Much is known about the biophysical mechanisms involved in cell crawling, but how
these processes are coordinated to produce directed motion is not well understood.
Here, we propose a new hypothesis whereby local cytoskeletal contraction generates
fluid flow through the lamellipodium, with the pressure at the front of the cell
facilitating actin polymerization which pushes the leading edge forward. The
contraction, in turn, is regulated by stress in the cytoskeleton. To test this
hypothesis, finite element models for a crawling cell are presented. These models are
based on nonlinear poroelasticity theory, modified to include the effects of active
contraction and growth, which are regulated by mechanical feedback laws. Results
from the models agree reasonably well with published experimental data for cell
speed, actin flow, and cytoskeletal deformation in migrating fish epidermal
keratocytes. The models also suggest that oscillations can occur for certain ranges of
parameter values.