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Updated: May 29, 2025

Analyses of Actin Dynamics, Clutch Coupling and Traction Force for Growth Cone Advance
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N-Cadherin based adhesion and Rac1 activity regulate tension polarization in the actin cortex.

Seyedsajad Moazzeni1,2, Kelly Kyker-Snowman2, Rick I Cohen2

  • 1Department of Mechanical & Aerospace Engineering, Rutgers, The State University of New Jersey, 98 Brett Rd, Piscataway, NJ, 08854, USA.

Scientific Reports
|February 5, 2025
PubMed
Summary

N-cadherin drives tension polarization in cells by regulating external and internal interface tensions. Rac1 acts as a switch, controlling actin-myosin contractility for tissue remodeling and cancer progression.

Keywords:
Cadherin-based cell adhesionCortical tensionMechanobiologyMechanotransductionMulticellular organizationTension polarization

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Area of Science:

  • Cell biology
  • Biophysics
  • Developmental biology

Background:

  • Tension-adhesion interplay is vital for multicellular organization, influencing tissue surface tension, cell sorting, and morphogenesis.
  • Cadherins are implicated in this process, but their precise roles and quantitative contributions remain unclear.
  • Understanding these mechanisms is crucial for fields ranging from developmental biology to cancer research.

Purpose of the Study:

  • To elucidate the role of N-cadherin in tension polarization within the actin cortical network.
  • To quantify the effects of N-cadherin density and cell-cell interfaces on tension differentials.
  • To identify the molecular mediators, such as Rac1, linking cadherins to actin-myosin contractility.

Main Methods:

  • Investigated tension polarization using biophysical techniques to measure forces at cell interfaces.
  • Manipulated N-cadherin surface density and cell cluster size to assess their impact on tension.
  • Utilized pharmacological inhibition of Rac1 to determine its role in the cadherin-actin contractility pathway.

Main Results:

  • N-cadherin critically drives tension polarization, increasing tension at the cell-medium interface and decreasing it at the cell-cell interface.
  • The magnitude of tension regulation is directly dependent on N-cadherin surface density.
  • Tension polarization strength correlates with the number of cell-cell interfaces in multicellular clusters.
  • Rac1 activation is essential for cadherin-mediated cortex remodeling and contractility via myosin II.
  • Rac1 inhibition disrupts tension polarization and coherence in cell clusters and spheroids.

Conclusions:

  • N-cadherin acts as a key regulator of tension polarization, with its effects quantitatively dependent on surface density and cellular context.
  • The Rac1-myosin II pathway mediates the link between cadherins and actin cortex remodeling, crucial for tissue mechanics.
  • These findings offer a unified perspective on tissue surface tension generation and present potential therapeutic targets for cancer treatment.