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Related Experiment Videos

Traf6 is essential for murine tooth cusp morphogenesis.

Atsushi Ohazama1, Jo-Maree Courtney, Abigail S Tucker

  • 1Department of Craniofacial Development, GKT Dental Institute, King's College, Guy's Hospital, London Bridge, London, United Kingdom.

Developmental Dynamics : an Official Publication of the American Association of Anatomists
|December 31, 2003
PubMed
Summary
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Tumor necrosis factor superfamily molecules regulate ectodermal development. This study identifies a novel pathway involving TROY/Traf6 in molar tooth cusp formation, distinct from ectodysplasin signaling.

Area of Science:

  • Developmental Biology
  • Genetics
  • Molecular Biology

Background:

  • Hypohidrotic ectodermal dysplasia (HED) affects ectodermal appendages like skin, hair, and teeth.
  • Mutations in tumor necrosis factor (TNF) superfamily members (ectodysplasin (EDA), EDA receptor (EDAR), EDAR-associated death domain (EDARADD)) cause HED.
  • The role of other TNF superfamily members in ectodermal development is less understood.

Purpose of the Study:

  • To investigate the role of the TNF orphan receptor TROY in tooth development.
  • To explore the involvement of TROY and its adaptor protein Traf6 in molar tooth cusp formation.
  • To determine if TROY/Traf6 signaling is independent of the known EDA pathway.

Main Methods:

  • In situ hybridization to examine gene coexpression patterns in murine tooth development.

Related Experiment Videos

  • Analysis of Traf6 mutant mice to assess tooth morphology.
  • Comparison of tooth abnormalities in Traf6 mutants with those in Eda signaling mutants.

    • Main Results:

    • TROY is strongly coexpressed with Edar in epithelial enamel knot signaling centers during murine tooth development.
    • Traf6 mutant mice exhibit molar tooth abnormalities more severe than those seen in Eda signaling molecule mutants.
    • This suggests a distinct role for TROY/Traf6 in molar tooth cusp formation.

    Conclusions:

    • A TNF pathway involving TROY/Traf6 is essential for molar tooth cusp formation, in addition to ectodysplasin.
    • This study identifies a critical role for Traf6 in tooth development.
    • The findings expand our understanding of the molecular mechanisms underlying ectodermal development and HED.