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Related Experiment Videos

Epithelium-mesenchyme transition during neural crest development

J L Duband1, F Monier, M Delannet

  • 1Laboratoire de Biologie Cellulaire du Développement, Institut Jacques-Monod, Université Paris, France.

Acta Anatomica
|January 1, 1995
PubMed
Summary

Neural crest cell migration is a key vertebrate trait involving an epithelium to mesenchyme transition (EMT). This study explores EMT events, cell adhesion changes, and extracellular matrix interactions during neural crest development.

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Area of Science:

  • Developmental Biology
  • Cell Biology
  • Vertebrate Embryology

Background:

  • The neural crest, defining vertebrates, originates from an epithelium to mesenchyme transition (EMT).
  • The zinc finger gene Slug is implicated in specifying EMT competence for neural crest cells.
  • Understanding the precise temporal events of neural crest EMT is crucial but incompletely understood.

Purpose of the Study:

  • To elucidate the molecular and cellular events characterizing neural crest EMT.
  • To investigate the roles of cell adhesion molecules, extracellular matrix, and cytoskeleton during neural crest migration.
  • To identify signaling pathways, such as TGF-beta, that regulate neural crest EMT.

Main Methods:

  • In situ observations and in vitro/in vivo experiments across different species and axial levels.

Related Experiment Videos

  • Analysis of cell-cell adhesion molecules (N-cadherin, T-cadherin, N-CAM) and their expression dynamics.
  • Assessment of extracellular matrix receptor (integrin) activity and matrix composition changes.
  • Investigation of cell shape, motility, and cytoskeletal alterations.
  • Examination of signaling pathways involving TGF-beta family growth factors and phosphorylation.

    • Main Results:

    • Neural crest EMT involves decreased cell-cell adhesion, notably loss of N-cadherin at migration onset.
    • Changes in integrin activity and extracellular matrix composition are observed.
    • Alterations in cell shape, motility, and cytoskeleton accompany EMT.
    • TGF-beta family growth factors, like dorsalin-I, can trigger these EMT-associated responses.
    • EMT involves complex signaling pathways with controlled phosphorylation events.

    Conclusions:

    • Neural crest EMT is a multi-faceted process involving coordinated changes in adhesion, matrix interaction, and cellular mechanics.
    • The spatiotemporal characteristics of neural crest EMT make it a valuable model for studying EMT in general.
    • Further research is needed to fully understand the intricate mechanisms governing neural crest EMT.