Microfilament-based motility in non-muscle cells

Small, J. Victor

doi:10.1016/s0955-0674(89)80040-7

Cited by 65 publications

(24 citation statements)

References 19 publications

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“…These findings are consistent with the conceptions that actin polymerization is required for formation of lamellipodia [Cassimeris et al, 1990;Small, 1989] and that polymerized actin provides elastic resistance to deformation [Janmey et al, 1992;Needham et al, 1989;Oster and Perelson, 1994]. Latrunculin A (Figs.…”

Section: Mechanisms Of Protrusionsupporting

confidence: 90%

“…The work of the past decades provides strong evidence that lamellipodia and actin polymerisation in lamellipodia are essential for locomotion of metazoan cells to occur [Stossel, 1993;Small, 1989Mitchison and Cramer, 1996;Zigmond et al, 1981;Cassimeris et al, 1990]. Untreated Walker carcinosarcoma cells in culture usually show lamellipodia.…”

Section: Role Of Lamellipodia In Locomotion Of Walker Carcinosarcoma mentioning

confidence: 99%

“…One of the classical arguments in favour of the concept that actin polymerization in lamellipodia drives locomotion is that inhibitors of actin polymerization, in particular cytochalasins, can depolymerize F-actin in lamellipodia and suppress formation of lamellipodia and locomotion [Small, 1989;Cassimeris et al, 1990;Keller and Zimmermann, 1986]. Latrunculin A, a toxin isolated from the Red Sea sponge Latrunculia magnifica Keller has been found to disrupt microfilament organization, to inhibit actin polymerization, and to suppress actin dependent cell functions [Spector et al, 1989;Oliveira et al, 1996;Ayscough et al, 1997] by affecting the polymerization of pure actin in a manner consistent with formation of a 1:1 molar complex with G-actin [Coué et al, 1987;Ayscough et al, 1997].…”

Section: Introductionmentioning

confidence: 99%

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Redundancy of lamellipodia in locomoting Walker carcinosarcoma cells

Keller

2000

Cell Motil. Cytoskeleton

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Locomoting metazoan cells usually form lamellipodia at the leading front and it is widely accepted that lamellipodia are required for locomotion. In this case, suppression of lamellipodia must stop locomotion. However, the experiments show that lamellipodia are redundant for locomotion of Walker carcinosarcoma cells. Low latrunculin A concentrations (10−7 M) transform polarised locomoting cells with lamellipodia into cells without morphologically recognisable protrusions showing an increased speed of locomotion and a reduced amount of cellular F‐actin. Whereas untreated cells show a fairly linear distribution of F‐actin along the plasma membrane, cells lacking morphologically recognizable protrusions at the front show modifications at the front consisting in an irregular distribution of F‐actin with formation of small or large patches of F‐actin alternating with small or large gaps in the F‐actin layer. This is associated with a reduced resistance to deformation pressure at the front of the cell. High concentrations of latrunculin A (>10−7 M) compromising contraction at the rear stop locomotion, suggesting that cortical contraction is important for locomotion to occur in these cells. The results are consistent with the view that actin polymerization is important for formation of lamellipodia but they are not compatible with the view that lamellipodia are essential for locomotion of Walker carcinosarcoma cells. A unifying hypothesis for the formation of different types of protrusions is proposed. Cell Motil. Cytoskeleton 46:247–256, 2000. © 2000 Wiley‐Liss, Inc.

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Section: Mechanisms Of Protrusionsupporting

confidence: 90%

Section: Role Of Lamellipodia In Locomotion Of Walker Carcinosarcoma mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Redundancy of lamellipodia in locomoting Walker carcinosarcoma cells

Keller

2000

Cell Motil. Cytoskeleton

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“…It is well known that cell migration is a complex process mediated by dynamic changes in the actinmyosin cytoskeleton. It is now generally thought that actin polymerization at the leading edge provides a crucial driving force for extension of growth cones (Dent and Gertler, 2003;Kalil and Dent, 2005), keratocytes (Svitkina et al, 1997;Pollard and Borisy, 2003;Jurado et al, 2005), fibroblasts (Wang, 1985;Galbraith and Sheetz, 1997), neutrophils (Torres and Coates, 1999;Parent, 2004) and Dictyostelium cells (Yumura et al, 1984;Yumura, 1996a;Yumura and Fukui, 1998;Parent, 2004), whereas the detachment and retraction of the rear of the cell from the substratum is thought to be induced by contraction through myosin-II-dependent processes in Dictyostelium cells (Yumura et al, 1984;Yumura and KitanishiYumura, 1990;Yumura, 1993;Small, 1989;Jay and Elson, 1992;Jay et al, 1995;Uchida et al, 2003) and fibroblasts (Chen, 1981;Galbraith and Sheetz, 1997).…”

Section: Introductionmentioning

confidence: 99%

Actin-based propulsive forces and myosin-II-based contractile forces in migratingDictyosteliumcells

Iwadate

Yumura

2008

Journal of Cell Science

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It has been suggested that myosin II exerts traction forces at the posterior ends and retracting pseudopodia of migrating cells, but there is no direct evidence. Here, using a combination of total internal reflection fluorescence (TIRF) microscopy and force microscopy with a high spatial resolution of ∼400 nm, we simultaneously recorded GFP-myosin II dynamics and traction forces under migrating Dictyostelium cells. Accumulation of filamentous myosin II and a subsequent increase in traction forces were detected in pseudopodia just before retraction. In the case of motorless myosin II, traction forces did not increase after accumulation, suggesting that the source of the retraction force is the motor activity of accumulated myosin II. Simultaneous recording of F-actin and traction forces revealed that traction forces were exerted under spot-like regions where F-actin accumulated. Cells migrated in a direction counter to the sum of the force vectors exerted at each spot, suggesting that the stress spots act as scaffolds to transmit the propulsive forces at the leading edge generated by actin polymerization.

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“…In fibroblasts adhesive complexes are regions of the plasma membrane where integrin receptors, actin filaments and associated proteins cluster together. During migration the small nascent adhesive complexes (focal complexes) at the front of the cell grow and strengthen into larger, more organized focal adhesions that serve as traction 'pads' over which the cell body moves (Small, 1989). The molecular nature of the contacts is poorly characterized in Dd, which does not express integrins, but one candidate molecule has recently been discovered (Fey et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

How cellular movement determines the collective force generated by the Dictyostelium discoideum slug

Dallon

Othmer

2004

Journal of Theoretical Biology

106

134

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How the collective motion of cells in a biological tissue originates in the behavior of a collection of individuals, each of which responds to the chemical and mechanical signals it receives from neighbors, is still poorly understood. Here we study this question for a particular system, the slug stage of the cellular slime mold Dictyostelium discoideum (Dd). We investigate how cells in the interior of a migrating slug can effectively transmit stress to the substrate and thereby contribute to the overall motive force. Theoretical analysis suggests necessary conditions on the behavior of individual cells, and computational results shed light on experimental results concerning the total force exerted by a migrating slug. The model predicts that only cells in contact with the substrate contribute to the translational motion of the slug. Since the model is not based specifically on the mechanical properties of Dd cells, the results suggest that this behavior will be found in many developing systems. r

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Microfilament-based motility in non-muscle cells

Cited by 65 publications

References 19 publications

Redundancy of lamellipodia in locomoting Walker carcinosarcoma cells

Redundancy of lamellipodia in locomoting Walker carcinosarcoma cells

Actin-based propulsive forces and myosin-II-based contractile forces in migratingDictyosteliumcells

How cellular movement determines the collective force generated by the Dictyostelium discoideum slug

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