Active gel model for one-dimensional cell migration coupling actin flow and adhesion dynamics

TL;DR

This paper presents a minimal active gel model that integrates actin flow and adhesion dynamics to explain one-dimensional cell migration, including symmetry breaking and bistability phenomena.

Contribution

It combines actin flow and adhesion receptor dynamics into a unified active gel model, revealing mechanisms for cell polarization and migration bistability.

Findings

Load sharing causes symmetry breaking with stronger front adhesion.

Bistability occurs at intermediate adhesion levels.

Local adhesion variations can switch cells between stationary and migrating states.

Abstract

Migration of animal cells is based on the interplay between actin polymerization at the front, adhesion along the cell-substrate interface, and actomyosin contractility at the back. Active gel theory has been used before to demonstrate that actomyosin contractility is sufficient for polarization and self-sustained cell migration in the absence of external cues, but did not consider the dynamics of adhesion. Likewise, migration models based on the mechanosensitive dynamics of adhesion receptors usually do not include the global dynamics of intracellular flow. Here we show that both aspects can be combined in a minimal active gel model for one-dimensional cell migration with dynamic adhesion. This model demonstrates that load sharing between the adhesion receptors leads to symmetry breaking, with stronger adhesion at the front, and that bistability of migration arises for intermediate adhesiveness. Local variations in adhesiveness are sufficient to switch between sessile and motile states, in qualitative agreement with experiments.