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Fibronectin requirement in branching morphogenesis.

Takayoshi Sakai1, Melinda Larsen, Kenneth M Yamada

  • 1Craniofacial Developmental Biology and Regeneration Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland 20892-4370, USA.

Nature
|June 20, 2003
PubMed
Summary
This summary is machine-generated.

Fibronectin is crucial for embryonic organ development, enabling cleft formation during branching morphogenesis. This extracellular matrix protein facilitates the transition from cell-cell to cell-matrix adhesion, essential for organ structure.

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Area of Science:

  • Developmental Biology
  • Cell Biology
  • Extracellular Matrix Biology

Background:

  • Organogenesis relies on epithelial branching morphogenesis, involving repetitive cleft and bud formation.
  • The precise molecular mechanisms driving these structural changes, particularly cleft formation, remain largely unknown.
  • Previous hypotheses suggested the involvement of localized regulatory proteins in guiding branching patterns.

Purpose of the Study:

  • To investigate the role of extracellular matrix proteins in initiating epithelial branching.
  • To determine the specific function of fibronectin in cleft formation during branching morphogenesis.
  • To elucidate the molecular mechanisms by which fibronectin influences epithelial structure.

Main Methods:

  • Localization and temporal expression analysis of fibronectin messenger RNA and protein in developing salivary glands.
  • Functional assays using small interfering RNA to reduce fibronectin levels and antibody inhibition of fibronectin and integrin.
  • Experiments with exogenous fibronectin to assess its impact on branching.
  • In vitro studies using cultured human salivary epithelial cells to examine fibronectin-induced adhesion changes.

Main Results:

  • Fibronectin expression was transient and focal in developing cleft regions, correlating with a loss of cadherin.
  • Suppression of fibronectin (via siRNA or antibodies) inhibited cleft formation and branching in salivary glands, lungs, and kidneys.
  • Addition of exogenous fibronectin promoted cleft formation and branching.
  • Fibrillar fibronectin induced cell-matrix adhesions and cadherin loss in cultured epithelial cells.

Conclusions:

  • Fibronectin is essential for cleft formation during the initiation of epithelial branching morphogenesis.
  • Fibronectin mediates a critical transition from cell-cell adhesion to cell-matrix adhesion, driving structural changes in developing organs.
  • These findings highlight fibronectin's indispensable role in the development of complex organ architectures.