Delamination of neural crest cells requires transient and reversible Wnt inhibition mediated by Dact1/2

M Angeles Rabadán1, Antonio Herrera2, Lucia Fanlo1

  • 1Department of Developmental Biology, Instituto de Biología Molecular de Barcelona, CSIC, Parc Científic de Barcelona, C/ Baldiri i Reixac 20, Barcelona 08028, Spain.

Development (Cambridge, England)
|April 29, 2016
PubMed

Insights

Neural crest cell delamination, a model for epithelial-to-mesenchymal transition (EMT), involves transient Wnt/β-catenin signaling inhibition. Scaffold proteins Dact1/2 are crucial for this process by regulating β-catenin activity.

Area of Science:

  • Developmental Biology
  • Cell Biology
  • Molecular Biology

Background:

  • Neural crest (NC) cell delamination is a key developmental process and a model for epithelial-to-mesenchymal transition (EMT).
  • Wnt/β-catenin signaling is known to influence EMT and cell migration during development.

Purpose of the Study:

  • To investigate the role of Wnt/β-catenin signaling in NC cell delamination.
  • To identify the molecular mechanisms regulating Wnt/β-catenin signaling during NC delamination.

Main Methods:

  • Utilized two in vivo models (Xenopus and chick embryos).
  • Investigated the expression and function of Dact1 and Dact2 proteins in pre-migratory NC cells.
  • Analyzed the effects of Dact1/2 on Wnt/β-catenin signaling and β-catenin subcellular localization.

Main Results:

  • Wnt/β-catenin signaling is transiently inhibited during NC delamination.
  • Scaffold proteins Dact1 and Dact2 are essential for NC delamination but not for migratory cell motility.
  • Dact1/2 inhibit Wnt/β-catenin signaling upstream of TCF transcriptional activity by regulating β-catenin's co-activator function without affecting its stability.

Conclusions:

  • Dact1 and Dact2 act as novel regulators of Wnt/β-catenin signaling during NC delamination.
  • This study reveals a new mechanism controlling β-catenin activity, impacting NC cell fate and migration.
  • The findings provide insights into the regulation of EMT during embryonic development.

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