Relevant bibliographies by topics / Filopodium

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'Filopodium'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Filopodium"

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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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McConnell, Russell E., J. Edward van Veen, Marina Vidaki, Adam V. Kwiatkowski, Aaron S. Meyer, and Frank B. Gertler. "A requirement for filopodia extension toward Slit during Robo-mediated axon repulsion." Journal of Cell Biology 213, no. 2 (April 18, 2016): 261–74. http://dx.doi.org/10.1083/jcb.201509062.

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Axons navigate long distances through complex 3D environments to interconnect the nervous system during development. Although the precise spatiotemporal effects of most axon guidance cues remain poorly characterized, a prevailing model posits that attractive guidance cues stimulate actin polymerization in neuronal growth cones whereas repulsive cues induce actin disassembly. Contrary to this model, we find that the repulsive guidance cue Slit stimulates the formation and elongation of actin-based filopodia from mouse dorsal root ganglion growth cones. Surprisingly, filopodia form and elongate toward sources of Slit, a response that we find is required for subsequent axonal repulsion away from Slit. Mechanistically, Slit evokes changes in filopodium dynamics by increasing direct binding of its receptor, Robo, to members of the actin-regulatory Ena/VASP family. Perturbing filopodium dynamics pharmacologically or genetically disrupts Slit-mediated repulsion and produces severe axon guidance defects in vivo. Thus, Slit locally stimulates directional filopodial extension, a process that is required for subsequent axonal repulsion downstream of the Robo receptor.
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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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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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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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Heidemann, S. R., P. Lamoureux, and R. E. Buxbaum. "Growth cone behavior and production of traction force." Journal of Cell Biology 111, no. 5 (November 1, 1990): 1949–57. http://dx.doi.org/10.1083/jcb.111.5.1949.

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The growth cone must push its substrate rearward via some traction force in order to propel itself forward. To determine which growth cone behaviors produce traction force, we observed chick sensory growth cones under conditions in which force production was accommodated by movement of obstacles in the environment, namely, neurites of other sensory neurons or glass fibers. The movements of these obstacles occurred via three, different, stereotyped growth cone behaviors: (a) filopodial contractions, (b) smooth rearward movement on the dorsal surface of the growth cone, and (c) interactions with ruffling lamellipodia. More than 70% of the obstacle movements were caused by filopodial contractions in which the obstacle attached at the extreme distal end of a filopodium and moved only as the filopodium changed its extension. Filopodial contractions were characterized by frequent changes of obstacle velocity and direction. Contraction of a single filopodium is estimated to exert 50-90 microdyn of force, which can account for the pull exerted by chick sensory growth cones. Importantly, all five cases of growth cones growing over the top of obstacle neurites (i.e., geometry that mimics the usual growth cone/substrate interaction), were of the filopodial contraction type. Some 25% of obstacle movements occurred by a smooth backward movement along the top surface of growth cones. Both the appearance and rate of movements were similar to that reported for retrograde flow of cortical actin near the dorsal growth cone surface. Although these retrograde flow movements also exerted enough force to account for growth cone pulling, we did not observe such movements on ventral growth cone surfaces. Occasionally obstacles were moved by interaction with ruffling lamellipodia. However, we obtained no evidence for attachment of the obstacles to ruffling lamellipodia or for directed obstacle movements by this mechanism. These data suggest that chick sensory growth cones move forward by contractile activity of filopodia, i.e., isometric contraction on a rigid substrate. Our data argue against retrograde flow of actin producing traction force.
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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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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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Miyashita, Motoaki, Hiroshi Ohnishi, Hideki Okazawa, Hiroyasu Tomonaga, Akiko Hayashi, Tetsuro-Takahiro Fujimoto, Nobuhiko Furuya, and Takashi Matozaki. "Promotion of Neurite and Filopodium Formation by CD47: Roles of Integrins, Rac, and Cdc42." Molecular Biology of the Cell 15, no. 8 (August 2004): 3950–63. http://dx.doi.org/10.1091/mbc.e04-01-0019.

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Axon extension during development is guided by many factors, but the signaling mechanisms responsible for its regulation remain largely unknown. We have now investigated the role of the transmembrane protein CD47 in this process in N1E-115 neuroblastoma cells. Forced expression of CD47 induced the formation of neurites and filopodia. Furthermore, an Fc fusion protein containing the extracellular region of the CD47 ligand SHPS-1 induced filopodium formation, and this effect was enhanced by CD47 overexpression. SHPS-1–Fc also promoted neurite and filopodium formation triggered by serum deprivation. Inhibition of Rac or Cdc42 preferentially blocked CD47-induced formation of neurites and filopodia, respectively. Overexpression of CD47 resulted in the activation of both Rac and Cdc42. The extracellular region of CD47 was sufficient for the induction of neurite formation by forced expression, but the entire structure of CD47 was required for enhancement of filopodium formation by SHPS-1–Fc. Neurite formation induced by CD47 was also inhibited by a mAb to the integrin β3 subunit. These results indicate that the interaction of SHPS-1 with CD47 promotes neurite and filopodium formation through the activation of Rac and Cdc42, and that integrins containing the β3 subunit participate in the effect of CD47 on neurite formation.
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Mallavarapu, Aneil, and Tim Mitchison. "Regulated Actin Cytoskeleton Assembly at Filopodium Tips Controls Their Extension and Retraction." Journal of Cell Biology 146, no. 5 (September 6, 1999): 1097–106. http://dx.doi.org/10.1083/jcb.146.5.1097.

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The extension and retraction of filopodia in response to extracellular cues is thought to be an important initial step that determines the direction of growth cone advance. We sought to understand how the dynamic behavior of the actin cytoskeleton is regulated to produce extension or retraction. By observing the movement of fiduciary marks on actin filaments in growth cones of a neuroblastoma cell line, we found that filopodium extension and retraction are governed by a balance between the rate of actin cytoskeleton assembly at the tip and retrograde flow. Both assembly and flow rate can vary with time in a single filopodium and between filopodia in a single growth cone. Regulation of assembly rate is the dominant factor in controlling filopodia behavior in our system.
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Dissertations / Theses on the topic "Filopodium"

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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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Lourenco, da Conceicao Luz Marta. "Cellular mechanisms involved in Wnt8 distribution and function in zebrafish neurectoderm patterning." Doctoral thesis, Technische Universität Dresden, 2007. https://tud.qucosa.de/id/qucosa%3A23716.

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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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Durkaya, Göksel. "Nanoscopic Investigation of Surface Morphology of Neural Growth Cones and Indium Containing Group-III Nitrides." Digital Archive @ GSU, 2009. http://digitalarchive.gsu.edu/phy_astr_diss/43.

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This research focuses on the nanoscopic investigation of the three-dimensional surface morphology of the neural growth cones from the snail Helisoma trivolvis, and InN and InGaN semiconductor material systems using Atomic Force Microscopy (AFM). In the analysis of the growth cones, the results obtained from AFM experiments have been used to construct a 3D architecture model for filopodia. The filopodia from B5 and B19 neurons have exhibited different tapering mechanisms. The volumetric analysis has been used to estimate free Ca2+ concentration in the filopodium. The Phase Contrast Microscopy (PCM) images of the growth cones have been corrected to thickness provided by AFM in order to analyze the spatial refractive index variations in the growth cone. AFM experiments have been carried out on InN and InGaN epilayers. Ternary InGaN alloys are promising for device applications tunable from ultraviolet (Eg[GaN]=3.4 eV) to near-infrared (Eg [InN]=0.7 eV). The real-time optical characteristics and ex-situ material properties of InGaN epilayers have been analyzed and compared to the surface morphological properties in order to investigate the relation between the growth conditions and overall physical properties. The effects of composition, group V/III molar ratio and temperature on the InGaN material characteristics have been studied and the growth of high quality indium-rich InGaN epilayers are demonstrated.
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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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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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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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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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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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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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Book chapters on the topic "Filopodium"

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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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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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Vignjevic, Danijela, John Peloquin, and Gary G. Borisy. "In Vitro Assembly of Filopodia‐Like Bundles." In Methods in Enzymology, 727–39. Elsevier, 2006. http://dx.doi.org/10.1016/s0076-6879(06)06057-5.

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Conference papers on the topic "Filopodium"

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Lee, Chau-Hwang. "Label-free observation of cancer-cell filopodium activities using structured illumination nanoprofilometry." In 2015 Opto-Electronics and Communications Conference (OECC). IEEE, 2015. http://dx.doi.org/10.1109/oecc.2015.7340191.

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Maska, Martin, Tereza Necasova, David Wiesner, Dmitry V. Sorokin, Igor Peterlik, Vladimir Ulman, and David Svoboda. "Toward Robust Fully 3D Filopodium Segmentation and Tracking in Time-Lapse Fluorescence Microscopy." In 2019 IEEE International Conference on Image Processing (ICIP). IEEE, 2019. http://dx.doi.org/10.1109/icip.2019.8803721.

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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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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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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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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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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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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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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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