Cascade pathway of filopodia formation downstream of SCAR

Biyasheva, Assel; Svitkina, Tatyana; Kunda, Patricia; Baum, Buzz; Borisy, Gary G.

doi:10.1242/jcs.00921

Cited by 105 publications

(97 citation statements)

References 46 publications

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“…This is consistent with our evidence that WAVE-1 regulates growth cone morphology and neurite outgrowth but is at odds with evidence that inhibition of Arp2/3-stimulated neurite outgrowth (Strasser et al, 2004). Analogous RNAi studies in Drosophila show that loss of dWAVE inhibits lamellipodia as well as filopodial formation (Biyasheva et al, 2004). How these different findings fit together is not yet clear.…”

Section: Discussionsupporting

confidence: 82%

A WAVE-1 and WRP Signaling Complex Regulates Spine Density, Synaptic Plasticity, and Memory

Soderling¹,

Guire²,

Kaech³

et al. 2007

J. Neurosci.

200

187

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The scaffolding protein WAVE-1 (Wiskott-Aldrich syndrome protein family member 1) directs signals from the GTPase Rac through the Arp2/3 complex to facilitate neuronal actin remodeling. The WAVE-associated GTPase activating protein called WRP is implicated in human mental retardation, and WAVE-1 knock-out mice have altered behavior. Neuronal time-lapse imaging, behavioral analyses, and electrophysiological recordings from genetically modified mice were used to show that WAVE-1 signaling complexes control aspects of neuronal morphogenesis and synaptic plasticity. Gene targeting experiments in mice demonstrate that WRP anchoring to WAVE-1 is a homeostatic mechanism that contributes to neuronal development and the fidelity of synaptic connectivity. This implies that signaling through WAVE-1 complexes is essential for neural plasticity and cognitive behavior.

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Section: Discussionsupporting

confidence: 82%

A WAVE-1 and WRP Signaling Complex Regulates Spine Density, Synaptic Plasticity, and Memory

Soderling¹,

Guire²,

Kaech³

et al. 2007

J. Neurosci.

200

187

View full text Add to dashboard Cite

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“…However, if filopodia were effectively and continuously initiated by the elongation of pre-existing lamellipodial filaments, why would we need actin filament nucleators operating in filopodia such as formins? Furthermore, if the convergent elongation model was physiologically relevant, one would expect an interference with the process by removal of lamellipodia, as previously proposed (Biyasheva et al, 2004). Although a more recent study has reaffirmed this conclusion in neurons (Korobova and Svitkina, 2008), several independent studies have continuously failed to establish a defect in filopodia initiation and protrusion effected by suppression of lamellipodia (Gomez et al, 2007, Nicholson-Dykstra and Higgs, 2008, Nobes and Hall, 1995, Sarmiento et al, 2008, Vidali et al, 2006.…”

Section: Models For Filament Generation In Filopodia: Convergent Elonmentioning

confidence: 69%

Filopodia: Complex models for simple rods

Faix

Breitsprecher

Stradal

et al. 2009

The International Journal of Biochemistry & Cell Biology

154

148

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CitationFilopodia: Complex models for simple rods., 41 (8- AbstractFilopodia are prominent cell surface protrusions filled with bundles of linear actin filaments that drive their protrusion. These structures are considered important sensory organelles, for instance in neuronal growth cones or during the fusion of sheets of epithelial tissues. In addition, they can serve a precursor function in adhesion site or stress fibre formation. Actin filament assembly is essential for filopodia formation and turnover, yet the precise molecular mechanisms of filament nucleation and/or elongation are controversial. Indeed, conflicting reports on the molecular requirements of filopodia initiation have prompted researchers to propose different types and/or alternative or redundant mechanisms mediating this process.However, recent data shed new light on these questions, and they indicate that the balance of a limited set of biochemical activities can determine the structural outcome of a given filopodium. Here we focus on discussing our current view of the relevance of these activities, and attempt to propose a molecular mechanism of filopodia assembly based on a single core machinery.2

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“…Filopodia are formed as the result of a failure in the formation of a branched actin network, due to the decrease in actin filament severing or the increase in free barbed end capping [56]. Some actin severing proteins, including gelsolin, are regulated by PLCc [57].…”

Section: Discussionmentioning

confidence: 99%

Phospholipase Cγ negatively regulates Rac/Cdc42 activation in antigen‐stimulated mast cells

El‐Sibai

Backer

2006

Eur J Immunol

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The Rho GTPases Rac and Cdc42 play a central role in the regulation of secretory and cytoskeletal responses in antigen-stimulated mast cells. In this study, we examine the kinetics and mechanism of Rac and Cdc42 activation in the rat basophilic leukemia RBL-2H3 cells. The activation kinetics of both Rac and Cdc42 show a biphasic profile, consisting of an early transient peak at 1 min and a late sustained activation phase at 20-40 min. The inhibition of phospholipase C (PLC)c causes a twofold increase in Rac and Cdc42 activation that coincides with a dramatic production of atypical filopodialike structures. Inhibition of protein kinase C using bisindolylmaleimide mimics the effect of PLCc inhibition on Rac activation, but not on Cdc42 activation. In contrast, depletion of intracellular calcium leads to a complete inhibition of the early activation peak of both Rac and Cdc42, without significant effects on the late sustained activation. These data suggest that PLCc is involved in a negative feedback loop that leads to the inhibition of Rac and Cdc42. They also suggest that the presence of intracellular calcium is a prerequisite for both Rac and Cdc42 activation. IntroductionMast cells participate in the pathogenesis of immediate hypersensitivity and allergic reactions in humans [1]. Moreover, mast cells are important contributors to airway hyper-responsiveness that occurs in asthmatic inflammation [2]. In response to allergens and other exogenous stimuli, mast cells accumulate in the airway smooth muscle and in the bronchial intraepithelial layer [3]. The activation of mast cells, through the crosslinking of the FceRI, leads to the release of pre-formed early-phase inflammatory mediators and vasoactive substances from granules. It also leads to the in situ production of cytokines and bioactive lipids that contribute to the late-phase manifestation of the asthmatic reaction [4].Aggregation of FceRI on the surface of mast cells in response to multivalent ligand binding initiates a cascade of downstream signaling effectors that leads to degranulation [5]. These include phosphatidylinositol 3-kinase (PI3K), the guanine nucleotide exchange factor Vav, and phospholipase C (PLC)c1 [6]. The early activation of PLCc1 results in the generation of inositol 1,4,5-triphosphate (IP 3 ) and diacylglycerol. These two second messengers lead to increases in cytoplasmic calcium and activation of calcium/diacylglycerol-regulated isoforms of protein kinase C (PKC) which culminate in granule margination and exocytosis [7]. PI3K plays an important regulatory role as an upstream activator of PLCc1, as well as a regulator of calcium flux during mast cell degranulation [8][9][10][11][12][13].Members of the Rho family of small GTPases also regulate signaling events in mast cells [14][15][16]. In the rat basophilic leukemia (RBL-2H3) cells, Rac and Cdc42 have been implicated in the control of the FceRImediated phagocytosis and the regulation of migration, In conjunction with the secretory response, antigenstimulated mast cells undergo drama...

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Cascade pathway of filopodia formation downstream of SCAR

Cited by 105 publications

References 46 publications

A WAVE-1 and WRP Signaling Complex Regulates Spine Density, Synaptic Plasticity, and Memory

A WAVE-1 and WRP Signaling Complex Regulates Spine Density, Synaptic Plasticity, and Memory

Filopodia: Complex models for simple rods

Phospholipase Cγ negatively regulates Rac/Cdc42 activation in antigen‐stimulated mast cells

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