Key result
Dynamical model shows varying myosin contractility drives stable limit cycle oscillations via a Hopf bifurcation.
Why the study?
Force fluctuations in focal adhesions suggest complex control of cell migration, but the explicit role of myosin motors in temporal traction force oscillations remains to be elucidated.
A dynamical model demonstrates that lowering myosin contractility transitions the motor-clutch system from decaying to stable limit cycle oscillations via a supercritical Hopf bifurcation.
Model suggests myosin tunes cellular oscillations; leaves open translation to cardiac mechanobiology in vivo.
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.
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Ghosh et al. (2020) studied this question. A dynamical model based on the molecular clutch hypothesis shows that varying myosin motor contractility drives the system from decaying to stable limit cycle oscillations via a Hopf bifurcation.
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