Mechanics and polarity in cell motility

TL;DR

This paper presents a minimal mathematical model explaining how actin dynamics and mechanical factors lead to bistable motility behavior in fish keratocytes, predicting cell shape, length, and velocity.

Contribution

It introduces a simplified model highlighting the mechanical and actin dynamics responsible for cell motility bistability, emphasizing actin phase exchange at cell edges.

Findings

Actin dynamics and active stress suffice to explain motile bistability.

Model predicts cell length and velocity based on substrate and cell parameters.

Mechanical perturbations can switch cell motility states.

Abstract

The motility of a fish keratocyte on a flat substrate exhibits two distinct regimes: the non-migrating and the migrating one. In both configurations the shape is fixed in time and, when the cell is moving, the velocity is constant in magnitude and direction. Transition from a stable configuration to the other one can be produced by a mechanical or chemotactic perturbation. In order to point out the mechanical nature of such a bistable behaviour, we focus on the actin dynamics inside the cell using a minimal mathematical model. While the protein diffusion, recruitment and segregation govern the polarization process, we show that the free actin mass balance, driven by diffusion, and the polymerized actin retrograde flow, regulated by the active stress, are sufficient ingredients to account for the motile bistability. The length and velocity of the cell are predicted on the basis of the parameters of the substrate and of the cell itself. The key physical ingredient of the theory is the exchange among actin phases at the edges of the cell, that plays a central role both in kinematics and in dynamics.