Molecular Mechanisms Regulating Actin Filament Dynamics at the Leading Edge of Motile Cells

Pollard, Thomas D.

doi:10.1002/0470011742.ch1

Cited by 1 publication

(2 citation statements)

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“…The characteristic velocities of this movement determined with respect to the leading edge membrane vary for different cell types between few hundreds of nanometers to several microns per minute (7,13). Branched actin filaments in the lamellipodium are nucleated by the Arp2/3 complex and their polymerization is regulated by a bunch of accessory proteins (14,15). It has been established that polymerization of the lamellipodium actin generates a mechanical force pushing the leading edge membrane forward (3,4,16,17).…”

Section: Lamellipodium-lamellum Interfacementioning

confidence: 99%

“…The gel undergoes polymerization against the membrane, which generates a force pushing the gel from the membrane toward the cell center and resulting in the retrograde actin movement. Although, in general, the cell leading edge may crawl with respect to the substrate, we assume in the main analysis that the rate of this crawling is much smaller than that of the retrograde movement of the actin gel, which is true for most cells, except, perhaps, for keratocytes (15,33). Hence, we neglect the leading edge movement, and take the velocity of the actin retrograde flow to be v retro ¼ 5mm=min (13).…”

Section: Model Actin Gel and Focal Adhesionsmentioning

confidence: 99%

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Role of Focal Adhesions and Mechanical Stresses in the Formation and Progression of the Lamellum Interface

Shemesh

Verkhovsky

Svitkina

et al. 2009

Biophysical Journal

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Actin network in the front part of a moving cell is organized into a lamellipodium and a lamellum. A distinct lamellipodium-lamellum interface is associated with focal adhesions and consists of a series of arclike segments linking neighboring focal adhesions in the front row. The interface advances by leaping onto new rows of focal adhesions maturating underneath the lamellipodium. We propose a mechanism of the lamellipodium-lamellum boundary generation, shape formation, and progression based on the elastic stresses generated in the lamellipodial actin gel by its friction against the focal adhesions. The crucial assumption of the model is that stretching stresses trigger actin gel disintegration. We compute the stress distribution throughout the actin gel and show that the gel-disintegrating stresses drive formation of a gel boundary passing through the row of focal adhesions. Our computations recover the lamellipodium-lamellum boundary shapes detected in cells and predict the mode of the boundary transition to the row of the newly maturing focal adhesions in agreement with the experimental observations. The model fully accounts for the current phenomenology of the lamellipodium-lamellum interface formation and advancing, and makes experimentally testable predictions on the dependence of these phenomena on the sizes of the focal adhesions, the character of the focal adhesion distribution on the substrate, and the velocity of the actin retrograde flow with respect to the focal adhesions. The phase diagram resulting from the model provides a background for quantitative classification of different cell types with respect to their ability to form a lamellipodium-lamellum interface. In addition, the model suggests a mechanism of nucleation of the dorsal and arclike actin bundles found in the lamellum.

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