  Cell crawling on flat substrates is based on intracellular flows of the actin
cytoskeleton that are driven by both actin polymerization at the front and
myosin contractility at the back. The new experimental tool of optogenetics
makes it possible to spatially control contraction and thereby possibly also
cell migration. Here we analyze this situation theoretically using a
one-dimensional active gel model in which the excluded volume interactions of
myosin and their aggregation into minifilaments is modeled by a supercritical
van der Waals fluid. This physically simple and transparent, but nonlinear and
thermodynamically rigorous model predicts bistability between sessile and
motile solutions. We then show that one can switch between these two states at
realistic parameter ranges via optogenetic activation or inhibition of
contractility, in agreement with recent experiments. We also predict the
required activation strengths and initiation times.
