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Cellular contractility changes are sufficient to drive epithelial scattering.

Jacob P Hoj1, John A Davis1, Kendra E Fullmer1

  • 1Physiology and Developmental Biology Brigham Young University, 574 WIDB Provo, UT 84602, USA.

Experimental Cell Research
|May 1, 2014
PubMed
Summary
This summary is machine-generated.

Epithelial scattering, crucial for development and invasion, involves cell detachment. This study reveals that increased cell-substrate adhesion and myosin-based contractility, rather than altered cell-cell adhesion, drive this process during epithelial-mesenchymal transitions.

Keywords:
AdhesionContractilityCytoskeletonEpithelial mesenchymal transitionEpithelial scatteringMyosin

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Area of Science:

  • Cell Biology
  • Developmental Biology
  • Biophysics

Background:

  • Epithelial scattering allows individual cells to detach and migrate, a process vital for development and epithelial-mesenchymal transitions (EMT).
  • The precise mechanisms driving cell-cell junction detachment during scattering, whether through adhesion remodeling or altered traction forces, remain debated.
  • Understanding these mechanisms is key to comprehending cell migration and invasion in biological processes.

Purpose of the Study:

  • To investigate the roles of cell-cell adhesion, cell-substrate adhesion, and contractility in hepatocyte growth factor (HGF)/scatter factor-induced epithelial scattering.
  • To elucidate how RhoA signaling and myosin contractility contribute to the detachment of epithelial cells during EMT.

Main Methods:

  • Assessing cell-cell adhesion strength in suspension.
  • Quantifying cell-substrate adhesions and focal adhesions in HGF-treated cells.
  • Manipulating substrate pliability and RhoA activity (using mutants and inhibitors like blebbistatin).
  • Measuring cell scattering, migration, and contractility.

Main Results:

  • HGF treatment did not alter cell-cell adhesion strength in suspended cells.
  • HGF treatment increased cell-substrate adhesion and focal adhesions, correlating with scattering.
  • Altering substrate pliability affected cell scattering ability.
  • RhoA activity and myosin II contractility were essential for HGF-induced scattering; restoring contractility could induce scattering independently of migration changes.

Conclusions:

  • Epithelial scattering during HGF-induced EMT is primarily driven by increased cell-substrate adhesion and RhoA-dependent myosin contractility, not by changes in cell-cell adhesion strength.
  • Myosin-based contractility appears sufficient to induce cell-cell detachment, highlighting its critical role in scattering.
  • These findings offer new insights into the biophysical mechanisms governing cell detachment and collective cell migration.