Actin machinery in vivo typically becomes polarized in response to external cues that trigger directional movement. In the absence of such signals, however, achieving polarization requires breaking part of the actin network. Such is the case for isolated cells at rest or for van der Gucht's experimental system, in which beads coated with actin polymerization proteins are mixed with actin monomers, ATP, and other proteins.During symmetry breaking, a fracture appeared at the outer actin rim, which then grew inward and expanded to open up a hole within the network. Once the hole was wide enough, the bead escaped through it and was pushed forward by a trailing actin comet.
Using physical models of gel fracturing dating back to 1920, Sykes' group determined that this spontaneous symmetry breaking is caused by the release of elastic stress. Growth of the polymerized and cross-linked actin network moves the network outwards, leading to the greatest tensile stress and stretching at the outer gel surface. Once the stretching stress exceeds the strength of the actin network, a fracture forms and releases stored elastic energy, thereby leading to actin network polarization. As van der Gucht says, “Any elastic material under stress will eventually break.”