Spatiotemporal Feedback between Actomyosin and Focal-Adhesion Systems Optimizes Rapid Cell Migration

Gupton, Stephanie L.; Waterman‐Storer, Clare M.

doi:10.1016/j.cell.2006.05.029

Cited by 552 publications

(623 citation statements)

References 46 publications

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“…However, how the mineralized matrix or mineral by itself may affect RhoGTPase activity and then osteoclast function is an open question. An emerging theme is that adhesion strength and substrate stiffness regulate cell migration and adhesion structure organization (de Rooij et al, 2005;Gupton and Waterman-Storer, 2006). In turn, cells adjust their internal stiffness to match that of their substrate (Solon et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Rho GTPases in osteoclasts: Orchestrators of podosome arrangement

Ory

Brazier

Pawlak

et al. 2008

European Journal of Cell Biology

130

101

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Cells from the myeloid lineage, namely macrophages, dendritic cells and osteoclasts develop podosomes instead of stress fibers and focal adhesions to adhere and migrate.Podosomes share many components with focal adhesions but differ in their molecular organization, with a dense core of polymerized actin surrounded by scaffolding proteins, kinases and integrins. Podosomes are found either isolated both in macrophages and dendritic cells or arranged into superstructures in osteoclasts. When osteoclasts resorb bone, they form an F-actin rich sealing zone, which is a dense array of connected podosomes that firmly anchors osteoclasts to bone. It delineates a compartment in which protons and proteases are secreted to dissolve and degrade the mineralized matrix. Since Rho GTPases have been shown to control F-actin stress fibers and focal adhesions in mesenchymal cells, the question of whether they could also control podosome formation and arrangement in cells from the myeloid lineage, and particularly in osteoclasts, rapidly emerged. This article considers recent advances made in our understanding of podosome arrangements in osteoclasts and how Rho GTPases may control it.

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Section: Discussionmentioning

confidence: 99%

Rho GTPases in osteoclasts: Orchestrators of podosome arrangement

Ory

Brazier

Pawlak

et al. 2008

European Journal of Cell Biology

130

101

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“…This difference may reflect differences in substrate adhesion strength between keratocytes and mammalian cells. It was established in theoretical and experimental studies (DiMilla et al, 1991;Gupton and Waterman-Storer, 2006) that the overall speed of the cell is not directly proportional to the strength of myosin-mediated contraction but that it depends of the balance of contractility and adhesion strength and on the optimal organization of the motile machinery where contractility and adhesion are interdependent. Inhibition of contractility in strongly adherent mammalian cells may compromise the forcedependent maturation of focal adhesions, rendering the cells less adherent and more motile.…”

Section: Discussionmentioning

confidence: 99%

Comparative Maps of Motion and Assembly of Filamentous Actin and Myosin II in Migrating Cells

Schaub

Bohnet

Laurent

et al. 2007

MBoC

120

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To understand the mechanism of cell migration, one needs to know how the parts of the motile machinery of the cell are assembled and how they move with respect to each other. Actin and myosin II are thought to be the major structural and force-generating components of this machinery (Mitchison and Cramer, 1996; Parent, 2004). The movement of myosin II along actin filaments is thought to generate contractile force contributing to cell translocation, but the relative motion of the two proteins has not been investigated. We use fluorescence speckle and conventional fluorescence microscopy, image analysis, and computer tracking techniques to generate comparative velocity and assembly maps of actin and myosin II over the entire cell in a simple model system of persistently migrating fish epidermal keratocytes. The results demonstrate contrasting polarized assembly patterns of the two components, indicate force generation at the lamellipodium-cell body transition zone, and suggest a mechanism of anisotropic network contraction via sliding of myosin II assemblies along divergent actin filaments. INTRODUCTIONCrawling cell motion involves a cycle of several distinct processes: protrusion at the front of the cell, attachment to the substratum, and forward translocation of the cell body followed or accompanied by detachment and withdrawal of the rear of the cell. Crawling motion is thought to be dependent on the actin-myosin II cytoskeletal system (Mitchison and Cramer, 1996): protrusion is thought to be driven by the assembly of actin network, which is anchored to the substratum through integrin-containing adhesions; forward translocation of the cell body and contraction of the rear are thought to depend on the interaction of the actin network with the motor protein myosin II. Actin assembly during the protrusion at the leading edge of motile cells has recently received the most attention both in experimental (Pantaloni et al., 2001;Pollard and Borisy, 2003;Ridley et al., 2003) and theoretical studies (for review, see Mogilner, 2006). In contrast, the mechanisms involved in the forward translocation of the cell body remain largely unclear: the exact layout and the mode of action of the contractile actin-myosin II machinery are controversial. Qualitative models proposed in the literature include shortening of small contractile units similar to muscle sarcomeres, myosin II-dependent transport along uniformly polarized actin arrays, and a dynamic network contraction mechanism where contraction results from alignment of actin filaments by myosin II assemblies (Cramer, 1999;Verkhovsky et al., 1999a). More sophisticated biophysical models aim to understand the contractile cytoskeletal machinery in quantitative physical terms. In the past, considering the cytoskeleton as a gel made of cross-linked semiflexible polymers has helped understanding its passive visco-elastic properties. More recently, attempts were made to develop biophysical models taking into account intrinsic activity of the cytoskeleton: polarized assembly of acti...

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“…, 1996 al. Palecek , 1998et al Gallant , 2005et al Gupton and Waterman-Storer, 2006 During cell attachment and spreading, initial adhesions evolve into small focal complexes that mature into focal adhesions connected to stress fibers. During this initial process, auto-assembly requires the application of a force on integrin receptors up to 2 pN.…”

Section: Interplay Between Focal Adhesions Podosome Type Adhesions Amentioning

confidence: 99%