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Multifaceted control of E-cadherin dynamics by Adaptor Protein Complex 1 during epithelial morphogenesis.

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Adaptor Protein 1 (AP-1) complex regulates cell adhesion and tissue shape. AP-1 knockdown causes E-cadherin loss, leading to cell death and preventing tissue overgrowth.

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Area of Science:

  • Cell Biology
  • Developmental Biology
  • Molecular Biology

Background:

  • Intracellular trafficking is crucial for distributing transmembrane proteins that control epithelial polarity and adhesion.
  • The Adaptor Protein 1 (AP-1) complex is a key regulator of vesicle sorting and cargo binding.

Purpose of the Study:

  • To investigate the role of the AP-1 complex in epithelial morphogenesis using the Drosophila wing model.
  • To understand how AP-1 influences cell adhesion, polarity, and tissue development.

Main Methods:

  • AP-1 complex knockdown in Drosophila wings.
  • Analysis of integrin targeting to basal adhesion sites.
  • Assessment of cell proliferation and cell death.
  • Investigation of E-cadherin localization and internalization.
  • Examination of E-cadherin expression levels.

Main Results:

  • AP-1 knockdown induced ectopic tissue folding and defects in integrin targeting.
  • Loss of AP-1 led to integrin-independent cell death, balancing increased proliferation and preventing hyperplasia.
  • A distinct AP-1 pool at adherens junctions was identified.
  • AP-1 knockdown caused E-cadherin hyperinternalization from adherens junctions, with enrichment at the Golgi and recycling endosomes.
  • E-cadherin hyperinternalization preceded cell death, suggesting a tumor-suppressive role.
  • Cells upregulated E-cadherin expression to compensate for increased internalization and maintain adhesion.

Conclusions:

  • The AP-1 complex plays a critical role in maintaining epithelial integrity and tissue morphogenesis.
  • AP-1 regulates E-cadherin trafficking and localization at adherens junctions.
  • E-cadherin hyperinternalization, triggered by AP-1 loss, acts as a tumor-suppressive mechanism by inducing cell death.
  • Cellular compensation mechanisms, like increased E-cadherin expression, attempt to preserve cell-cell adhesion.