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Updated: Jan 1, 2026

Measuring Cell-Edge Protrusion Dynamics during Spreading using Live-Cell Microscopy
Published on: November 1, 2021
Actin protrusions push at apical junctions to maintain E-cadherin adhesion.
John Xiao He Li1, Vivian W Tang1, William M Brieher2
1Department of Cell and Developmental Biology, University of Illinois at Urbana-Champaign, Urbana, IL 61801.
Actin microspikes continuously push on cell junctions, maintaining epithelial cell adhesion. This protrusive activity prevents myosin II from disrupting cadherin bonds, ensuring cell sheet integrity.
Area of Science:
- Cell biology
- Biophysics
Background:
- Cadherin-mediated cell-cell adhesion is crucial for tissue integrity.
- The exact role of actin in maintaining established cell-cell adhesion is not fully understood.
Purpose of the Study:
- To investigate the role of actin protrusive activity in maintaining cell-cell adhesion in confluent epithelial sheets.
- To identify the molecular mechanisms underlying actin's role in cadherin adhesion.
Main Methods:
- Live cell imaging of Madin-Darby canine kidney (MDCK) cells.
- Electron microscopy.
- RNA interference (RNAi) to deplete actin assembly factors.
- Myosin II activity assays.
Main Results:
- Actin microspikes containing E-cadherin were observed at apical junctions of MDCK cells.
- Microspike activity correlated with the formation and maintenance of cadherin clusters.
- Depletion of Arp2/3, EVL, and CRMP-1 led to myosin II-dependent unzipping of cadherin bonds.
Conclusions:
- Actin polymerization-dependent protrusive activity is essential for maintaining cadherin-mediated cell-cell adhesion in epithelial sheets.
- This activity counteracts myosin II-dependent contractility, preventing the disruption of cell junctions.
- Arp2/3, EVL, and CRMP-1 are critical for the actin-based protrusive forces that stabilize cell adhesion.
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