Deconstructing the role of myosin contractility in force fluctuations within focal adhesions

TL;DR

This study investigates how myosin motor contractility influences force fluctuations in focal adhesions, revealing a transition from decaying to sustained oscillations through a supercritical Hopf bifurcation, supported by analytical and simulation results.

Contribution

It provides a detailed dynamical model linking myosin activity to force oscillations in focal adhesions, highlighting the role of motor contractility in cellular force regulation.

Findings

Lowering myosin contractility induces oscillatory force behavior.

The system transitions from decaying to limit cycle oscillations via a Hopf bifurcation.

Model predictions align with experimental frequency ranges.

Abstract

Force fluctuations exhibited in focal adhesions (FAs) that connect a cell to its extracellular environment, point to the complex role of the underlying machinery that controls cell migration. To elucidate the explicit role of myosin motors in the temporal traction force oscillations, we vary the contractility of these motors in a dynamical model based on the molecular clutch hypothesis. As the contractility is lowered, effected both by changing the motor velocity and the rate of attachment/detachment, we show analytically in an experimentally relevant parameter space that the system goes from decaying oscillations to stable limit cycle oscillations through a supercritical Hopf bifurcation. As a function of motor activity and the number of clutches, the system exhibits a wide array of dynamical states. We corroborate our analytical results with stochastic simulations of the motor-clutch system. We obtain limit cycle oscillations in the parameter regime as predicted by our model. The frequency range of oscillations in the average clutch and motor deformation compares well with experimental results.