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Fibronectin matrix composition and organization can regulate cell migration during amphibian development.

T Darribère1, J E Schwarzbauer

  • 1Université P. et M. Curie, U.M.R. CNRS 7622, Laboratoire de Biologie Moléculaire et Cellulaire du Développement, Equipe Adhesion et Migration Cellulaires, 9 Quai Saint-Bernard, 75252, Paris, France. darriber@ccr.jussieu.fr

Mechanisms of Development
|March 23, 2000
PubMed
Summary

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Fibronectin matrix structure is crucial for vertebrate development. Altering fibronectin assembly and composition disrupts cell adhesion and migration, leading to developmental defects like impaired gastrulation.

Area of Science:

  • Developmental Biology
  • Cell Biology
  • Extracellular Matrix Research

Background:

  • Fibronectin (FN) is a vital extracellular matrix protein essential for vertebrate development.
  • FN forms a cell-surface fibrillar matrix regulating cell morphology, migration, and proliferation.

Purpose of the Study:

  • To investigate the role of fibronectin matrix structure in early vertebrate development.
  • To analyze the impact of specific fibronectin mutations on matrix assembly and function.

Main Methods:

  • Introduction of normal and mutant recombinant fibronectins (recFNs) into Pleurodeles waltl embryos.
  • Analysis of recFN assembly into fibrillar matrices and aggregates.
  • Assessment of cell adhesion, spreading, and migration in vitro and in vivo on chimeric matrices.

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Main Results:

  • Native and specific mutant recFNs (FN(A-B-), FN(RGD-), FN(syn-), FNDeltaIII(1)) assembled into fibrillar matrices.
  • A distinct recFN (FNDeltaIII(1-7)) formed aggregates and inhibited endogenous FN matrix assembly.
  • Perturbed cell behaviors and developmental defects, including mesoderm patterning defects and inhibited gastrulation, were observed.

Conclusions:

  • Fibronectin matrix fibrillar structure is critical for regulating cell adhesion and migration during vertebrate development.
  • Matrix composition significantly influences developmental processes.
  • Specific fibronectin mutations can disrupt normal embryonic development.