Mechanical stress as a regulator of cell motility

TL;DR

This paper presents a one-dimensional model showing how mechanical stresses like stretching and squeezing influence cell motility, polarization, and integrity, with implications for contact inhibition and epithelial transition.

Contribution

It introduces a transparent analytical model linking applied stress to cell motility states, highlighting the roles of internal activity and external stress in cell behavior.

Findings

Stretching can initiate cell motility and polarization.

Squeezing can arrest motility and cause cell collapse.

A phase diagram maps static, motile, and collapsed states.

Abstract

The motility of a cell can be triggered or inhibited not only by an applied force but also by a mechanically neutral force couple. This type of loading, represented by an applied stress and commonly interpreted as either squeezing or stretching, can originate from extrinsic interaction of a cell with its neighbors. To quantify the effect of applied stresses on cell motility we use an analytically transparent one-dimensional model accounting for active myosin contraction and induced actin turnover. We show that stretching can polarize static cells and initiate cell motility while squeezing can symmetrize and arrest moving cells. We show further that sufficiently strong squeezing can lead to the loss of cell integrity. The overall behavior of the system depends on the two dimensionless parameters characterizing internal driving (chemical activity) and external loading (applied stress). We construct a phase diagram in this parameter space distinguishing between, static, motile and collapsed states. The obtained results are relevant for the mechanical understanding of contact inhibition and the epithelial-to-mesenchymal transition.