Contribution of myosin II activity to cell spreading dynamics.
Myosin II activity and actin polymerization at the leading edge of the cell are known to be essential sources of cellular stress. However, a quantitative account of their separate contributions is still lacking; so is the influence of the coupling between the two phenomena on cell spreading dynamics. We present a simple analytic elastic theory of cell spreading dynamics that quantitatively demonstrates how actin polymerization and myosin activity cooperate in the generation of cellular stress during spreading. Consistent with experiments, myosin activity is assumed to polarize in response to the stresses generated during spreading. The characteristic response time and the overall spreading time are predicted to determine different evolution profiles of cell spreading dynamics. These include, a (regular) monotonic increase of cell projected area with time, a non-monotonic (overshooting) profile with a maximum, and damped oscillatory modes. In addition, two populations of myosin II motors are distinguished based on their location in the lamella; those located above the major adhesion zone at the cell periphery are shown to facilitate spreading whereas those in deeper regions of the lamella are shown to oppose spreading. We demonstrate that the attenuation of myosin activity in the two regions may result in reciprocal effects on spreading. These findings provide important new insight into the function of myosin II motors in the course of spreading.
Institute of Dental Sciences and Fritz Haber Center for Molecular Dynamics, Hebrew University of Jerusalem, 91120, Israel. Assaf.Zemel@ekmd.huji.ac.il.
Noam
N
Nisenholz
Aishwarya
A
Paknikar
Sarah
S
Köster
Assaf
A
Zemel
D001696:Biomechanical Phenomena; D002448:Cell Adhesion; D002465:Cell Movement; D008954:Models, Biological; D024462:Myosin Type II / Q000378:metabolism*
D024462:Myosin Type II