Chemoattractant-induced lamellipod extension

Bailly, Maryse; Condeelis, John S.; Segall, Jeffrey E.

doi:10.1002/(sici)1097-0029(19981201)43:5<433::aid-jemt9>3.0.co;2-2

Cited by 64 publications

(42 citation statements)

References 108 publications

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“…Interestingly, the localization of Rho at 1 versus 3 min was different. At 1 min, Rho was localized to a narrow band that extended approximately 0.5 μm into the cell (Fig 1B middle panel), which is the zone of f-actin accumulation in EGF-stimulated MTLn3 cells [34]. We presume that this is staining pattern is largely due to RhoA, since RhoB is confined to endosomes [35].…”

Section: Spatial and Temporal Analysis Of Rho Activation In Egf-stimumentioning

confidence: 87%

RhoA/ROCK-mediated switching between Cdc42- and Rac1-dependent protrusion in MTLn3 carcinoma cells

El‐Sibai

Pertz

Pang

et al. 2008

Experimental Cell Research

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Rho GTPases are versatile regulators of cell shape that act on the actin cytoskeleton. Studies using Rho GTPase mutants have shown that, in some cells, Rac1 and Cdc42 regulate the formation of lamellipodia and filopodia, respectively at the leading edge, whereas RhoA mediates contraction at the rear of moving cells. However, recent reports have described a zone of RhoA/ROCK activation at the front of cells undergoing motility. In this study, we use a FRET-based RhoA biosensor to show that RhoA activation localizes to the leading edge of EGF-stimulated cells. Inhibition of Rho or ROCK enhanced protrusion, yet markedly inhibited cell motility; these changes correlated with a marked activation of Rac-1 at the cell edge. Surprisingly, whereas EGF-stimulated protrusion in control MTLn3 cells is Rac-independent and Cdc42-dependent, the opposite pattern is observed in MTLn3 cells after inhibition of ROCK. Thus, Rho and ROCK suppress Rac-1 activation at the leading edge, and inhibition of ROCK causes a switch between Cdc42 and Rac-1 as the dominant Rho GTPase driving protrusion in carcinoma cells. These data describe a novel role for Rho in coordinating signaling by Rac and Cdc42.

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Section: Spatial and Temporal Analysis Of Rho Activation In Egf-stimumentioning

confidence: 87%

RhoA/ROCK-mediated switching between Cdc42- and Rac1-dependent protrusion in MTLn3 carcinoma cells

El‐Sibai

Pertz

Pang

et al. 2008

Experimental Cell Research

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“…Overexpressed growth factors and constitutively activated oncogenes are able to directly induce cell motility and invasion, in addition to their more well known mitogenic properties (Partin et al, 1988;Stolz and Michalopoulos, 1994). EGF is a chemoattractant for tumor cells (Bailly et al, 1998) and paracrine stimulation of tumor cells by EGF is required for tumor cell motility in vivo (Wyckoff et al, 2004). These growth factors are dependent upon the function of members of the Ras superfamily of small guanine 5 0 -triphosphate binding proteins.…”

Section: Introductionmentioning

confidence: 99%

Transcription factors control invasion: AP-1 the first among equals

et al. 2006

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“…Theory and observation suggest that changes in cell direction are governed by local behavior around the edges of the leading lamella [19,4]. Supposing the taxis is generated by the difference in the stimulus (in this case, electric potential) between the two ends of the lamella, the directional sensitivity would be greatest when the cell is moving perpendicular to the electric field.…”

Section: A Model For Topotaxis In a Uniform Electric Fieldmentioning

confidence: 99%

Stochastic models for cell motion and taxis

Ionides

Fang

Isseroff

et al. 2004

Journal of Mathematical Biology

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Certain biological experiments investigating cell motion result in time lapse video microscopy data which may be modeled using stochastic differential equations. These models suggest statistics for quantifying experimental results and testing relevant hypotheses, and carry implications for the qualitative behavior of cells and for underlying biophysical mechanisms. Directional cell motion in response to a stimulus, termed taxis, has previously been modeled at a phenomenological level using the Keller-Segel diffusion equation. The Keller-Segel model cannot distinguish certain modes of taxis, and this motivates the introduction of a richer class of models which is nevertheless still amenable to statistical analysis. A state space model formulation is used to link models proposed for cell velocity to observed data. Sequential Monte Carlo methods enable parameter estimation via maximum likelihood for a range of applicable models. One particular experimental situation, involving the effect of an electric field on cell behavior, is considered in detail. In this case, an Ornstein-Uhlenbeck model for cell velocity is found to compare favorably with a nonlinear diffusion model.

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Chemoattractant-induced lamellipod extension

Cited by 64 publications

References 108 publications

RhoA/ROCK-mediated switching between Cdc42- and Rac1-dependent protrusion in MTLn3 carcinoma cells

RhoA/ROCK-mediated switching between Cdc42- and Rac1-dependent protrusion in MTLn3 carcinoma cells

Transcription factors control invasion: AP-1 the first among equals

Stochastic models for cell motion and taxis

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