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E-cadherin-mediated cell-cell attachment activates Cdc42.

S H Kim1, Z Li, D B Sacks

  • 1Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.

The Journal of Biological Chemistry
|August 22, 2000
PubMed
Summary
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E-cadherin initiates cell-cell adhesion and activates Cdc42 (a Rho family GTPase), demonstrating a bi-directional signaling pathway. This interaction is specific to E-cadherin-mediated adhesion in epithelial cells.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • E-cadherin mediates calcium-dependent cell-cell adhesion.
  • Cdc42, a Rho family GTPase, regulates cytoskeleton and cell cycle.
  • Rho family proteins are known to modulate E-cadherin function.

Purpose of the Study:

  • To investigate the role of Cdc42 in E-cadherin-mediated cell-cell adhesion.
  • To elucidate the interaction between E-cadherin and Cdc42 signaling pathways.

Main Methods:

  • Developed an assay for active Cdc42 using the GTPase-binding domain of Wiskott-Aldrich syndrome protein.
  • Measured Cdc42 activity in MCF-7 epithelial cells during E-cadherin-mediated adhesion.
  • Utilized green fluorescent protein-tagged Wiskott-Aldrich syndrome protein/GTPase-binding domain to visualize endogenous Cdc42 activation in live cells.

Related Experiment Videos

Main Results:

  • E-cadherin-mediated cell-cell attachment significantly increased active Cdc42 levels in MCF-7 cells over time.
  • Cdc42 activity remained unchanged in MCF-7 cells treated with anti-E-cadherin antibodies.
  • No increase in Cdc42 activity was observed in E-cadherin-negative MDA-MB-231 cells.
  • Live-cell imaging confirmed E-cadherin-induced activation of endogenous Cdc42.

Conclusions:

  • E-cadherin directly activates Cdc42.
  • Demonstrated bi-directional signaling interactions between Rho and E-cadherin pathways.
  • Highlights the specific role of E-cadherin in regulating Cdc42 activity during cell adhesion.