Academic literature on the topic 'Filopodia'

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Journal articles on the topic "Filopodia"

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Krndija, Denis, and Michael Fairhead. "IGF1R undergoes active and directed centripetal transport on filopodia upon receptor activation." Biochemical Journal 476, no. 23 (December 3, 2019): 3583–93. http://dx.doi.org/10.1042/bcj20190665.

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Filopodia are thin, actin-based membrane protrusions with roles in sensing external mechanical and chemical cues, such as growth factor gradients in tissues. It was proposed that the chemical sensing role of filopodia is achieved through clearance of activated signaling receptors from filopodia. Type I insulin-like growth factor receptor (IGF1R) is a key regulator of normal development and growth, as well as tumor development and progression. Its biological roles depend on its activation upon IGF1 binding at the cell membrane. IGF1R behavior at the cell membrane and in particular in filopodia, has not been established. We found that IGF1 activation led to a gradual reduction in IGF1R puncta in filopodia, and that this clearance depended on actin, non-muscle myosin II, and IGF1R kinase activity. Using single particle tracking of filopodial IGF1R, we established that ligand-free IGF1R undergoes non-directional unidimensional diffusion along the filopodium. Moreover, after initial diffusion, the ligand-bound IGF1R is actively transported along the filopodium towards the filopodium base, and consequently cleared from the filopodium. Our results show that IGF1R can move directionally on the plasma membrane protrusions, supporting a sensory role for filopodia in interpreting local IGF1 gradients.
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Leijnse, Natascha, Lene B. Oddershede, and Poul M. Bendix. "Helical buckling of actin inside filopodia generates traction." Proceedings of the National Academy of Sciences 112, no. 1 (December 22, 2014): 136–41. http://dx.doi.org/10.1073/pnas.1411761112.

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Cells can interact with their surroundings via filopodia, which are membrane protrusions that extend beyond the cell body. Filopodia are essential during dynamic cellular processes like motility, invasion, and cell–cell communication. Filopodia contain cross-linked actin filaments, attached to the surrounding cell membrane via protein linkers such as integrins. These actin filaments are thought to play a pivotal role in force transduction, bending, and rotation. We investigated whether, and how, actin within filopodia is responsible for filopodia dynamics by conducting simultaneous force spectroscopy and confocal imaging of F-actin in membrane protrusions. The actin shaft was observed to periodically undergo helical coiling and rotational motion, which occurred simultaneously with retrograde movement of actin inside the filopodium. The cells were found to retract beads attached to the filopodial tip, and retraction was found to correlate with rotation and coiling of the actin shaft. These results suggest a previously unidentified mechanism by which a cell can use rotation of the filopodial actin shaft to induce coiling and hence axial shortening of the filopodial actin bundle.
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Lau, Pak-ming, Robert S. Zucker, and David Bentley. "Induction of Filopodia by Direct Local Elevation of Intracellular Calcium Ion Concentration." Journal of Cell Biology 145, no. 6 (June 14, 1999): 1265–76. http://dx.doi.org/10.1083/jcb.145.6.1265.

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In neuronal growth cones, cycles of filopodial protrusion and retraction are important in growth cone translocation and steering. Alteration in intracellular calcium ion concentration has been shown by several indirect methods to be critically involved in the regulation of filopodial activity. Here, we investigate whether direct elevation of [Ca2+]i, which is restricted in time and space and is isolated from earlier steps in intracellular signaling pathways, can initiate filopodial protrusion. We raised [Ca2+]i level transiently in small areas of nascent axons near growth cones in situ by localized photolysis of caged Ca2+ compounds. After photolysis, [Ca2+]i increased from ∼60 nM to ∼1 μM within the illuminated zone, and then returned to resting level in ∼10–15 s. New filopodia arose in this area within 1–5 min, and persisted for ∼15 min. Elevation of calcium concentration within a single filopodium induced new branch filopodia. In neurons coinjected with rhodamine-phalloidin, F-actin was observed in dynamic cortical patches along nascent axons; after photolysis, new filopodia often emerged from these patches. These results indicate that local transient [Ca2+]i elevation is sufficient to induce new filopodia from nascent axons or from existing filopodia.
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Marchenko, Olena O., Sulagna Das, Ji Yu, Igor L. Novak, Vladimir I. Rodionov, Nadia Efimova, Tatyana Svitkina, Charles W. Wolgemuth, and Leslie M. Loew. "A minimal actomyosin-based model predicts the dynamics of filopodia on neuronal dendrites." Molecular Biology of the Cell 28, no. 8 (April 15, 2017): 1021–33. http://dx.doi.org/10.1091/mbc.e16-06-0461.

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Dendritic filopodia are actin-filled dynamic subcellular structures that sprout on neuronal dendrites during neurogenesis. The exploratory motion of the filopodia is crucial for synaptogenesis, but the underlying mechanisms are poorly understood. To study filopodial motility, we collected and analyzed image data on filopodia in cultured rat hippocampal neurons. We hypothesized that mechanical feedback among the actin retrograde flow, myosin activity, and substrate adhesion gives rise to various filopodial behaviors. We formulated a minimal one-dimensional partial differential equation model that reproduced the range of observed motility. To validate our model, we systematically manipulated experimental correlates of parameters in the model: substrate adhesion strength, actin polymerization rate, myosin contractility, and the integrity of the putative microtubule-based barrier at the filopodium base. The model predicts the response of the system to each of these experimental perturbations, supporting the hypothesis that our actomyosin-driven mechanism controls dendritic filopodia dynamics.
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Saha, Tanumoy, Isabel Rathmann, Abhiyan Viplav, Sadhana Panzade, Isabell Begemann, Christiane Rasch, Jürgen Klingauf, Maja Matis, and Milos Galic. "Automated analysis of filopodial length and spatially resolved protein concentration via adaptive shape tracking." Molecular Biology of the Cell 27, no. 22 (November 7, 2016): 3616–26. http://dx.doi.org/10.1091/mbc.e16-06-0406.

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Filopodia are dynamic, actin-rich structures that transiently form on a variety of cell types. To understand the underlying control mechanisms requires precise monitoring of localization and concentration of individual regulatory and structural proteins as filopodia elongate and subsequently retract. Although several methods exist that analyze changes in filopodial shape, a software solution to reliably correlate growth dynamics with spatially resolved protein concentration along the filopodium independent of bending, lateral shift, or tilting is missing. Here we introduce a novel approach based on the convex-hull algorithm for parallel analysis of growth dynamics and relative spatiotemporal protein concentration along flexible filopodial protrusions. Detailed in silico tests using various geometries confirm that our technique accurately tracks growth dynamics and relative protein concentration along the filopodial length for a broad range of signal distributions. To validate our technique in living cells, we measure filopodial dynamics and quantify spatiotemporal localization of filopodia-associated proteins during the filopodial extension–retraction cycle in a variety of cell types in vitro and in vivo. Together these results show that the technique is suitable for simultaneous analysis of growth dynamics and spatiotemporal protein enrichment along filopodia. To allow readily application by other laboratories, we share source code and instructions for software handling.
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Xue, Fei, Deanna M. Janzen, and David A. Knecht. "Contribution of Filopodia to Cell Migration: A Mechanical Link between Protrusion and Contraction." International Journal of Cell Biology 2010 (2010): 1–13. http://dx.doi.org/10.1155/2010/507821.

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Numerous F-actin containing structures are involved in regulating protrusion of membrane at the leading edge of motile cells. We have investigated the structure and dynamics of filopodia as they relate to events at the leading edge and the function of the trailing actin networks. We have found that although filopodia contain parallel bundles of actin, they contain a surprisingly nonuniform spatial and temporal distribution of actin binding proteins. Along the length of the actin filaments in a single filopodium, the most distal portion contains primarily T-plastin, while the proximal portion is primarily bound byα-actinin and coronin. Some filopodia are stationary, but lateral filopodia move with respect to the leading edge. They appear to form a mechanical link between the actin polymerization network at the front of the cell and the myosin motor activity in the cell body. The direction of lateral filopodial movement is associated with the direction of cell migration. When lateral filopodia initiate from and move toward only one side of a cell, the cell will turn opposite to the direction of filopodial flow. Therefore, this filopodia-myosin II system allows actin polymerization driven protrusion forces and myosin II mediated contractile force to be mechanically coordinated.
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Kim, Min-Cheol, Yaron R. Silberberg, Rohan Abeyaratne, Roger D. Kamm, and H. Harry Asada. "Computational modeling of three-dimensional ECM-rigidity sensing to guide directed cell migration." Proceedings of the National Academy of Sciences 115, no. 3 (January 2, 2018): E390—E399. http://dx.doi.org/10.1073/pnas.1717230115.

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Filopodia have a key role in sensing both chemical and mechanical cues in surrounding extracellular matrix (ECM). However, quantitative understanding is still missing in the filopodial mechanosensing of local ECM stiffness, resulting from dynamic interactions between filopodia and the surrounding 3D ECM fibers. Here we present a method for characterizing the stiffness of ECM that is sensed by filopodia based on the theory of elasticity and discrete ECM fiber. We have applied this method to a filopodial mechanosensing model for predicting directed cell migration toward stiffer ECM. This model provides us with a distribution of force and displacement as well as their time rate of changes near the tip of a filopodium when it is bound to the surrounding ECM fibers. Aggregating these effects in each local region of 3D ECM, we express the local ECM stiffness sensed by the cell and explain polarity in the cellular durotaxis mechanism.
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Young, Lorna E., Ernest G. Heimsath, and Henry N. Higgs. "Cell type–dependent mechanisms for formin-mediated assembly of filopodia." Molecular Biology of the Cell 26, no. 25 (December 15, 2015): 4646–59. http://dx.doi.org/10.1091/mbc.e15-09-0626.

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Filopodia are finger-like protrusions from the plasma membrane and are of fundamental importance to cellular physiology, but the mechanisms governing their assembly are still in question. One model, called convergent elongation, proposes that filopodia arise from Arp2/3 complex–nucleated dendritic actin networks, with factors such as formins elongating these filaments into filopodia. We test this model using constitutively active constructs of two formins, FMNL3 and mDia2. Surprisingly, filopodial assembly requirements differ between suspension and adherent cells. In suspension cells, Arp2/3 complex is required for filopodial assembly through either formin. In contrast, a subset of filopodia remains after Arp2/3 complex inhibition in adherent cells. In adherent cells only, mDia1 and VASP also contribute to filopodial assembly, and filopodia are disproportionately associated with focal adhesions. We propose an extension of the existing models for filopodial assembly in which any cluster of actin filament barbed ends in proximity to the plasma membrane, either Arp2/3 complex dependent or independent, can initiate filopodial assembly by specific formins.
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Urbančič, Vasja, Richard Butler, Benjamin Richier, Manuel Peter, Julia Mason, Frederick J. Livesey, Christine E. Holt, and Jennifer L. Gallop. "Filopodyan: An open-source pipeline for the analysis of filopodia." Journal of Cell Biology 216, no. 10 (July 31, 2017): 3405–22. http://dx.doi.org/10.1083/jcb.201705113.

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Filopodia have important sensory and mechanical roles in motile cells. The recruitment of actin regulators, such as ENA/VASP proteins, to sites of protrusion underlies diverse molecular mechanisms of filopodia formation and extension. We developed Filopodyan (filopodia dynamics analysis) in Fiji and R to measure fluorescence in filopodia and at their tips and bases concurrently with their morphological and dynamic properties. Filopodyan supports high-throughput phenotype characterization as well as detailed interactive editing of filopodia reconstructions through an intuitive graphical user interface. Our highly customizable pipeline is widely applicable, capable of detecting filopodia in four different cell types in vitro and in vivo. We use Filopodyan to quantify the recruitment of ENA and VASP preceding filopodia formation in neuronal growth cones, and uncover a molecular heterogeneity whereby different filopodia display markedly different responses to changes in the accumulation of ENA and VASP fluorescence in their tips over time.
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Steketee, Michael, Kenneth Balazovich, and Kathryn W. Tosney. "Filopodial Initiation and a Novel Filament-organizing Center, the Focal Ring." Molecular Biology of the Cell 12, no. 8 (August 2001): 2378–95. http://dx.doi.org/10.1091/mbc.12.8.2378.

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This study examines filopodial initiation and implicates a putative actin filament organizer, the focal ring. Filopodia were optically recorded as they emerged from veils, the active lamellar extensions of growth cones. Motile histories revealed three events that consistently preceded filopodial emergence: an influx of cytoplasm into adjacent filopodia, a focal increase in phase density at veil margins, and protrusion of nubs that transform into filopodia. The cytoplasmic influx probably supplies materials needed for initiation. In correlated time lapse-immunocytochemistry, these focal phase densities corresponded to adhesions. These adhesions persisted at filopodial bases, regardless of subsequent movements. In correlated time lapse-electron microscopy, these adhesion sites contained a focal ring (an oblate, donut-shaped structure ∼120 nm in diameter) with radiating actin filaments. Filament geometry may explain filopodial emergence at 30 degree angles relative to adjacent filopodia. A model is proposed in which focal rings play a vital role in initiating and stabilizing filopodia: 1) they anchor actin filaments at adhesions, thereby facilitating tension development and filopodial emergence; 2) “axial” filaments connect focal rings to nub tips, thereby organizing filament bundling and ensuring the bundle intersects an adhesion; and 3) “lateral” filaments interconnect focal rings and filament bundles, thereby helping stabilize lamellar margins and filopodia.
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Dissertations / Theses on the topic "Filopodia"

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Mortara, R. A. "Microfilament-membrane interactions in isolated P815 filopodia." Thesis, University of Cambridge, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.372923.

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RAIMO, SERENA. "UNRAVELING A NEW ROLE OF TFEB IN FILOPODIA FORMATION." Doctoral thesis, Università degli Studi di Milano, 2018. http://hdl.handle.net/2434/562675.

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The microphthalmia family (MITF, TFEB, TFE3, and TFEC) of transcription factors is emerging as global regulators of cancer cell survival and energy metabolism, both through the promotion of lysosomal genes as well as newly uncharacterized targets. During my Ph.D. thesis project, I revealed a new set of TFEB target genes that when activated could contribute to cell migration and invasiveness in cancer. During my work, I found that TFEB regulates the filopodial initiator's factors IRSp53 and EPS8 causing a change in cell shape and an increase in filopodia number that correlates with an augmented motility and invasiveness of the cell. On the contrary, depletion of TFEB and TFE3 leads to down-regulation of EPS8 and IRSp53, and a decrease of filopodia numbers. I confirmed the entire study in the Melanoma cell line (501Mel), a model of cancer, that are cells with a high degree of motility, showing that also in this system, there is an increase in the number of filopodia as well as of EPS8 and IRSp53 levels. This phenotype was completely reversed by depletion of MITF or TFEB and TFE3, demonstrating that the upregulation of these transcription factors could contribute to the invasive phenotype of melanoma cells. Altogether these data revealed a new role of MITF transcription factors as regulators of a transcriptional program that could control metastatic cancer initialization.
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Gauthier-Campbell, Catherine. "Regulation of filopodia dynamics is critical for proper synapse formation." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/722.

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Despite the importance of proper synaptogenesis in the CNS, the molecular mechanisms that regulate the formation and development of synapses remain poorly understood. Indeed, the mechanisms through which initial synaptic contacts are established and modified during synaptogenesis have not been fully determined and a precise understanding of these mechanisms may shed light on synaptic development, plasticity and many CNS developmental diseases. The development and formation of spiny synapses has been thought to occur via filopodia shortening followed by the recruitment of proper postsynaptic proteins, however the precise function of filopodia remains controversial. Thus the goal of this study was to investigate the dynamics of dendritic filopodia and determine their role in the development of synaptic contacts. We initially define and characterize short lipidated motifs that are sufficient to induce process outgrowth. Indeed, the palmitoylated protein motifs of GAP-43 and paralemmin are sufficient to induce filopodial extensions in heterologous cells and to increase the number of filopodia and dendritic branches in neurons. We showed that the morphological changes induced by these FIMs (filopodia inducing motifs) require on-going protein palmitoylation and are modulated by a specific GTPase, Cdc42, that regulates actin dynamics. We also show that their function is palmitoylation dependent and is dynamically regulated by reversible protein palmitoylation. Significantly, our work suggests a general role for those palmitoylated motifs in the development of structures important for synapse formation and maturation. We combined several approaches to monitor the formation and development of filopodia. We show that filopodia continuously explore the environment and probe for appropriate contacts with presynaptic partners. We find that shortly after establishing a contact with axons, filopodia induce the recruitment of presynaptic elements. Remarkably, we find that expression of acylated motifs or the constitutively active form of cdc-42 enhances filopodia number and motility, but reduces the recruitment of synaptophysin positive presynaptic elements and the probability of forming stable axo-dendritic contacts. We provide evidence for the rapid transformation of filopodia to spines within hours of imaging live neurons and reveal potential molecules that accelerate this process.
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Arstikaitis, Pamela. "The role of filopodia in the formation of spine synapses." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/32688.

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In the mammalian brain, excitatory (glutamatergic) synapses are mainly located on dendritic spines; bulbous protrusions enriched with F-actin. Dendritic filopodia are thin protrusions thought to be involved in the development of spines. However, limited evidence illustrating the emergence of spines from filopodia has been found. In addition, the molecular machinery required for filopodia induction and transformation to spines is not well understood. Paralemmin-1 has been shown to induce cell expansion and process formation and is concentrated at the plasma membrane, in part through a lipid modification known as palmitoylation. Palmitoylation of paralemmin-1 may also serve as a signal for its delivery to subcellular lipid microdomains to induce changes in cell morphology and membrane dynamics making it a candidate synapse-inducing molecule. Using live imaging as well as loss and gain-of-function approaches, our analysis identifies paralemmin-1 as a regulator of filopodia induction, synapse formation, and spine maturation. We show neuronal activity-driven translocation of paralemmin-1 to membranes induces rapid protrusion expansion, emphasizing the importance of paralemmin-1 in paradigms that control structural changes associated with synaptic plasticity and learning. Finally, we show that knockdown of paralemmin-1 results in loss of filopodia and compromises spine maturation induced by Shank1b, a protein that facilitates rapid transformation of newly formed filopodia to spines. To investigate the role of filopodia in synapse formation, we contrasted the roles of molecules that affect filopodia elaboration and motility, versus those that impact synapse induction and maturation. Expression of the palmitoylated protein motifs found in growth associated protein 43kDa, enhanced filopodia number and motility, but reduced the probability of forming a stable axon-dendrite contact. Conversely, expression of neuroligin-1 (NLG-1), a synapse inducing cell adhesion molecule, resulted in a decrease in filopodia motility, but an increase in the number of stable axonal contacts. Moreover, siRNA knockdown of NLG-1, reduced the number of presynaptic contacts formed. Postsynaptic scaffolding proteins such as Shank1b, a protein that induces the maturation of spine synapses, reduced filopodia number, but increased the stabilization of the initial contact with axons. These results suggest that increased filopodia stability and not density may be the rate-limiting step for synapse formation.
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Lee, Kwonmoo. "Self-assembly of filopodia-like structures on supported lipid bilayers." Thesis, Massachusetts Institute of Technology, 2010. http://hdl.handle.net/1721.1/62648.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Physics, 2010.
Cataloged from PDF version of thesis.
Includes bibliographical references (p. 98-121).
Filopodia are finger-like protrusive structures of cells, comprised of actin bundles, which can serve as sensory organelles. To probe their pathway of assembly we have reconstituted filopodia-like structures (FLSs) by applying frog egg extracts to supported lipid bilayers containing phosphatidylinositol(4,5)bisphosphate, PI(4,5)P 2. The FLSs recapitulate important characteristics of filopodia - they assemble parallel actin bundles from the lipid membrane and they form in the presence of capping activity. Known filopodial tip components such as Diaphanous-related formin and VASP localize to the membrane base of the structures, and bundling protein fascin to the shaft. Actin subunits assemble at the tip and translocate into the shaft. FLS assembly requires negativelycharged lipid membranes, with specific requirements for PI(4,5)P 2 and, for maximal efficiency, phosphatidyl-serine. The focal nature of FLSs is not a result of templating by PI(4,5)P2 microdomains but instead by the self-organization of tip complex assembly on uniform PI(4,5)P 2-enriched regions. BAR domain protein toca-1 recruits N-WASP then the Arp2/3 complex and actin assembly follow. Elongation proteins Diaphanous-related formin, VASP and fascin are recruited later. The Arp2/3 complex is absolutely required for FLS initiation but is not required for elongation, which may involve multiple factors including formins. We propose a model for filopodia formation involving an initial clustering of Arp 2/3 complex regulators, self-assembly of filopodial tip complexes on the membrane, resulting in the outgrowth of parallel actin bundles.
by Kwonmoo Lee.
Ph.D.
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De, Arpan. "Role of RHO- Family Guanosine Triphosphatase Effectors in Filopodia Dynamics." Bowling Green State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=bgsu1440176135.

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Lourenco, da Conceicao Luz Marta. "Cellular mechanisms involved in Wnt8 distribution and function in zebrafish neurectoderm patterning." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2008. http://nbn-resolving.de/urn:nbn:de:bsz:14-ds-1228815553128-55176.

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Wnt proteins have key roles in patterning of multicellular animals, acting at a distance from their sites of production. However, it is not well understood how these molecules propagate. This question has become even more puzzling by the discovery that Wnts harbour post-translational lipid-modifications, which enhance association with membranes and may therefore limit propagation by simple diffusion in an aqueous environment. The cellular mechanisms involved in Wnt propagation are largely unknown for vertebrate organisms. Here, I discuss my findings on the cellular localization of zebrafish Wnt8, as an example of a vertebrate Wnt. Wnt8 is a key signal for positioning the midbrain-hindbrain brain boundary (MHB) organizer along the anterior-posterior axis of the developing brain in vertebrates. However, it is not clear how this protein propagates from its source, the blastoderm margin, to the target cells, in the prospective neural plate. For this purpose, I have analysed a biologically active, fluorescently tagged Wnt8 in live zebrafish embryos. Wnt8 was present in live tissue in membrane associated punctate structures. In Wnt8 expressing cells these puncta localise to filopodial cellular processes, from which the protein is released to neighbouring cells. This filopodial release requires posttranslational palmitoylation. Although palmitoylation-defective Wnt8 retains auto- and juxtacrine signaling activity, it fails to signal over a long-range. Additionally, this Wnt8 palmitoylation is necessary for regulation of its neural plate target genes. These results suggest that vertebrate Wnt proteins use cell-to-cell contact through filopodia as a shortrange propagation mechanism while released palmitoylated Wnt is required for longrange signaling activity. Furthermore, I show that a Wnt8 receptor, Frizzled9 can negatively influence Wnt8 propagation and signaling range. Finally, I was able to determine the presence of an endogenous Wnt8 gradient in the neurectoderm. I discuss these findings in the context of Wnt8 signaling function in mediating anterior-posterior patterning during early brain development.
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Ezeanochie, Tochukwu Chinedu. "Modelling and Simulation of Filopodial Protrusion." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/32781.

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The effect of substrate surface topology on the interaction of living cells with inanimate substrates is a well-established phenomenon. When cells are placed on biomaterials, they outgrow protrusions called filopodia that sense surface features in their immediate surroundings and initiate the formation of stable cell adhesion complexes closer to the cell body. Adhesion proteins permit filopodia to constantly explore the surrounding microenvironment. A better understanding of the relationship of filopodia with surface features is highly relevant for exploiting custom-made surfaces to guide cell activity. In this work, mathematical modeling and simulation were used to describe different phenomena related to the interaction of a filopodium with its microenvironment, with the aim of reproducing experimentally observed phenomena associated to filopodia growth and interactions with substrates. The Kelvin Voigt model was used for the viscoelastic response of filopodia. Result predict filopodia protrusion under test conditions and helps improving our understanding on the effect of substrate topology on the biomechanical response of filopodial extensions.
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Evers, Jan Felix. "The role of dendritic filopodia in postembryonic remodelling of dendritic architecture." [S.l. : s.n.], 2005. http://www.diss.fu-berlin.de/2005/153/index.html.

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Michiels, Rebecca [Verfasser], and Alexander [Akademischer Betreuer] Rohrbach. "Investigation of filopodia dynamics in macrophage cells by photonic force microscopy." Freiburg : Universität, 2019. http://d-nb.info/1185977295/34.

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Books on the topic "Filopodia"

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Gori, Marcello, Sara Forti, and Mario Gori. Non Posso Darti Altro Che Parole: Filopoesia. Independently Published, 2018.

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Book chapters on the topic "Filopodia"

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Jacquemet, Guillaume, Hellyeh Hamidi, and Johanna Ivaska. "Filopodia Quantification Using FiloQuant." In Computer Optimized Microscopy, 359–73. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9686-5_16.

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Jacquemet, Guillaume. "Mapping the Localization of Proteins Within Filopodia Using FiloMap." In Cell Migration in Three Dimensions, 51–61. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2887-4_4.

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Small, J. Victor, and Klemens Rottner. "Elementary Cellular Processes Driven by Actin Assembly: Lamellipodia and Filopodia." In Actin-based Motility, 3–33. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9301-1_1.

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Gallo, Gianluca. "The Neuronal Actin Cytoskeleton and the Protrusion of Lamellipodia and Filopodia." In Advances in Neurobiology, 7–22. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-7368-9_2.

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Hely, Tim A., Arjen van Ooyen, and David J. Willshaw. "A Simulation of Growth Cone Filopodia Dynamics Based on Turing Morphogenesis Patterns." In Information Processing in Cells and Tissues, 69–73. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5345-8_8.

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Aarts, L. H. J., H. B. Nielander, A. B. Oestreicher, L. H. Schrama, W. H. Gispen, and P. Schotman. "Overexpression of B-50/GAP-43 Induces Formation of Filopodia in PC12 Cells." In Neurochemistry, 1107–10. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5405-9_186.

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Peterlík, Igor, David Svoboda, Vladimír Ulman, Dmitry V. Sorokin, and Martin Maška. "Model-Based Generation of Synthetic 3D Time-Lapse Sequences of Multiple Mutually Interacting Motile Cells with Filopodia." In Simulation and Synthesis in Medical Imaging, 71–79. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-030-00536-8_8.

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"Filopodia." In Encyclopedia of Parasitology, 1013. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-43978-4_1197.

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Robles, E., S. J. Smith, and M. P. Meyer. "Synaptic Precursors: Filopodia." In Encyclopedia of Neuroscience, 779–86. Elsevier, 2009. http://dx.doi.org/10.1016/b978-008045046-9.00361-2.

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Svitkina, T. M. "Filopodia and Lamellipodia." In Encyclopedia of Cell Biology, 683–93. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-394447-4.20066-7.

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Conference papers on the topic "Filopodia"

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Maska, Martin, Xabier Morales, Arrate Munoz-Barrutia, Ana Rouzaut, and Carlos Ortiz-de-Solorzano. "Automatic quantification of filopodia-based cell migration." In 2013 IEEE 10th International Symposium on Biomedical Imaging (ISBI 2013). IEEE, 2013. http://dx.doi.org/10.1109/isbi.2013.6556563.

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Ahmed, Sohail, Amy Chou, K. P. Sem, Sudaharan Thankiah, Graham Wright, John Lim, and Srivats Hariharan. "Using dSTORM to probe the molecular architecture of filopodia." In SPIE BiOS, edited by Jörg Enderlein, Ingo Gregor, Zygmunt K. Gryczynski, Rainer Erdmann, and Felix Koberling. SPIE, 2014. http://dx.doi.org/10.1117/12.2058123.

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Bathe, Mark, Claus Heussinger, Mireille Claessens, Andreas Bausch, and Erwin Frey. "Cytoskeletal Bundle Mechanics." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176170.

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Abstract:
Filamentous actin (F-actin) is a stiff biopolymer that is tightly crosslinked in vivo by actin-binding proteins (ABPs) to form stiff bundles that form major constituents of a multitude of slender cytoskeletal processes including stereocilia, filopodia, microvilli, neurosensory bristles, cytoskeletal stress fibers, and the acrosomal process of sperm cells (Fig. 1). The mechanical properties of these cytoskeletal processes play key roles in a broad range of cellular functions — the bending stiffness of stereocilia mediates the mechanochemical transduction of mechanical stimuli such as acoustic waves to detect sound, the critical buckling load of filopodia and acrosomal processes determines their ability to withstand compressive mechanical forces generated during cellular locomotion and fertilization, and the entropic stretching stiffness of cytoskeletal bundles mediates cytoskeletal mechanical resistance to cellular deformation. Thus, a detailed understanding of F-actin bundle mechanics is fundamental to gaining a mechanistic understanding of cytoskeletal function.
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Jung, Uijin, Tetsuo Kan, Kenta Kuwana, Kiyoshi Matsumoto, and Isao Shimoyama. "Si nano-pillars for measuring traction force exerted by filopodia." In TRANSDUCERS 2011 - 2011 16th International Solid-State Sensors, Actuators and Microsystems Conference. IEEE, 2011. http://dx.doi.org/10.1109/transducers.2011.5969359.

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Wang, Jing, Svetlana V. Boriskina, Hongyun Wang, and Björn M. Reinhard. "Illuminating Epidermal Growth Factor Receptor Densities on Filopodia through Plasmon Coupling." In Optical Sensors. Washington, D.C.: OSA, 2012. http://dx.doi.org/10.1364/sensors.2012.sth2b.3.

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Heckman, Carol A., and Surya P. Amarachintha. "Abstract 3032: Role of ruffles and filopodia in adhesion gradient sensing." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3032.

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Lee, Chau-Hwang, Tsi-Hsuan Hsu, Wei-Yu Liao, Pan-Chyr Yang, Chun-Chieh Wang, and Jian-Long Xiao. "Cancer Cell Filopodia Characterized by Super-resolution Bright-field Optical Microscopy." In CLEO 2007. IEEE, 2007. http://dx.doi.org/10.1109/cleo.2007.4452966.

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De Moura, Carlos, Mauricio Kritz, Thiago Leal, and Andreas Prokop. "Biological Systems at Sub-cellular Scale: Investigation of G-actin Transport in Filopodia." In CNMAC 2016 - XXXVI Congresso Nacional de Matemática Aplicada e Computacional. SBMAC, 2017. http://dx.doi.org/10.5540/03.2017.005.01.0068.

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Kiso, Marina, Sunao Tanaka, Masakazu Toi, and Fumiaki Sato. "Abstract 1885: VEGFA/NRP1 signal contributes to filopodia formation in breast cancer cells." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1885.

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Sorokin, Dmitry V., Igor Peterlik, Vladimir Ulman, David Svoboda, and Martin Maska. "Model-based generation of synthetic 3D time-lapse sequences of motile cells with growing filopodia." In 2017 IEEE 14th International Symposium on Biomedical Imaging (ISBI 2017). IEEE, 2017. http://dx.doi.org/10.1109/isbi.2017.7950644.

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