Fig. 1. The steady-state and stimulated protrusion models. (A) In the steady-state model [based on Pollard et al. (Pollard et al., 2000)], cofilin functions only as a G-actin-recycling factor, depolymerizing filaments to G-actin at the base of the lamellipodium to sustain steady-state actin polymerization at the leading edge when G-actin is limiting (e.g. in continuously moving cells such as keratocytes). Dendritic nucleation at the leading edge occurs from the Arp2/3 complex at the interface with the cell membrane. (B) The stimulated protrusion model applies to situations when motility is not continuous and G-actin is not limiting. In this case, initiation of movement involves the localized activation of cofilin at the leading edge. Severing of actin filaments in the quiescent cortical cytoskeleton by cofilin creates free barbed ends that define the site of activation of the Arp2/3 complex. Polymerization of actin occurs from a pool of pre-existing G-actin and is not tightly coupled to depolymerization.