This is a model for molecular mechanisms contolling actin filament dynamics in nonmuscle cells (Fig. CM11B).
There are 10 steps in the figure. In the first step all the ATP-actin monomers are bound to profilin, there are no free barbed ends; the actin cytoskeletal components are held in a metastable state, poised for assembly. Activation of WASp family proteins (Step 2) leads to activation of the Arp2/3 complex and this creates new barbed ends and subsequently new filaments (Step 3). These filaments grow rapidly (Step 4) and push the membrane forward (Step 5). After a short while, growth of the barbed ends is terminated by capping (Step 6). ATP hydrolysis and Pi dissociation (Step 7) triggers severing and depolymerization of actin filaments by ADF/cofilins (Step 8). LIM kinase inhibits ADF/cofilins (Step 9). Nucleotide exchange catalyzed by profilin recycles ADP-actin to ATP-actin monomer in the pool (Step 10).
Accordingly, the molecular mechanism of motion in nonmuscle cells is a very complex cycle that converts the energy of the hydrolysis of actin-bound ATP into mechanical force through the polymerization and depolymerization of actin filaments ( treadmilling of actin filaments). In a continuously moving cell, assembly and dysassembly of actin filaments are balanced.
Reviews of Pollard et al. (2000), Higgs and Pollard (2001), and Pantaloni et al. (2001) are recommended for a further understanding of the molecular mechanism of motion in nonmuscle cells.
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