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Vinculin-dependent Cadherin mechanosensing regulates efficient epithelial barrier formation
Floor Twiss1, Quint Le Duc, Suzanne Van Der Horst
1Hubrecht Institute for Developmental Biology and Stem Cell Research and University Medical Centre Utrecht , PO Box 85164, 3508 AD Utrecht , The Netherlands.
Biology Open
|December 6, 2012
Summary
Epithelial barrier formation relies on E-cadherin junctions linking to the actomyosin cytoskeleton. Specialized Focal Adherens Junctions (FAJs) with Vinculin drive rapid barrier establishment by sensing mechanical cues.
Area of Science:
- Cell Biology
- Biophysics
- Developmental Biology
Background:
- Epithelial cell-cell adhesion is vital for embryonic development and tissue repair.
- Proper formation and stabilization of these adhesions are critical for epithelial barrier function.
- Cellular processes integrate chemical and mechanical signals to regulate adhesion.
Purpose of the Study:
- Investigate the role of the actomyosin cytoskeleton in epithelial barrier formation.
- Elucidate the connection between cell-junction complexes and the actomyosin cytoskeleton.
- Determine the function of Focal Adherens Junctions (FAJs) in epithelial barrier establishment.
Main Methods:
- Utilized Madin-Darby Canine Kidney (MDCK) cells to model epithelial barrier formation.
- Examined the E-cadherin complex's interaction with the actomyosin cytoskeleton.
- Assessed the role of α-catenin and Vinculin in junctional complex dynamics.
- Measured Trans Epithelial Electrical Resistance (TER) to quantify barrier integrity.
- Perturbed actomyosin contraction and Vinculin recruitment to assess effects on barrier formation.
Main Results:
- The E-cadherin complex functionally links cell-cell contacts to the actomyosin cytoskeleton.
- Tensile, punctate cell-cell junctions, termed Focal Adherens Junctions (FAJs), recruit Vinculin and connect to F-actin bundles.
- FAJs are transient structures present during rapid barrier establishment and disappear as adhesions mature.
- Blocking actomyosin contraction or Vinculin recruitment delays barrier formation.
- Increased Vinculin presence accelerates barrier formation.
Conclusions:
- E-cadherin-based FAJs connect nascent cell-cell adhesions to the contractile actomyosin cytoskeleton.
- FAJs act as sites of E-cadherin mechanosensing.
- Vinculin recruitment to FAJs is a key driver of epithelial barrier formation.
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