Abstract
Although many of the regulators of actin assembly are known, we do not understand how these components act together to organize cell shape and movement. To address this question, we analyzed the spatial dynamics of a key actin regulator–the Scar/WAVE complex–which plays an important role in regulating cell shape in both metazoans and plants. We have recently discovered that the Hem‐1/Nap1 component of the Scar/WAVE complex localizes to propagating waves that appear to organize the leading edge of a motile immune cell, the human neutrophil. Actin is both an output and input to the Scar/WAVE complex: the complex stimulates actin assembly, and actin polymer is also required to remove the complex from the membrane. These reciprocal interactions appear to generate propagated waves of actin nucleation that exhibit many of the properties of morphogenesis in motile cells, such as the ability of cells to flow around barriers and the intricate spatial organization of protrusion at the leading edge. We propose that cell motility results from the collective behavior of multiple self‐organizing waves.
Highlights
Rac and its downstream effector Scar/WAVE are central regulators of cell shape and movement [1,2,3,4]
The Hem-1 component of the leukocyte WAVE2 complex is required for actin polymerization and proper leading edge morphology in neutrophils [6], and its homologues play important roles in regulating cell shape or movement for Dictyostelium [7], plants [8], worms [9], insects [10,11,12], and mammals [1,13,14]
We show here that the leading edge of neutrophils contains moving waves of Hem-1, whose collective behavior corresponds to the morphology of the leading edge
Summary
Rac and its downstream effector Scar/WAVE are central regulators of cell shape and movement [1,2,3,4]. We show here that the leading edge of neutrophils contains moving waves of Hem-1 (including complexes which contain WAVE2), whose collective behavior corresponds to the morphology of the leading edge. These waves are not formed by lateral movement of individual proteins but, like action potentials, are the result of propagated cycles of activation and inhibition. These waves reveal a far more complex and dynamic interaction between inducers of actin nucleation and the cytoskeleton than is represented in current models of cell motility
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