Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Edar/Eda interactions regulate enamel knot formation in tooth morphogenesis.

A S Tucker1, D J Headon, P Schneider

  • 1MRC Centre for Developmental Neurobiology, King's College, Guy's Hospital, London Bridge, London SE1 1UL, UK.

Development (Cambridge, England)
|October 12, 2000
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Aberrant Proliferation and Cell Fate Underlie Oral Defects in a Mouse Model of EvC Syndrome.

Journal of dental research·2026
Same author

Tooth-bone attachment tissue is produced by cells with a mixture of odontoblastic and osteoblastic features in reptiles.

Journal of anatomy·2025
Same author

Activating Endogenous Condylar Stem Cells to Enhance TMJ Repair.

Journal of dental research·2025
Same author

Vascular Invasion of the Dental Epithelium Is Essential for Ameloblasts.

Journal of dental research·2025
Same author

FSP1/S100A4-Expressing Stem/Progenitor Cells Are Essential for Temporomandibular Joint Growth and Homeostasis.

Journal of dental research·2025
Same author

CACNA1S mutation-associated dental anomalies: A calcium channelopathy.

Oral diseases·2023
Same journal

Expanding the C. elegans toolkit with gonad explants.

Development (Cambridge, England)·2026
Same journal

Nuclear Factor Y controls nutrient-adaptive epithelial growth by regulating mTOR in the Drosophila midgut.

Development (Cambridge, England)·2026
Same journal

Primordial germ cells differentially contribute to the germline in zebrafish.

Development (Cambridge, England)·2026
Same journal

Dissecting planar and vertical organiser signals in early chick neural development.

Development (Cambridge, England)·2026
Same journal

Real-time transcriptomic profiling of hPSC-derived cartilage during development identifies a key role for the extracellular matrix in homeostasis and protection.

Development (Cambridge, England)·2026
Same journal

In preprints - housekeeping the housekeeping genes.

Development (Cambridge, England)·2026
See all related articles

The tabby and downless mouse mutants reveal distinct roles for Ectodysplasin-A (Eda) and its receptor Edar in tooth development. Their interaction is crucial, but the downless mutant

Area of Science:

  • Developmental Biology
  • Genetics
  • Molecular Biology

Background:

  • Tabby (Ta) and downless (Dl) mouse mutants exhibit similar defects in teeth, hair, and sweat glands.
  • The genes responsible, Ectodysplasin-A (Eda) for Ta and Edar for Dl, encode interacting TNF pathway members.
  • Understanding their specific roles in development, particularly tooth morphogenesis, is crucial.

Purpose of the Study:

  • To investigate the distinct roles of Eda and Edar in mouse tooth development.
  • To analyze the molecular and cellular defects in tabby and downless mutant tooth germs.
  • To elucidate the signaling pathways involved in tooth cusp formation.

Main Methods:

  • Comparative analysis of gene expression patterns for Eda and Edar during mouse tooth development.

Related Experiment Videos

  • Detailed morphological and molecular analysis of downless mutant tooth germs.
  • In vitro experiments using soluble Edar to assess its interaction with Eda and its effect on tooth germs.

    • Main Results:

    • Eda and Edar interact in vitro, but their expression patterns during tooth development are not in adjacent cells.
    • Downless mutant teeth show defects in the enamel knot, forming an 'enamel rope' instead of a distinct knot, with altered signaling.
    • Adding soluble Edar mimicked the tabby phenotype, implicating endogenous Eda, but did not replicate the downless phenotype.

    Conclusions:

    • Eda and Edar signaling pathways play distinct roles in tooth cusp morphogenesis, affecting the enamel knot structure differently.
    • The downless phenotype suggests additional factors or ligand-independent Edar activation mechanisms.
    • The Lef1 pathway functions independently in a parallel pathway during tooth development.