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A Network Contraction Model for Cell Translocation and Retrograde Flow
A.B.Verkhovsky, T.M.Svitkina, and G.G. Borisy
In: Cell Behaviour: Control and Mechanism of Motility, 1999, 207-222.
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Abstract:

Kinetic and structural analysis of the actin-myosin II system in mammalian fibroblasts and fish epidermal keratocytes suggests that the cell's motility machinery arises behind the leading edge in the form of myosin filament clusters immersed in an actin filament network. We discuss how the contraction of this actin-myosin II network is related to the formation of actin-myosin filament bundles, cell translocation and retrograde flow.


Figures:

Figure 1 (64K) - Forces acting between the lamellipodium and the cell body may drive both cell body translocation and retrograde flow
Figure 2 (96K) - Schematic representation of mechanisms of cell body translocation
Figure 3 (96K) - Overall distribution of myosin II (red) and actin (cyan) in REF-52 fibroblast (a) and fish epidermal keratocyte (b)
Figure 4 (128K) - Dynamics of myosin features in REF-52 fibroblast (a), locomoting fish keratocyte (b) and fish keratocyte tethered at the edge of an epithelioid colony (c)
Figure 5 (96K) - Clusters of myosin filaments in REF-52 fibroblast (a) and fish epidermal keratocyte (b)
Figure 6 (64K) - Diagram showing how myosin filament clusters can transform actin network
Figure 7 (96K) - Compression of an actin-myosin network into a bundle at the lamellipodial/cell body transition zone of a fish keratocyte is coupled to forward translocation


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