Optogenetic control of intracellular flows and cell migration: a comprehensive mathematical analysis with a minimal active gel model

TL;DR

This paper presents a mathematical model analyzing how optogenetic control of actomyosin contraction influences cell migration, revealing conditions under which contraction can initiate, enhance, or arrest cell motility.

Contribution

It introduces a minimal active gel model incorporating optogenetic activation, elucidating how contraction affects cell movement and polarization.

Findings

Optogenetic activation of contraction can initiate cell locomotion.

Contraction can enhance motility in polymerizing cells.

Properly designed activation can arrest cell movement.

Abstract

The actin cytoskeleton of cells is in continuous motion due to both polymerization of new filaments and their contraction by myosin II molecular motors. Through adhesion to the substrate, such intracellular flow can be converted into cell migration. Recently, optogenetics has emerged as a new powerful experimental method to control both actin polymerization and myosin II contraction. While optogenetic control of polymerization can initiate cell migration by generating protrusion, it is less clear if and how optogenetic control of contraction can also affect cell migration. Here we analyze the latter situation using a minimal variant of active gel theory into which we include optogenetic activation as a spatiotemporally constrained perturbation. The model can describe the symmetrical flow of the actomyosin system observed in optogenetic experiments, but not the long-lasting polarization required for cell migration. Motile solutions become possible if cytoskeletal polymerization is included through the boundary conditions. Optogenetic activation of contraction can then initiate locomotion in a symmetrically spreading cell and strengthen motility in an asymmetrically polymerizing one. If designed appropriately, it can also arrest motility even for protrusive boundaries.