Active elastic dimers: Cells moving on rigid tracks

TL;DR

This paper presents a minimal one-dimensional model of cell migration on rigid tracks, highlighting the roles of active stress fibers, integrin catch/slip bonds, and alpha-actinin, providing insights into cell motility mechanisms without needing actin nucleation.

Contribution

It introduces a simplified active elastic dimer model that captures key features of cell migration, emphasizing the importance of bond behavior and contractility in movement.

Findings

Model reproduces realistic cell speeds with estimated parameters.

Hysteresis and active noise influence cell motility dynamics.

Alpha-actinin plays a crucial role in three-dimensional cell movement.

Abstract

Experiments suggest that the migration of some cells in the three-dimensional extra cellular matrix bears strong resemblance to one-dimensional cell migration. Motivated by this observation, we construct and study a minimal one-dimensional model cell made of two beads and an active spring moving along a rigid track. The active spring models the stress fibers with their myosin-driven contractility and alpha-actinin-driven extendability, while the friction coefficients of the two beads describe the catch/slip bond behavior of the integrins in focal adhesions. In the absence of active noise, net motion arises from an interplay between active contractility (and passive extendability) of the stress fibers and an asymmetry between the front and back of the cell due to catch bond behavior of integrins at the front of the cell and slip bond behavior of integrins at the back. We obtain reasonable cell speeds with independently estimated parameters. We also study the effects of hysteresis in the active spring, due to catch bond behavior and the dynamics of cross-linking, and the addition of active noise on the motion of the cell. Our model highlights the role of alpha-actinin in three-dimensional cell motility and does not require Arp2/3 actin filament nucleation for net motion.