the developmentally arrested Lef1(-/-) tooth rudiments fails to express Fgf4, Shh, and Bmp4, but not Wnt10a. We identify the Fgf4 gene as a direct transcriptional target for LEF1 and show that beads soaked with recombinant FGF4 protein can fully overcome the developmental arrest of Lef1(-/-) tooth germs. In addition, we find that FGF4 beads induce rapidly the expression of Fgf3 in dental mesenchyme and that both epithelial and mesenchymal FGF proteins induce the delayed expression of Shh in the epithelium. Taken together, these data indicate that a single target of LEF1 can account for the function of LEF1 in tooth development and for a relay of a Wnt signal reception to a cascade of FGF signaling activities, allowing for a sequential and reciprocal communication between epithelium and mesenchyme.

Indexed as

Zebrafish ProteinsAnimalsbeta CateninBone Morphogenetic Protein 4Bone Morphogenetic ProteinsCell DifferentiationCytoskeletal ProteinsDNA-Binding ProteinsElectrophoretic Mobility Shift AssayEmbryonic InductionEpithelial CellsFibroblast Growth Factor 4Fibroblast Growth FactorsGene ExpressionGene Expression Regulation, DevelopmentalHedgehog Proteinsbeta CateninBmp4 protein, mousebmp4 protein, zebrafishBone Morphogenetic Protein 4Bone Morphogenetic ProteinsCTNNB1 protein, mouseCytoskeletal ProteinsDNA-Binding ProteinsFgf4 protein, mouseFibroblast Growth Factor 4Fibroblast Growth FactorsHedgehog ProteinsLef1 protein, mouseLymphoid Enhancer-Binding Factor 1Proto-Oncogene ProteinsRecombinant ProteinsTrans-ActivatorsTranscription FactorsWnt ProteinsZebrafish Proteins

Identifiers

PMID12502739
PMCPMC187508
OpenAlexW2100057652

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.