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Journal ArticleDOI

Two distinct actin networks drive the protrusion of migrating cells

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TLDR
Computational analysis of fluorescent speckle microscopy movies of migrating epithelial cells revealed this process is mediated by two spatially colocalized but kinematically, kinetically, molecularly, and functionally distinct actin networks.
Abstract
Cell migration initiates by extension of the actin cytoskeleton at the leading edge. Computational analysis of fluorescent speckle microscopy movies of migrating epithelial cells revealed this process is mediated by two spatially colocalized but kinematically, kinetically, molecularly, and functionally distinct actin networks. A lamellipodium network assembled at the leading edge but completely disassembled within 1 to 3 micrometers. It was weakly coupled to the rest of the cytoskeleton and promoted the random protrusion and retraction of the leading edge. Productive cell advance was a function of the second colocalized network, the lamella, where actomyosin contraction was integrated with substrate adhesion.

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Citations
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Journal ArticleDOI

Myo1c facilitates G-actin transport to the leading edge of migrating endothelial cells

TL;DR: Myo1c directly interacts with G-actin and is important for its transport to the leading edge during endothelial cell migration.
Journal ArticleDOI

Guidance of Axons by Local Coupling of Retrograde Flow to Point Contact Adhesions.

TL;DR: This study provides the best evidence that growth cone–ECM adhesions clutch RF locally to guide axon outgrowth and guidance in vivo, and correlation with clutching of filamentous actin retrograde flow (RF) strongly suggest guides developing axons.
Book ChapterDOI

Cell volume regulatory ion transport in the regulation of cell migration.

TL;DR: The role of the cell volume regulatory ion transport mechanisms as they participate in the regulation of cell migration is focused on and special emphasis is given to their interplay with the cytoskeleton, their meaning for substrate adhesion and to the polarized fashion of their subcellular distribution.
References
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Journal ArticleDOI

Cell Migration: A Physically Integrated Molecular Process

TL;DR: The authors are grateful for financial support from the National Institutes of Health (grants GM23244 and GM53905), and to very helpful comments on the manuscript from Elliot Elson, Vlodya Gelfand, Paul Matsudaira, Julie Theriot, and Sally Zigmond.
Journal ArticleDOI

Cellular Motility Driven by Assembly and Disassembly of Actin Filaments

TL;DR: A core set of proteins including actin, Arp2/3 complex, profilin, capping protein, and ADF/cofilin can reconstitute the process in vitro, and mathematical models of the constituent reactions predict the rate of motion.
Journal ArticleDOI

The interaction of Arp2/3 complex with actin: Nucleation, high affinity pointed end capping, and formation of branching networks of filaments

TL;DR: It is shown that Arp2/3 complex purified from Acanthamoeba caps the pointed ends of actin filaments with high affinity and increases the critical concentration for polymerization at the pointed end from 0.6 to 1.0 microM.
Journal ArticleDOI

Dissecting Temporal and Spatial Control of Cytokinesis with a Myosin II Inhibitor

TL;DR: It is shown that exit from the cytokinetic phase of the cell cycle depends on ubiquitin-mediated proteolysis and continuous signals from microtubules are required to maintain the position of the cleavage furrow, and these signals control the localization of myosin II independently of other furrow components.
Journal ArticleDOI

Actions of cytochalasins on the organization of actin filaments and microtubules in a neuronal growth cone.

TL;DR: Results suggest that actin normally polymerizes at the leading edge and then flows rearward at a rate between 3-6 microns/min, which is consistent with their being secondary to effects of CB on lamellar F-actin.
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