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Updated: Dec 30, 2025

De Novo Generation of Somatic Stem Cells by YAP/TAZ
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DLC1 is a direct target of activated YAP/TAZ that drives collective migration and sprouting angiogenesis

Miesje van der Stoel1, Lilian Schimmel2, Kalim Nawaz2

  • 1Amsterdam UMC, University of Amsterdam, location AMC, Department of Medical Biochemistry, Amsterdam Cardiovascular Sciences, 1105 AZ Amsterdam, The Netherlands.

Journal of Cell Science
|January 23, 2020
PubMed

Insights

This study identifies deleted-in-liver-cancer 1 (DLC1) as a key regulator in endothelial YAP/TAZ signaling, crucial for blood vessel formation (angiogenesis) and vascular homeostasis.

Area of Science:

  • Vascular biology
  • Cell signaling
  • Molecular mechanisms

Background:

  • Endothelial YAP/TAZ signaling is vital for angiogenesis and vascular homeostasis.
  • The precise molecular mechanisms by which YAP/TAZ regulate the vasculature are not fully understood.

Purpose of the Study:

  • To elucidate the molecular mechanisms of YAP/TAZ in endothelial cells.
  • To identify direct targets of YAP/TAZ-TEAD complexes in angiogenesis.

Main Methods:

  • Investigated the role of deleted-in-liver-cancer 1 (DLC1) as a YAP/TAZ transcriptional target.
  • Utilized substrate stiffening and VEGF stimulation to modulate DLC1 expression.
  • Examined the impact of DLC1 depletion and ectopic expression on endothelial cell behavior.

Main Results:

  • DLC1 is a direct transcriptional target of YAP/TAZ-TEAD, induced by substrate stiffness and VEGF.
  • DLC1 limits F-actin, focal adhesion lifetime, and traction forces in endothelial cells.
  • Endothelial DLC1 depletion impairs cell polarization and angiogenic sprouting; its ectopic expression rescues these defects in YAP-depleted cells.

Conclusions:

  • DLC1 plays a critical role in YAP/TAZ-mediated endothelial adhesion remodeling.
  • DLC1 is essential for collective cell migration and angiogenic sprouting.
  • DLC1 represents a key downstream effector of YAP/TAZ signaling in angiogenesis.
Keywords:
AdhesionAngiogenesisEndotheliumIntegrinMechanotransductionYAP

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