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Relevant bibliographies by topics / Cytoskeleton model

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Academic literature on the topic 'Cytoskeleton model'

Author: Grafiati

Published: 4 June 2021

Last updated: 14 February 2022

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Journal articles on the topic "Cytoskeleton model"

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Durand-Smet, Pauline, Tamsin A. Spelman, Elliot M. Meyerowitz, and Henrik Jönsson. "Cytoskeletal organization in isolated plant cells under geometry control." Proceedings of the National Academy of Sciences 117, no. 29 (July 8, 2020): 17399–408. http://dx.doi.org/10.1073/pnas.2003184117.

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The cytoskeleton plays a key role in establishing robust cell shape. In animals, it is well established that cell shape can also influence cytoskeletal organization. Cytoskeletal proteins are well conserved between animal and plant kingdoms; nevertheless, because plant cells exhibit major structural differences to animal cells, the question arises whether the plant cytoskeleton also responds to geometrical cues. Recent numerical simulations predicted that a geometry-based rule is sufficient to explain the microtubule (MT) organization observed in cells. Due to their high flexural rigidity and persistence length of the order of a few millimeters, MTs are rigid over cellular dimensions and are thus expected to align along their long axis if constrained in specific geometries. This hypothesis remains to be testedin cellulo. Here, we explore the relative contribution of geometry to the final organization of actin and MT cytoskeletons in single plant cells ofArabidopsis thaliana. We show that the cytoskeleton aligns with the long axis of the cells. We find that actin organization relies on MTs but not the opposite. We develop a model of self-organizing MTs in three dimensions, which predicts the importance of MT severing, which we confirm experimentally. This work is a first step toward assessing quantitatively how cellular geometry contributes to the control of cytoskeletal organization in living plant cells.

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Akram, Zain, Ishtiaq Ahmed, Heike Mack, Ramandeep Kaur, Richard C. Silva, Beatriz A. Castilho, Sylvie Friant, Evelyn Sattlegger, and Alan L. Munn. "Yeast as a Model to Understand Actin-Mediated Cellular Functions in Mammals—Illustrated with Four Actin Cytoskeleton Proteins." Cells 9, no. 3 (March 10, 2020): 672. http://dx.doi.org/10.3390/cells9030672.

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The budding yeast Saccharomyces cerevisiae has an actin cytoskeleton that comprises a set of protein components analogous to those found in the actin cytoskeletons of higher eukaryotes. Furthermore, the actin cytoskeletons of S. cerevisiae and of higher eukaryotes have some similar physiological roles. The genetic tractability of budding yeast and the availability of a stable haploid cell type facilitates the application of molecular genetic approaches to assign functions to the various actin cytoskeleton components. This has provided information that is in general complementary to that provided by studies of the equivalent proteins of higher eukaryotes and hence has enabled a more complete view of the role of these proteins. Several human functional homologues of yeast actin effectors are implicated in diseases. A better understanding of the molecular mechanisms underpinning the functions of these proteins is critical to develop improved therapeutic strategies. In this article we chose as examples four evolutionarily conserved proteins that associate with the actin cytoskeleton: (1) yeast Hof1p/mammalian PSTPIP1, (2) yeast Rvs167p/mammalian BIN1, (3) yeast eEF1A/eEF1A1 and eEF1A2 and (4) yeast Yih1p/mammalian IMPACT. We compare the knowledge on the functions of these actin cytoskeleton-associated proteins that has arisen from studies of their homologues in yeast with information that has been obtained from in vivo studies using live animals or in vitro studies using cultured animal cell lines.

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Wang, Jizeng, and Long Li. "Coupled elasticity–diffusion model for the effects of cytoskeleton deformation on cellular uptake of cylindrical nanoparticles." Journal of The Royal Society Interface 12, no. 102 (January 2015): 20141023. http://dx.doi.org/10.1098/rsif.2014.1023.

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Molecular dynamic simulations and experiments have recently demonstrated how cylindrical nanoparticles (CNPs) with large aspect ratios penetrate animal cells and inevitably deform cytoskeletons. Thus, a coupled elasticity–diffusion model was adopted to elucidate this interesting biological phenomenon by considering the effects of elastic deformations of cytoskeleton and membrane, ligand–receptor binding and receptor diffusion. The mechanism by which the binding energy drives the CNPs with different orientations to enter host cells was explored. This mechanism involved overcoming the resistance caused by cytoskeleton and membrane deformations and the change in configurational entropy of the ligand–receptor bonds and free receptors. Results showed that deformation of the cytoskeleton significantly influenced the engulfing process by effectively slowing down and even hindering the entry of the CNPs. Additionally, the engulfing depth was determined quantitatively. CNPs preferred or tended to vertically attack target cells until they were stuck in the cytoskeleton as implied by the speed of vertically oriented CNPs that showed much faster initial engulfing speeds than horizontally oriented CNPs. These results elucidated the most recent molecular dynamics simulations and experimental observations on the cellular uptake of carbon nanotubes and phagocytosis of filamentous Escherichia coli bacteria. The most efficient engulfment showed the stiffness-dependent optimal radius of the CNPs. Cytoskeleton stiffness exhibited more significant influence on the optimal sizes of the vertical uptake than the horizontal uptake.

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Ning, Liang, Hani Y. Suleiman, and Jeffrey H. Miner. "Synaptopodin deficiency exacerbates kidney disease in a mouse model of Alport syndrome." American Journal of Physiology-Renal Physiology 321, no. 1 (July 1, 2021): F12—F25. http://dx.doi.org/10.1152/ajprenal.00035.2021.

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Alport syndrome (AS) is a hereditary disease of the glomerular basement with hematuria and proteinuria. Podocytes eventually exhibit foot process effacement, indicating actin cytoskeletal changes. To investigate how cytoskeletal changes impact podocytes, we generated Alport mice lacking synaptopodin, an actin-binding protein in foot processes. Analysis showed a more rapid disease progression, demonstrating that synaptopodin is protective. This suggests that the actin cytoskeleton is a target for therapy in AS and perhaps other glomerular diseases.

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REDONDO, Pedro C., Ana I. LAJAS, Ginés M. SALIDO, Antonio GONZALEZ, Juan A. ROSADO, and José A. PARIENTE. "Evidence for secretion-like coupling involving pp60src in the activation and maintenance of store-mediated Ca2+ entry in mouse pancreatic acinar cells." Biochemical Journal 370, no. 1 (February 15, 2003): 255–63. http://dx.doi.org/10.1042/bj20021505.

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Store-mediated Ca2+ entry (SMCE) is one of the main pathways for Ca2+ influx in non-excitable cells. Recent studies favour a secretion-like coupling mechanism to explain SMCE, where Ca2+ entry is mediated by an interaction of the endoplasmic reticulum (ER) with the plasma membrane (PM) and is modulated by the actin cytoskeleton. To explore this possibility further we have now investigated the role of the actin cytoskeleton in the activation and maintenance of SMCE in pancreatic acinar cells, a more specialized secretory cell type which might be an ideal cellular model to investigate further the properties of the secretion-like coupling model. In these cells, the cytoskeletal disrupters cytochalasin D and latrunculin A inhibited both the activation and maintenance of SMCE. In addition, stabilization of a cortical actin barrier by jasplakinolide prevented the activation, but not the maintenance, of SMCE, suggesting that, as for secretion, the actin cytoskeleton plays a double role in SMCE as a negative modulator of the interaction between the ER and PM, but is also required for this mechanism, since the cytoskeleton disrupters impaired Ca2+ entry. Finally, depletion of the intracellular Ca2+ stores induces cytoskeletal association and activation of pp60src, which is independent on Ca2+ entry. pp60src activation requires the integrity of the actin cytoskeleton and participates in the initial phase of the activation of SMCE in pancreatic acinar cells.

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Jean, Ronald P., Christopher S. Chen, and Alexander A. Spector. "Finite-Element Analysis of the Adhesion-Cytoskeleton-Nucleus Mechanotransduction Pathway During Endothelial Cell Rounding: Axisymmetric Model." Journal of Biomechanical Engineering 127, no. 4 (January 20, 2005): 594–600. http://dx.doi.org/10.1115/1.1933997.

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Endothelial cells possess a mechanical network connecting adhesions on the basal surface, the cytoskeleton, and the nucleus. Transmission of force at adhesions via this pathway can deform the nucleus, ultimately resulting in an alteration of gene expression and other cellular changes (mechanotransduction). Previously, we measured cell adhesion area and apparent nuclear stretch during endothelial cell rounding. Here, we reconstruct the stress map of the nucleus from the observed strains using finite-element modeling. To simulate the disruption of adhesions, we prescribe displacement boundary conditions at the basal surface of the axisymmetric model cell. We consider different scenarios of the cytoskeletal arrangement, and represent the cytoskeleton as either discrete fibers or as an effective homogeneous layer. When the nucleus is in the initial (spread) state, cytoskeletal tension holds the nucleus in an elongated, ellipsoidal configuration. Loss of cytoskeletal tension during cell rounding is represented by reactive forces acting on the nucleus in the model. In our simulations of cell rounding, we found that, for both representations of the cytoskeleton, the loss of cytoskeletal tension contributed more to the observed nuclear deformation than passive properties. Since the simulations make no assumption about the heterogeneity of the nucleus, the stress components both within and on the surface of the nucleus were calculated. The nuclear stress map showed that the nucleus experiences stress on the order of magnitude that can be significant for the function of DNA molecules and chromatin fibers. This study of endothelial cell mechanobiology suggests the possibility that mechanotransduction could result, in part, from nuclear deformation, and may be relevant to angiogenesis, wound healing, and endothelial barrier dysfunction.

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Symington, Alison L., Selma Zimmerman, and A. M. Zimmerman. "The influence of hydrostatic pressure on the distribution of histone mRNA in HeLa cells." Biochemistry and Cell Biology 71, no. 3-4 (March 1, 1993): 150–55. http://dx.doi.org/10.1139/o93-024.

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Hydrostatic pressure and HeLa S3 cells were used (as a model system) to investigate the relationship of the cytoskeleton and histone gene expression. Exposure of HeLa S3 cells to hydrostatic pressure of 1000 – 10 000 psi (6.89 × 103 – 6.89 × 104 kPa) disrupts the cytoskeleton and reduces H1 and core histone mRNA and actin mRNA levels as determined by hybridization to specific DNA probes. Soluble and insoluble cell fractions were isolated from HeLa cells after lysis in Triton X-100 buffered with PIPES and being subjected to low-speed centrifugation. The insoluble fraction was designated the cytoskeletal fraction. At atmospheric pressure, 76% of H4 histone mRNA is associated with the cytoskeletal fraction and 24% of the H4 histone mRNA is in the soluble fraction. At 6000 and 10 000 psi for a duration of 10 min, H4 mRNA levels in the cytoskeletal fraction were reduced to 52 and 41%, respectively. The reduction of mRNA in the cytoskeletal fraction is accompanied by a corresponding increase of mRNA in the soluble cell fraction. The other core (H2A, H2B, and H3) and H1 histone mRNA transcripts exhibited similar sensitivity to pressure treatment. The effects of pressure on histone gene regulation may be mediated through alteration of mRNA–cytoskeleton association.Key words: cytoskeleton, HeLa cells, histone mRNA, hydrostatic pressure.

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Clark, J. I., J. M. Clark, L. L. David, and H. Matsushima. "Lens cytoskeleton and transparency: A model." Eye 13, no. 3 (May 1999): 417–24. http://dx.doi.org/10.1038/eye.1999.116.

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Liu, Fei, Dan Wu, Xiaoyong Wu, and Ken Chen. "Analyses of the cell mechanical damage during microinjection." Soft Matter 11, no. 7 (2015): 1434–42. http://dx.doi.org/10.1039/c4sm02773f.

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The structure of the cell mechanical model. The cell model contains the membrane networks, the internal cytoskeleton, ACPs, motors and their functions, including the binding/unbinding and the folding/unfolding of the proteins, the polymerization/depolymerization of cytoskeletal filaments, and the walk of motors.

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Dufort, Paul A., and Charles J. Lumsden. "Cellular automaton model of the actin cytoskeleton." Cell Motility and the Cytoskeleton 25, no. 1 (1993): 87–104. http://dx.doi.org/10.1002/cm.970250110.

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Dissertations / Theses on the topic "Cytoskeleton model"

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Lane, D. C. "A mathematical investigation of a mechanochemical model for the cytoskeleton." Thesis, University of Oxford, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.379843.

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Dewolf, Christine Elizabeth. "Properties of model biological membranes." Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244082.

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Muddana, Hari Shankar. "Integrated biomechanical model of cells embedded in extracellular matrix." [College Station, Tex. : Texas A&M University, 2006. http://hdl.handle.net/1969.1/ETD-TAMU-1074.

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Monreal, Gretel. "Ventricular Remodeling in a Large Animal Model of Heart Failure." The Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=osu1210007937.

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Lewis, Sara Ann. "Functions of Drosophila Pak (p21-activated kinase) in Morphogenesis: A Mechanistic Model based on Cellular, Molecular, and Genetic Studies." Diss., The University of Arizona, 2015. http://hdl.handle.net/10150/594389.

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Intellectual disability (ID) is a common phenotype of brain-development disorders and is heterogeneous in etiology with numerous genetic causes. PAK3 is one gene with multiple mutations causing ID. Affected individuals have microcephaly, and other brain-structure defects have been reported. Additionally, PAK3 is in a genetic network with eighteen other genes whose mutations cause ID, suggesting the molecular mechanisms by which PAK3 regulates of cognitive function may be shared by other genetic ID disorders. Studies in rodent models have shown that the orthologs of PAK3 are important for regulating dendrite spine morphology and postnatal brain size. In Drosophila melanogaster, the morphological processes of oogenesis, dorsal closure during embryogenesis, and salivary gland-lumen formation require Pak, the Drosophila ortholog of PAK3. Additionally, Pak is important for development of the subsynaptic reticulum of the neuromuscular junction, sensory axon pathfinding and terminal arborization in the Drosophila central nervous system (CNS). However, the role of Pak in mushroom body (MB) structure and intrinsic neurite arbor morphogenesis, as well as details of the underlying cellular and molecular mechanisms are unknown. To address this gap, I used Drosophila models of PAK3 gene mutations, Pak, and a combination of immunostaining, primary cell culture, and genetic interaction studies to elucidate these mechanisms. I performed a detailed characterization of the previously reported adult Pak phenotypes of decreased survival as well as leg and wing morphology. I found that decreased survival is a low-penetrance phenotype that is enhanced by chromosomes from the same mutagenesis. Defects of the adult wing include folding and misalignment between the layers, blisters, and missing or partial cross veins. The Pak-mutant legs are short and often misdirected in the pupal case with morphological defects in the shape of the leg segments themselves. The mushroom bodies are important insect learning and memory brain structures whose lobes are composed of axon bundles with individual axons bifurcating to form the α and β lobes. Mutations in Pak cause defects in the length, thickness, and direction of the MB α and β lobes. These defects increase in severity during metamorphosis, when neurogenesis and differentiation of these structures occur, suggesting that Pak stabilizes the branches of the α/β mushroom body neurons. Pak-mutant cultured neurons have reduced neurite arbor size with defects in neurite caliber. Initial outgrowth was normal, followed by a decrease in neurite branch number, again supporting the role of Pak in neurite-branch stability. There are defects in the cytoskeleton in growth cones at six hours post-plating as well as in neurons after three days in vitro. The Pak-mutant phenotype severity depends on the phosphorylation status of myosin regulatory light chain, supporting the mechanistic hypothesis that Pak regulates neurite-branch stability by inhibiting myosin light chain kinase. The neuronal phenotype of decreased branch stability suggests a mechanism of excessive retraction as the cellular pathogenesis underlying PAK3 mutation-associated brain disorders. I used western blotting to characterize the protein products of four nonsense mutations in Drosophila Pak to interpret genotype-phenotype relationships. Each allele has molecularly unique consequences: Pak¹¹, stop-codon read through and truncated protein; Pak¹⁶, no read through, but truncated protein; Pak⁶, read through with no truncated protein; Pak ¹⁴, neither readthrough nor truncated protein. Truncated proteins produced by Pak¹¹ and Pak¹⁶ alleles retained partial function for survival, wing blistering, leg morphology, and neurite length. Conversely, truncated protein increased the severity of the mushroom body defects. Truncated proteins have no effect on neuron branch number, wing folding, or vein defects. Together, these results demonstrate a role of Pak in regulating epithelial morphology, brain structure, and neurite arbor size and complexity. These closely resemble features of the human disorder, providing evidence that this is a good genetic model for this cause of ID.

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Bauer, David. "Využití tensegritních struktur pro modelování mechanického chování hladkých svalových buněk." Master's thesis, Vysoké učení technické v Brně. Fakulta strojního inženýrství, 2011. http://www.nusl.cz/ntk/nusl-229836.

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The master’s thesis deals with the computational modelling of the mechanical testing of isolated smooth muscle cells. The main aims are to create computational model of a cell, to simulate single-axis tensile test and to modify the model so that the model reflects real mechanical response. The model of the cell includes cytoplasm, nucleus, cell membrane and cytoskeleton which is modelled as a tensegrite structure. On this model the tensile test was simulated in case of the cell with cytoskeleton and the cell with distributed the cytoskeleton. Force-elongation curves, which were obtained from this simulation, were compared with experimental data which were taken from literature. Tensile properties were measured on freshly isolated cells from rat thoracic aorta, cultured cells, and cells treated with cytochalasin D to disrupt their actin filaments. It was found that the cytoskeleton influence on the cell load in computational model was smaller than in the real cell. Therefore the model was modified by changing material propreties and geometry so that the model of the cell corresponded with the different types of experimentally measured cells.

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Yadav, Preeti [Verfasser], and Michael [Gutachter] Sendtner. "Studying Neuronal Cytoskeleton Defects and Synaptic Defects in Mouse Model of Amyotrophic Lateral Sclerosis and Spinal Muscular Atrophy / Preeti Yadav. Gutachter: Michael Sendtner." Würzburg : Universität Würzburg, 2016. http://d-nb.info/1113535075/34.

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Kovari, Daniel T. "Investigations of the spreading and closure mechanisms of phagocytosis in J774a.1 macrophages." Diss., Georgia Institute of Technology, 2015. http://hdl.handle.net/1853/54882.

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Phagocytosis is the process by which cells engulf foreign bodies. It is the hallmark behavior of white blood cells, being the process through which those cells ingest and degrade pathogens and debris. To date a large amount of research has focused on documenting the existence and role of biochemical components involved with phagocytosis. Scores of signaling molecules have been implicated in the complex signal cascade which drives the process. These molecules are small (typically no larger than 5 nanometers) and operate in a crowded, chemically “noisy,” environment, yet they coordinate the cell's activity over comparatively expansive distances (as large as 20 micrometers). How these molecular processes scale-up to coordinate the activities of the cell over such massive distances is largely unknown. Using a planar analog of phagocytosis termed “frustrated phagocytosis,” we experimentally demonstrate that phagocytosis occurs in three distinct phases: initial cell-antigen binding, symmetric spreading, and late-stage contraction. Initial binding and symmetric spreading appears to be both mechanically and chemically similar to the quasi-universal cellular behaviors of adhesion and migration. Adhesion and migration have received extensive attention from the biophysics community in recent years. Leveraging these similarities, we adapt the biomechanical frameworks used in models of migration to phagocytosis. We show that macroscopic properties such as a cell's effective viscosity and membrane cortical tension can be used to model cell behavior during phagocytosis. Our experiments reveal that late-stage contraction distinguishes frustrated phagocytosis from other spreading behaviors. This contraction is myosin dependent. Additionally we demonstrate, for the first time, that late-stage contraction corresponds with formation of a contractile F-actin belt. Based on the dynamic contraction model (DC) developed to explain actin structure during cell migration we propose a DC model of phagocytosis which posits that contractile belt formation is the result of a late-stage myosin activity coupled with F-actin.

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Ganay, Thibault. "Caractérisation du modèle murin de la Neuropathie à Axones Géants : rôle de la gigaxonine dans la survie neuronale et l'organisation du cytosquelette." Thesis, Aix-Marseille 2, 2011. http://www.theses.fr/2011AIX22075.

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La Neuropathie à Axones Géants (NAG) est une maladie neurodégénérative rare et fatale caractérisée par une détérioration du système nerveux central et périphérique, impliquant les fonctions motrices et sensorielles. La détérioration massive du système nerveux est accompagnée d'une désorganisation générale des Filaments Intermédiaires ce qui la différencie de nombreuses maladies neurodégénératives où seuls les neurofilaments(NFs) sont affectés. La protéine déficiente, la gigaxonine, est la sous-unité d'une ubiquitine ligase E3, responsable de la reconnaissance spécifique des substrats MAP1B, MAP1S et TBCB, seuls connus à ce jour.Dans le but d'étudier le rôle de la gigaxonine sur la survie neuronale, la désorganisation du cytosquelette et d'avoir un modèle animal suffisamment fort pour envisager des tests thérapeutiques, j'ai caractérisé un modèle murin de NAG. Pour ce faire, j'ai réalisé une étude comportementale des fonctions motrices et sensorielles ainsi qu'une étude histopathologique. Les souris NAG (129/SvJ) développent un phénotype moteur modéré dès 60 semaines alors que les souris NAG (C57BL/6) présentent un phénotype sensoriel dès 60 semaines. Les données histopathologiques ne présentent pas de mort neuronale mais les NFs sont sévèrement altérés. Les NFs sont plus abondant, leur diamètre est augmenté et leur orientation hétérogène, comme c'est observé chez les patients NAG.Nos résultats montrent que l'absence de gigaxonine induit un phénotype moteur et sensoriel modéré mais par contre reproduit la désorganisation massive des NFs observée chez les patients. Ce modèle va nous permettred'étudier le rôle de la gigaxonine, une ligase E3, sur l'organisation des NFs et ainsi comprendre les processus pathologiques impliqués dans d'autres maladies neurodégénératives caractérisée par une accumulation des NFs et un dysfonctionnement du système ubiquitine-protéasome comme les maladies d'Azheimer, de Parkinson etd'huntington ou la sclérose latérale amyotrophique
Giant Axonal Neuropathy (GAN) is a rare and fatale neurodegenerative disorder characterized by a deterioration of the peripheral and central nervous system. The broad deterioration of the nervous system is accompanied with a general disorganization of the Intermediate Filaments which makes it different from other neurodegenerative disorders wherein only neurofilaments (NFs) are affected. The defective protein, gigaxonin, is the substrate adaptator of an E3 ubiquitin ligase, in charge of the specific recognition of MAP1B, MAP1S and TBCB. In order to study the role of gigaxonin on neuronal survival, the cytoskeleton disorganization and to have a relevant GAN animal model to evaluate efficacy of GAN treatments, I have characterized a GAN mouse model. I did a motor and sensory behavioural study and an histopathologic study. The GAN mice (129/SvJ) shown mild motordeficits starting at 60 weeks of age while sensory deficits were evidenced in C57BL/6 GAN mice. No apparent neurodegeneration was evidenced in GAN mice, but dysregulation of NFs was massive. NFs were more abundant, they shown the abnormal increased diameter and misorientation that are characteristics of the human pathology. Our results show that gigaxonin depletion induces mild motor and sensory deficits but recapitulates the severe NFs dysregulation seen in patients. Our model will allow us to study the role of the gigaxonin-E3 ligase in organizing NFs and understand the pathological processes engaged in other neurodegenerative disorders characterized by accumulation of NFs and dysfunction of the Ubiquitin Proteasome System, such as Amyotrophic Lateral Sclerosis, Huntington's, Alzheimer's and Parkinson's diseases

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Henninger, Nils. "Inhibiting Axon Degeneration in a Mouse Model of Acute Brain Injury Through Deletion of Sarm1." eScholarship@UMMS, 2017. http://escholarship.umassmed.edu/gsbs_diss/900.

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Traumatic brain injury (TBI) is a leading cause of disability worldwide. Annually, 150 to 200/1,000,000 people become disabled as a result of brain trauma. Axonal degeneration is a critical, early event following TBI of all severities but whether axon degeneration is a driver of TBI remains unclear. Molecular pathways underlying the pathology of TBI have not been defined and there is no efficacious treatment for TBI. Despite this significant societal impact, surprisingly little is known about the molecular mechanisms that actively drive axon degeneration in any context and particularly following TBI. Although severe brain injury may cause immediate disruption of axons (primary axotomy), it is now recognized that the most frequent form of traumatic axonal injury (TAI) is mediated by a cascade of events that ultimately result in secondary axonal disconnection (secondary axotomy) within hours to days. Proposed mechanisms include immediate post-traumatic cytoskeletal destabilization as a direct result of mechanical breakage of microtubules, as well as catastrophic local calcium dysregulation resulting in microtubule depolymerization, impaired axonal transport, unmitigated accumulation of cargoes, local axonal swelling, and finally disconnection. The portion of the axon that is distal to the axotomy site remains initially morphologically intact. However, it undergoes sudden rapid fragmentation along its full distal length ~72 h after the original axotomy, a process termed Wallerian degeneration. Remarkably, mice mutant for the Wallerian degeneration slow (Wlds) protein exhibit ~tenfold (for 2–3 weeks) suppressed Wallerian degeneration. Yet, pharmacological replication of the Wlds mechanism has proven difficult. Further, no one has studied whether Wlds protects from TAI. Lastly, owing to Wlds presumed gain-of-function and its absence in wild-type animals, direct evidence in support of a putative endogenous axon death signaling pathway is lacking, which is critical to identify original treatment targets and the development of viable therapeutic approaches. Novel insight into the pathophysiology of Wallerian degeneration was gained by the discovery that mutant Drosophila flies lacking dSarm (sterile a/Armadillo/Toll-Interleukin receptor homology domain protein) cell-autonomously recapitulated the Wlds phenotype. The pro-degenerative function of the dSarm gene (and its mouse homolog Sarm1) is widespread in mammals as shown by in vitro protection of superior cervical ganglion, dorsal root ganglion, and cortical neuron axons, as well as remarkable in-vivo long-term survival (>2 weeks) of transected sciatic mouse Sarm1 null axons. Although the molecular mechanism of function remains to be clarified, its discovery provides direct evidence that Sarm1 is the first endogenous gene required for Wallerian degeneration, driving a highly conserved genetic axon death program. The central goals of this thesis were to determine (1) whether post-traumatic axonal integrity is preserved in mice lacking Sarm1, and (2) whether loss of Sarm1 is associated with improved functional outcome after TBI. I show that mice lacking the mouse Toll receptor adaptor Sarm1 gene demonstrate multiple improved TBI-associated phenotypes after injury in a closed-head mild TBI model. Sarm1-/- mice developed fewer beta amyloid precursor protein (βAPP) aggregates in axons of the corpus callosum after TBI as compared to Sarm1+/+ mice. Furthermore, mice lacking Sarm1 had reduced plasma concentrations of the phosphorylated axonal neurofilament subunit H, indicating that axonal integrity is maintained after TBI. Strikingly, whereas wild type mice exhibited a number of behavioral deficits after TBI, I observed a strong, early preservation of neurological function in Sarm1-/- animals. Finally, using in vivo proton magnetic resonance spectroscopy, I found tissue signatures consistent with substantially preserved neuronal energy metabolism in Sarm1-/- mice compared to controls immediately following TBI. My results indicate that the Sarm1-mediated prodegenerative pathway promotes pathogenesis in TBI and suggest that anti-Sarm1 therapeutics are a viable approach for preserving neurological function after TBI.

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Books on the topic "Cytoskeleton model"

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Hameroff, Stuart R. Ultimate computing: Biomolecular consciousness and nanotechnology. Amsterdam: North-Holland, 1987.

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Ultimatecomputing: Biomolecular consciousness and nano technology. Amsterdam: North-Holland, 1987.

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Mofrad, Mohammad R. K., and Roger D. Kamm. Cytoskeletal Mechanics: Models and Measurements in Cell Mechanics. Cambridge University Press, 2011.

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Cytoskeletal Mechanics: Models and Measurements (Cambridge Texts in Biomedical Engineering). Cambridge University Press, 2006.

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Read, Nick D. Fungal cell structure and organization. Edited by Christopher C. Kibbler, Richard Barton, Neil A. R. Gow, Susan Howell, Donna M. MacCallum, and Rohini J. Manuel. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755388.003.0004.

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Human pathogenic fungi produce three basic ‘cell’ types: hyphae, yeast cells, and spores. The organization and subcellular structure of these different cell types and their modes of growth and formation are reviewed. Growth and form is the consequence of how new cell surface is formed. This is generated by the delivery of vesicles to the surface which provides new membrane and the enzymes for cell wall synthesis. To generate these various cell types, the pathway of vesicle secretion to the surface has to be carefully regulated. These vesicles have to be transported through the cell by the cytoskeleton, and in filamentous cells these vesicles accumulate at a supply centre called the Spitzenkörper before docking and fusion with the hyphal apex. Ultimately, membrane is also endocytosed and recycled behind actively expanding regions of the fungal surface. These various processes are described and particular emphasis is given to the structural and organizational features of fungal cells that play roles in their pathogenesis and virulence.

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Book chapters on the topic "Cytoskeleton model"

1

Spira, Micha E., and Hadas Erez. "From an Axon into a Growth Cone After Axotomy: A Model for Cytoskeletal Dynamics." In The Cytoskeleton, 237–63. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-266-7_10.

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Santos, Luís Carlos, Emilia Laura Munteanu, and Nicolas Biais. "An In Vitro Model System to Test Mechano-microbiological Interactions Between Bacteria and Host Cells." In Cytoskeleton Methods and Protocols, 195–212. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3124-8_10.

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Reggio, Hubert, Daniel Louvard, and Evelyne Coudrier. "Membrane Cytoskeleton Interactions, A Model System : The Intestinal Microvilli." In Cellular and Molecular Control of Direct Cell Interactions, 319–22. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-5092-7_18.

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Keković, G., D. Raković, M. V. Satarić, and Dj Koruga. "A Kink-Soliton Model of Charge Transport through Microtubular Cytoskeleton." In Materials Science Forum, 507–12. Stafa: Trans Tech Publications Ltd., 2005. http://dx.doi.org/10.4028/0-87849-971-7.507.

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Bretschneider, Till. "Reinforcement of Cytoskeleton-Matrix Bonds and Tensiotaxis: A Cell-Based Model." In Function and Regulation of Cellular Systems, 279–86. Basel: Birkhäuser Basel, 2004. http://dx.doi.org/10.1007/978-3-0348-7895-1_28.

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Woolf, Nancy J., Avner Priel, and Jack A. Tuszynski. "The Cytoskeleton as a Nanoscale Information Processor: Electrical Properties and an Actin-Microtubule Network Model." In Nanoneuroscience, 85–127. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-03584-5_3.

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Hufnagel, Linda A. "The Cilioprotist Cytoskeleton, a Model for Understanding How Cell Architecture and Pattern Are Specified: Recent Discoveries from Ciliates and Comparable Model Systems." In Methods in Molecular Biology, 251–95. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1661-1_13.

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Lin, Shin, Mary A. Risinger, and James A. Butler. "A Model for Protein-Protein Interactions Involved in the Linkage of the Actin Cytoskeleton to Transmembrane Receptors for Extracellular Matrix Proteins." In Springer Series in Biophysics, 341–44. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-73925-5_61.

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Lindemann, Charles B., and Kathleen A. Lesich. "Detergent-Extracted Models for the Study of Cilia or Flagella." In Cytoskeleton Methods and Protocols, 337–53. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-376-3_19.

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Hackney, C. M., and D. N. Furness. "Observations on the Cytoskeleton and Related Structures of Mammalian Cochlear Hair Cells." In Cochlear Mechanisms: Structure, Function, and Models, 11–20. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5640-0_2.

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Conference papers on the topic "Cytoskeleton model"

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Allen, Kathleen B., and Bradley Layton. "A Mechanical Model for Cytoskeleton and Membrane Interactions in Neuronal Growth Cones." In ASME 2007 International Mechanical Engineering Congress and Exposition. ASMEDC, 2007. http://dx.doi.org/10.1115/imece2007-42008.

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Revealing the molecular events of neuronal growth is critical to obtaining a deeper understanding of nervous system development, neural injury response, and neural tissue engineering. Central to this is the need to understand the mechanical interactions among the cytoskeleton and the cell membrane, and how these interactions affect the overall growth mechanics of neurons. Using ANSYS, the force produced by a cytoskeletal protein acting against a deformable membrane was modeled, and the deformation, stress, and strain were computed for the membrane. Parameters to represent the flexural rigidities of the well-studied actin and tubulin cytoskeletal proteins as well as the mechanical properties of neuronal growth cones were used in the simulations. Our model predicts that while a single actin filament is able to produce a force sufficient to cause membrane deformation and thus growth, it is also possible that the actin filament may cause the membrane to rupture, if a dilatational strain of more than 3–4% occurs. Additionally, neurotoxins or pharmaceuticals that alter the mechanical properties of either the cell membrane or cytoskeletal proteins could disrupt the balance of forces required for neurons to not only push out and grow correctly, but also to sustain their shapes as high-aspect-ratio structures once growth is complete. Understanding how cytoskeletal elements have coevolved mechanically with their respective cell membranes will yield insights into the events that gave rise to the sequences and quaternary structures of the major cytoskeletal elements.

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Coghlan, Karen M., Patrick McGarry, Mohammad R. K. Mofrad, and Peter E. McHugh. "Development of a Discrete Finite Element Cell Model." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176734.

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Computational models have proven useful in the study of cell mechanics and mechanotransduction. While most finite element (FE) models of cells are commonly described in terms of the laws of continuum mechanics, a model that can accurately represent the microstructure of the filamentous network of the cytoskeleton would be required to relate mechanics to biology at the microscale level. An alternative approach to a continuum is presented here, whereby the discrete nature of the cytoskeleton of the cell is emphasized and the known structural properties of the cytoskeleton of the cell are utilized.

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Mehrbod, Mehrdad, and Mohammad R. K. Mofrad. "On the Mechanics of Microtubule Filaments." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53896.

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Quantitative understanding of cell mechanics has challenged biological scientists during the past couple of decades. one of the promising attempts towards mechanical modeling of the cytoskeleton has been the “tensegrity” cytoskeletal model, which simplifies the complex network of cytoskeletal filaments as a structure merely composed of compression-bearing elements (hinge-ended struts) and tensile members (cables). This discrete model can interestingly explain many experimental observations in cell mechanics. However, evidence suggests that the simplicity of this model may undermine the accuracy of its predictions [1–2]. Continuum mechanics predicts that a free, simply-supported beam tends to buckle in the first mode of buckling and that is the case for an in vitro loading of a single microtubule. However, in vivo imaging of microtubules indicates that the buckling mostly occurs in higher modes. This buckling mode switch takes place mostly because of lateral support of microtubules via their connections to actin and intermediate filaments, which themselves are tensile members of the tensegrity cytoskeleton model. Since these loads are exerted throughout the microtubule length, they introduce a considerable amount of microtubule bending behavior. The objective of this paper is to explore the influence of this flexural behavior on the accuracy of the tensegrity model, given the model’s underlying assumption that “every single member bears solely either tensile or compressive behavior”.

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Nakamura, Masanori, Ray Noguchi, Yoshihiro Ujihara, Hiroshi Miyazaki, and Shigeo Wada. "Proposal of a Mechano-Cell Model With Membrane, Cytoskeleton and Nucleus." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192527.

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The mechanical properties of cells have been of great interest to scientists from early studies which suggested that mechanical stress-induced alterations in cell shape and structure are critical for control of many cell functions. Although various loading tests of a cell have been designed to understand the cellular mechanical properties, the heterogeneous intracellular structure such as cytoskeletons brings about difficulties in interpreting experimental data.

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Lykotrafitis, George, and He Li. "Two-Component Coarse-Grain Model for Erythrocyte Membrane." In ASME 2011 International Mechanical Engineering Congress and Exposition. ASMEDC, 2011. http://dx.doi.org/10.1115/imece2011-62133.

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Biological membranes are vital components of living cells as they function to maintain the structural integrity of the cells. Red blood cell (RBC) membrane comprises the lipid bilayer and the cytoskeleton network. The lipid bilayer consists of phospholipids, integral membrane proteins, peripheral proteins and cholesterol. It behaves as a 2D fluid. The cytoskeleton is a network of spectrin tetramers linked at the actin junctions. It is connected to the lipid bilayer primarily via Band-3 and ankyrin proteins. In this paper, we introduce a coarse-grained model with high computational efficiency for simulating a variety of dynamic and topological problems involving erythrocyte membranes. Coarse-grained agents are used to represent a cluster of lipid molecules and proteins with a diameter on the order of lipid bilayer thickness and carry both translational and rotational freedom. The membrane cytoskeleton is modeled as a canonical exagonal network of entropic springs that behave as Worm-Like-Chains (WLC). By simultaneously invoking these characteristics, the proposed model facilitates simulations that span large length-scales (∼ μm) and time-scales (∼ ms). The behavior of the model under shearing at different rates is studied. At low strain rates, the resulted shear stress is mainly due to the spectrin network and it shows the characteristic non-linear behavior of entropic networks, while the viscosity of the fluid-like lipid bilayer contributes to the resulting shear stress at higher strain rates. The apparent ease of this model in combining the spectrin network with the lipid bilayer presents a major advantage over conventional continuum methods such as finite element or finite difference methods for cell membranes.

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Kaunas, Roland. "A Theoretical Model of Stretch-Induced Stress Fiber Remodeling." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193241.

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Cyclic stretching of endothelial cells (ECs), such as occurs in arteries during the cardiac cycle, induces ECs and their actin stress fibers to orient perpendicular to the direction of maximum stretch. This perpendicular alignment response is strengthened by increasing the magnitudes of stretch and cell contractility (1). The actin cytoskeleton is a dynamic structure that regulates cell shape changes and mechanical properties. It has been shown that actin stress fibers are ‘prestretched’ under normal, non-perturbed, conditions (2), consistent with the ideas of ‘prestress’ that have motivated tensegrity cell models (3). It has also been shown that ‘tractional forces’ generated by cells at focal adhesions tend to increase proportionately with increasing focal adhesion area, thus suggesting that cells tend to maintain constant the stress borne by a focal adhesion (4). By implication, this suggests that cells try to maintain constant the stress in actin stress fibers. Thus, it seems that cells reorganize or turnover cytoskeletal proteins and adhesion complexes so as to maintain constant a preferred mechanical state. Mizutani et al. (5) referred to this as cellular tensional homeostasis, although they did not suggest a model or theory to account for this dynamic process.

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Han, Sangyoon J., and Nathan J. Sniadecki. "Traction Forces During Cell Migration Predicted by the Multiphysics Model." In ASME 2011 International Mechanical Engineering Congress and Exposition. ASMEDC, 2011. http://dx.doi.org/10.1115/imece2011-63843.

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Cells rely on traction forces in order to crawl across a substrate. These traction forces come from dynamic changes in focal adhesions, cytoskeletal structures, and chemical and mechanical signals from the extracellular matrix. Several computational models have been developed that help explain the trajectory or accumulation of cells during migration, but little attention has been placed on traction forces during this process. Here, we investigated the spatial and temporal dynamics of traction forces by using a multiphysics model that describes the cycle of steps for a migrating cell on an array of posts. The migration cycle includes extension of the leading edge, formation of new adhesions at the front, contraction of the cytoskeleton, and the release of adhesions at the rear. In the model, an activation signal triggers the assembly of actin and myosin into a stress fiber, which generates a cytoskeletal tension in a manner similar to Hill’s muscle model. In addition, the role that adhesion dynamics has in regulating cytoskeletal tension has been added to the model. The multiphysics model was simulated in Matlab for 1-D simulations, and in Comsol for 2-D simulations. The model was able to predict the spatial distribution of traction forces observed with previous experiments in which large forces were seen at the leading and trailing edges. The large traction force at the trailing edge during the extension phase likely contributes to detachment of the focal adhesion by overcoming its adhesion strength with the post. Moreover, the model found that the mechanical work of a migrating cell underwent a cyclic relationship that rose with the formation of a new adhesion and fell with the release of an adhesion at its rear. We applied a third activation signal at the time of release and found it helped to maintain a more consistent level of work during migration. Therefore, the results from both our 1-D and 2-D migration simulations strongly suggest that cells use biochemical activation to supplement the loss in cytoskeletal tension upon adhesion release.

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Pathak, Amit, Vikram S. Deshpande, Robert M. McMeeking, and Anthony G. Evans. "Simulation of the Coupling of Cell Contractility and Focal Adhesion Formation." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176108.

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The remodeling of the cytoskeleton and focal adhesion distributions for cells on substrates with micro-patterned ligand patches is investigated using a bio-chemo-mechanical model. All the cells have approximately the same area and we investigate the effect of ligand pattern shape on the cytoskeletal arrangements and focal adhesion distributions. The model for the cytoskeleton accounts for the dynamic rearrangement of the actin/myosin stress fibers and entails the highly non-linear interactions between signaling, the kinetics of tension-dependent stress-fiber formation/dissolution and stress dependent contractility. This model is coupled with a focal adhesion (FA) model that accounts for the mechano-sensitivity of the adhesions from thermodynamic considerations. This coupled stress fiber and focal adhesion model is shown to capture a variety of key experimental observations including: (i) the formation of high stress fiber and focal adhesion concentrations at the periphery of circular and triangular, convex–shaped ligand patterns; (ii) the development of high focal adhesion concentrations along the edges of the V, T, Y and U shaped concave ligand patterns; and (iii) the formation of highly aligned stress fibers along the un-adhered edges of cells on the concave ligand patterns. When appropriately calibrated, the model also accurately predicts the radii of curvature of the un-adhered edges of cells on the concave-shaped ligand patterns.

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Vernerey, Franck J. "Biophysical Model of the Coupled Mechanisms of Cell Adhesion, Contraction and Spreading." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80309.

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Recent research has shown that cell spreading is highly dependent on the contractility of its cytoskeleton and the mechanical properties of its surrounding environment. This extended abstract introduces a mathematical formulation of cell spreading and contraction that couples the processes of stress fiber formation, protrusion growth through actin polymerization at the cell edge and dynamics of cross-membrane protein (integrins) enabling cell-substrate attachment. The evolving cell’s cytoskeleton is modeled as a mixture of fluid, proteins and filaments that can exchange mass and generate contraction. In particular, besides self-assembling into stress fibers, actin monomers are able to polymerize into an actin meshwork at the cell’s boundary in order to push the membrane forward and generate protrusion. These processes are possible via the development of cell-substrate attachment complexes that arise from the mechano-sensitive equilibrium of membrane proteins, known as integrins. Numerical simulations show that the proposed model is able to capture the dependency of cell spreading and contraction on substrate stiffness and chemistry. The very good agreement between model predictions and experimental observations suggests that mechanics plays a strong role into the coupled mechanisms of contraction, adhesion and spreading of adherent cells.

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Li, He, and George Lykotrafitis. "Modeling Diffusion and Vesiculation in Defective Human Erythrocyte Membrane." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14203.

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The hemolytic disorders of hereditary spherocytosis (HS) and hereditary elliptocytosis (HE) affect the lives of millions of individuals worldwide. In HS and HE, connections in the vertical and horizontal directions between components of the RBC membrane (see Fig. 1(a)), are disrupted due to defective proteins, leading to loss of the structural and functional integrity of the membrane (1–2). Moreover, disruptions of either the vertical interactions or horizontal interactions affect the lateral diffusivity of the mobile band 3 proteins, as the motion of band 3 in the RBC membrane is confined by the cytoskeleton (3). Although a number of coarse-grained molecular dynamics (CGMD) RBC membrane models have been developed in the past two decades, very few RBC membrane models have been used to study the disordered band 3 diffusion and membrane vesiculation in HS and HE. The implicit representations of either the lipid bilayer or the cytoskeleton in these membrane models limit their applications in the membrane instability problems in HS and HE. In this extended abstract, we develop a two-component CGMD human RBC membrane model that explicitly comprises both the lipid bilayer and the cytoskeleton. In this way, the interactions between the cytoskeleton and the proteins embedded in the lipid bilayer can be simulated. The proposed model allows us to measure the band 3 lateral mobility and simulate the process of membrane vesiculation in the membrane with protein defects.

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