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  11. Cadherin Adhesion Complexes Direct Cell Aggregation In The Epithelial Transition Of Wnt-induced Nephron Progenitor Cells

Cadherin adhesion complexes direct cell aggregation in the epithelial transition of Wnt-induced nephron progenitor cells

Balint Der1,2,3, Helena Bugacov1,4, Bohdana-Myroslava Briantseva1

  • 1Department of Stem Cell Biology and Regenerative Medicine, Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research, Keck School of Medicine, University of Southern California, Los Angeles 90033, USA.

Development (Cambridge, England)
|September 30, 2024

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View abstract on PubMed

Summary
This summary is machine-generated.

Beta-catenin (Ctnnb1) links Wnt signaling to cell aggregation during kidney development. This process, crucial for nephrogenesis, involves cadherin-mediated cell adhesion and is essential for mesenchymal-to-epithelial transition in nephron progenitor cells.

Area of Science:

  • Developmental Biology
  • Cell Biology
  • Renal Physiology

Background:

  • Nephron formation in mammalian kidney development is initiated by nephron progenitor cells (NPCs).
  • Wnt signaling activates a β-catenin (Ctnnb1)-driven transcriptional program and mesenchymal-to-epithelial transition (MET) in NPCs.

Purpose of the Study:

  • To investigate the role of β-catenin in NPC aggregation and MET during kidney development.
  • To elucidate the molecular mechanisms underlying Wnt-induced NPC aggregation and its dependence on cell adhesion molecules.

Main Methods:

  • Utilized an in vitro mouse NPC culture model.
  • Employed genetic manipulation (gene removal) to assess the function of β-catenin, cadherins, and catenins.
  • Modulated extracellular calcium levels to study cell-cell contact dynamics.
Keywords:
Cadherin cell adhesionInductionKidneyNephron progenitor

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  • Performed molecular analyses to identify cadherin expression and β-catenin-mediated transcriptional changes.

    • Main Results:

    • Wnt pathway activation induced NPC aggregation, a key step in MET, dependent on β-catenin.
    • NPC aggregation was Ca2+-dependent, implicating cadherin-mediated cell adhesion.
    • β-catenin upregulated cadherin 3 (Cdh3) and cadherin 4 (Cdh4) during NPC MET.
    • Genetic removal of cadherins or disruption of α-catenin interactions abolished aggregation but not Wnt pathway induction.

    Conclusions:

    • β-catenin is a critical mediator linking Wnt-driven transcriptional programs to NPC morphogenesis.
    • Cadherin-mediated cell adhesion, regulated by β-catenin, is essential for NPC aggregation during kidney development.
    • These findings clarify the molecular basis of nephrogenesis and offer insights into developmental kidney diseases.
    Renal vesicle
    Wnt
    β-Catenin