Dissertationen zum Thema „Myosine1g“
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Janardhana, Kurup Akshai. „Étude de la myosine nonconventionelle myosine1g dans l'asymétrie droite-gauche du poisson zèbre“. Electronic Thesis or Diss., Université Côte d'Azur, 2022. http://www.theses.fr/2022COAZ6028.
Der volle Inhalt der QuelleLeft-Right (LR) asymmetry refers to the asymmetric placement of organs across the midline. Dysregulation of LR asymmetry establishment during animal development can lead to misplaced organs - a situation that can be lethal.I use zebrafish as a model to study the mechanisms that establish LR asymmetry. In zebrafish, a ciliated organ - Kupffer's Vesicle (KV) acts as a central LR organizer (LRO). The Nodal ligand Southpaw (Spaw) and its antagonist Dand5 are initially expressed in a symmetric fashion around the LRO. The beating of cilia in the LRO establishes a directional fluid flow that represses Dand5 on the left, allowing Spaw to spread on the left side through auto-induction and thereby direct the laterality of heart, brain and viscera.In contrast to many vertebrates, Drosophila establishes LR asymmetry independently of cilia using chiral cell remodeling controlled by the unconventional Myosin Myo1D. Our group showed previously that zebrafish Myo1D regulates LR asymmetry by orienting KV cilia and promoting the formation of a symmetry-breaking fluid flow. In addition to myo1d, the zebrafish genome encodes the closely related gene myo1g. The objective of my PhD work has been to study the contribution of Myo1G to the establishment of zebrafish LR asymmetry.KV acts as a central LRO that controls the laterality of the different organs of the animal. Accordingly, myo1d mutants that have an altered LRO flow present LR defects at the level of the heart, brain and viscera. In contrast, myo1g mutants present LR defects in heart and brain but not viscera, suggesting that myo1g may exert a flow-independent function in LR asymmetry.In order to directly test this hypothesis, I inactivated myo1g in dnaaf1 mutants which lack ciliary motility and present therefore no LRO flow. While the asymmetric movement of cardiac precursors is randomized to either the left or right side in dnaaf1 single mutants, asymmetric precursor cell movement is altogether lost in myo1g ; dnaaf1 double mutants, demonstrating thereby that myo1g functions indeed independently of the LRO flow.My work reveals that in contrast to Myo1D which regulates LRO cilia orientation, Myo1G is required for the Nodal-mediated transfer of laterality information from the central LRO to different target tissues. In myo1g mutants, spaw expression remains limited to the posterior of the embryo, properly guiding the laterality establishment of the posterior viscera, whereas the anterior heart and brain fail to establish laterality.In the context of the establishment of Zebrafish LR asymmetry, the Nodal ligand Spaw binds to a receptor complex formed by Acvr2, Alk4 and the co-receptor Oep. Productive ligand/receptor interactions trigger the phosphorylation of the downstream transcription factors Smad2/3, which then translocate into the nucleus to activate downstream genes. Nodal signal transduction induces spaw itself (which therefore propagates through auto-induction) as well the Nodal antagonist lefty1.When I injected equal amounts of spaw mRNA in WT and myo1g mutants and assessed the response by monitoring lefty1 activation, myo1g mutant embryos displayed a weaker response to spaw overexpression than their WT siblings, indicating thereby an impairment in Nodal signal transduction. In contrast, misexpression of constitutively activated smad2 produced equivalent responses in WT and myo1g mutant animals.Of particular interest, previous studies have implicated Myosin1 proteins in the endocytic trafficking of TGFβ receptor molecules. Different endocytic pathways have been shown to either promote TGFβ receptor signal transduction or conversely trigger receptor degradation. My work shows that myo1g mutants present a decrease in the number of Nodal-receptor positives endosomes, suggesting thereby that Myo1G may regulate LR asymmetry by controlling TGFβ receptor trafficking
El, Bahloul Amel. „Caractérisation fonctionnelle et structurale de trois myosines non conventionnelles : la myosine VI, la myosine VIIa et la myosine IB d'Acanthamoeba“. Paris 11, 2004. http://www.theses.fr/2004PA112138.
Der volle Inhalt der QuelleHarricane-Vors, Marie-Cécile. „Etudes in vitro de l'interaction entre l'actine et des protéines associées : gelsoline, caldesmone, myosine“. Montpellier 1, 1990. http://www.theses.fr/1990MON11303.
Der volle Inhalt der QuelleLheureux, Karine. „Transduction mécano-chimique dans le muscle squelettique : étude comparative des complexes acto-myosine à l'état monomérique et filamenteux“. Montpellier 1, 1995. http://www.theses.fr/1995MON1T015.
Der volle Inhalt der QuelleBonafé, Nathalie. „Structure et régulation du complexe actine-myosine dans le muscle squelettique“. Montpellier 1, 1994. http://www.theses.fr/1994MON1T009.
Der volle Inhalt der QuelleStordeur, Jean-Marc. „Evaluation de la taille de l'infarctus du myocarde thrombolysé par le dosage de la myosine plasmatique“. Montpellier 1, 1991. http://www.theses.fr/1991MON11213.
Der volle Inhalt der QuelleSeyer, Pascal. „Etude de l'implication directe de l'activité mitochondriale dans la régulation de la différenciation des myoblastes“. École nationale supérieure agronomique (Montpellier), 2005. http://www.theses.fr/2005ENSA0027.
Der volle Inhalt der QuelleGuimard, Laurent. „Modélisation et synthèse de peptides interagissant avec une protéine cible : application au complexe calmoduline-RS20“. Montpellier 1, 1995. http://www.theses.fr/1995MON1T037.
Der volle Inhalt der QuelleBarjot, Catherine. „Propriétés in vitro des cellules satellites des muscles lents et rapides de lapin, et modalités de la régénération musculaire in vivo“. Montpellier 1, 1995. http://www.theses.fr/1995MON1T036.
Der volle Inhalt der QuelleRauzi, Matteo. „Mapping Subcellular Forces Controlling Morphogenesis“. Thesis, Aix-Marseille 2, 2010. http://www.theses.fr/2010AIX22025.
Der volle Inhalt der QuelleDuring embryonic development tissue remodeling leads to shape changes: for example, tissues can elongate, invaginate, and stretch. Distinct signaling pathways regulate in space and time these behaviors through the control ofthe actin cytoskeleton and of myosin-based tension required for cell shapechange. What is the spatiotemporal pattern of subcellular forcesthat orient tissue morphogenesis? What is the nature of the generated forces and finally, what lies at the origin of such forces? These are the main questions that my thesis tries to illuminate. I use the germbandelongation of the Drosophila embryo as a model system to investigate themechanics of tissue morphogenesis
Vigouroux, Clémence. „Regulation of actin assembly and mechanotransduction in cell-matrix adhesion complexes by the protein RIAM The PIP2-talin-RIAM-VASP pathway controls actin polymerization and organisation Talin dissociates from RIAM and associates to vinculin sequentially in response to the actomyosin force Integrin-bound talin head inhibits actin filament barbed-end elongation“. Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASL015.
Der volle Inhalt der QuelleDuring cell migration, adhesion complexes control the production of force and the adaptation to the mechanical properties of the environment. The aim of this project was to understand the molecular mechanisms by which these complexes control the force produced by actin assembly and encode mechanical information into biochemical reactions. The first study shows that the proteins talin, RIAM and VASP assemble on the surface of a membrane to stimulate actin assembly by a novel. mechanism The second part is based on the reconstitution of the mechanosensitive machinery of the adhesion complexes with pure proteins on a micropatterned surface observed in microscopy. The study reveals that the stretchable protein talin exchanges its partner RIAM for vinculin in response to the force transmitted by the actin cytoskeleton. Talin thus codes mechanical information by recruiting partners that correspond to its degree of stretch
Blanchoin, Laurent. „Interaction actine-myosine. Caracterisation des complexes formes entre l'actine et le sous-fragment-1 de la myosine“. Paris 6, 1996. http://www.theses.fr/1996PA066044.
Der volle Inhalt der QuelleDürrbach, Antoine. „Role des myosines 1 dans le transport intracellulaire“. Paris 6, 1997. http://www.theses.fr/1997PA066070.
Der volle Inhalt der QuelleDürrwang, Ulrike. „Funktionelle Charakterisierung unkonventioneller Myosine aus Dictyostelium discoideum“. [S.l. : s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=967265800.
Der volle Inhalt der QuelleLagny, Thibaut. „Myosine 1b – Mécanique membranaire et dynamique cellulaire“. Thesis, Paris Sciences et Lettres (ComUE), 2018. http://www.theses.fr/2018PSLET007.
Der volle Inhalt der QuelleThe unconventional motor protein myosin 1b is involved in a variety of cellular processes, controlling, e.g. endomembrane shape, axon development, and cell segregation. The mechanism by which myosin 1b is able to fulfil its functions in a variety of cellular locations remains unknown to date, yet the described phenotypes suggest a role of myosin 1b at the interface between membranes and actin. Notably, it is required for efficient cell segregation after activation of the EphB2 receptor which induces cell contraction.This thesis presents a detailed characterization of the effects of myosin 1b on (1) the mechanical properties of the cell membrane, studied by membrane tether pulling with an optical tweezer, and (2) the dynamics of the actin cytoskeleton and transmembrane proteins, studied by a variety of microscopy-based methods.Here we show that class 1 myosins do not generally change effective membrane tension in adherent cells, likely due to efficient compensation mechanisms. Furthermore, we show that friction between the actin cortex and the plasma membrane depends on the total density of membrane-cortex linkers and the relative fraction of bound proteins. The observed deficiency in cell contraction in absence of myosin 1b is thus independent of a persistent, global change in effective membrane tension.In the second part of this thesis, we show that myosin 1b likely does not change EphB2’s receptor dynamics in the plasma membrane, i.e. its diffusion and clustering behavior.Finally, using TIRF-SIM imaging and quantitative description of actin flows, we reveal that myosin 1b has an intriguing yet non-intuitive effect on actin dynamics at the cellular ventral surface.In conclusion, even if the mechanism by which myosin 1b changes cellular response to EphB2 stimulation still remains unknown, we have finally been able to pinpoint its function to a well-defined and quantifiable observation, i.e. changed actin flow dynamics. Future experiments will be able to address this observation and dissect its underlying mechanism. This will allow concluding on whether myosin 1b has a common effect that governs all its described biological roles
Coureux, Pierre-Damien. „Etudes structurales d'un moteur moléculaire : la myosine“. Paris 11, 2004. http://www.theses.fr/2004PA112073.
Der volle Inhalt der QuelleMolecular motors are proteins that are able to produce a force : they convert the chemical energy released from ATP hydrolysis into mechanical force. This interesting feature is shared among three molecular motors families : myosins, kinesins and dyneins. Myosins, our favorite family, are involved in a litany of cellular functions as muscular contraction, hearing, vision, skin pigmentation, digestion, brain development, intracellular traffic, cellular division or phagocytosis. To understand the basis of force generation, and one day to use molecular motors as therapeutic targets, class II and V myosins were studied for their interesting features. These myosins share the same production force mechanism, but they have totally different functions in the cell (one forms filaments and contracts muscular fibers whereas the other is a dimer and carries vesicules). Kinetic and structural results on those two myosins classes helped to better understand the catalytic cycle of myosin with its partner, actin. Some new conformational states of myosin V, isolated by crystallography, allowed us to describe the structural elements responsible of the strong interaction between myosin and actin, and the effect of the nucleotide on the actomyosin complex. The studies lead on different myosin II mutants gave some parts of answer on a key step on myosin production force ; one of the hydrolysis products release. These mutants participated to a better understanding of the aim of some residues in the kinetic differences within the myosin superfamily
Isabet, Tatiana. „Etudes structurales d'un moteur moleculaire : la myosine“. Paris 6, 2011. http://www.theses.fr/2011PA066319.
Der volle Inhalt der QuelleBhat, Alka. „Les dynamiques d'agrégats de myosine et leurs rôles dans les fermetures d'epithelia“. Thesis, Strasbourg, 2019. http://www.theses.fr/2019STRAJ070.
Der volle Inhalt der QuelleMyosin clusters have been reported in a variety of systems, such as Drosophila, C. elegans, and acto-myosin in vitro assays. However, their integration in a general framework is still lacking. In theory, actin filaments and myosin motors are predicted to follow generic rules of self-organisation. Recent findings from the laboratory reported that cluster dynamics within cytokinetic rings are associated with biological functions, i.e. stress generation when radial, and transport when tangential. In this study, we show that these simple rules hold as well for acto-myosin ring wound closure in epithelial monolayers. By using microfabrication, cell biology, quantitative imaging and theoretical physics, we report that radial and tangential clusters are related to local closures and stalled portions of rings, respectively. This conserved mechanism between single and multi-cellular system suggests that these myosin clusters dynamics could be used as generic read-out for mapping and predicting changes in shapes in developing embryos
Plaçais, Pierre-Yves. „Propriétés mécaniques de la myosine II in vitro : de la molécule unique aux effets collectifs“. Phd thesis, Université Pierre et Marie Curie - Paris VI, 2008. http://tel.archives-ouvertes.fr/tel-00410100.
Der volle Inhalt der QuelleNous avons construit un dispositif reproduisant in vitro une configuration semblable. Nous avons observé qu'une assemblée de myosines II musculaires, consommant de l'ATP en interagissant avec un filament d'actine, et soumise à une force de rappel élastique exercée par une pince optique, est un système minimal capable d'osciller spontanément. La relation force-vitesse du système présente un comportement non-monotone lié à l'activité des moteurs. Cette propriété fournit un mécanisme pour interpréter les oscillations spontanées, comme il l'a été suggéré par différentes études théoriques antérieures.
Par ailleurs, des expériences préliminaires à l'échelle de la molécule individuelle indiquent que la raideur de l'accrochage actine-myosine II pourrait dépendre de la tension imposée au filament d'actine. Cette propriété pourrait expliquer les écarts entre les raideurs mesurées in vitro et estimées à partir d'expériences sur les fibres musculaires.
Masson, d'Autume Adèle de. „Lymphocytes B régulateurs dans la GVH chronique humaine et rôle de la myosine 18A dans la cytotoxicité des lymphocytes NK“. Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCC177/document.
Der volle Inhalt der QuelleAllogeneic hematopoietic stem cell transplantation (HSCT) remains the only curative treatment for many patients with haematological malignancies. In almost half of the cases, it is complicated by chronic graft-versus-host disease (cGVHD). Regulatory B cells are a population of B cells secreting interleukin (IL)-10 that can inhibit the immune responses. We have shown that in patients with active cGVHD, the frequency of regulatory B cells is decreased in the peripheral blood. Regulatory B cells are enriched in the memory B cell and plasmablast B cell pools. Increased plasmablasts frequencies and decreased memory B cells frequencies were found in patients with active cGVHD, suggesting alterations in the terminal differentiation of B cells. Our work also focused on NK cells that have a cytotoxic role. We identified one surface receptor of NK cells, CD245, as myosin 18A. Myosin 18A is involved in the organization of the cytoskeleton and is a receptor of the surfactant A. We have shown that myosin 18A was a coactivating receptor of the NK cytotoxicity and that this increase in cytotoxicity could be linked to the stimulation of the expression of CD137 (4-1BB) on the surface of the NK lymphocyte. These results suggest a potential therapeutic role of the use of specific CD245 agonist antibodies
Hartmann, Falk Alexander Karl. „Molekulare Grundlagen der Regulation und Modulation der Motorfunktion von Myosinen“. Hannover Technische Informationsbibliothek und Universitätsbibliothek Hannover, 2010. http://d-nb.info/1000893731/34.
Der volle Inhalt der QuelleBrandstaetter, Hemma. „Cellular function of the myosin1c motor protein in membrane trafficking“. Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609957.
Der volle Inhalt der QuelleCormery, Bruno. „Adaptations fonctionnelles des unités motrices à la suite d'une paralysie complète induite par l'application chronique de tetrodotoxine sur le nerf sciatique“. Aix-Marseille 2, 2000. http://www.theses.fr/2000AIX22065.
Der volle Inhalt der QuelleKorfage, Joannes Antonius Maria. „Myosin heavy chain composition of the human jaw muscles“. [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2004. http://dare.uva.nl/document/75060.
Der volle Inhalt der QuellePlanelles, Herrero Vicente José. „Bases mécanistiques et structurales de la régulation de l'activité des myosines“. Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066465.
Der volle Inhalt der QuelleMolecular motors are essential agents of force production in the cells: they convert the chemical energy released by the hydrolysis of ATP into mechanical work. This thesis focuses on myosins, a family of molecular motors responsible for actin-based motility. Myosin VI is unique among all of the myosin superfamily members in that it moves in the opposite direction of all other known myosins. Previous work revealed myosin VI tail ability to fold back, constituting a potential auto-inhibited state that prevents motor activity. Several myosin VI partners, binding to the C-terminal tail of the myosin, have been identified and shown to recruit the motor for different functions. In the first chapter of this thesis, the mechanism allowing the regulation of myosin VI activity has been studied using biochemical and biophysical analysis (SAXS, light scattering, microscopy, binding assays and mutagenesis). GIPC1, the most studied myosin VI partners, promotes myosin dimerization and activation. During my PhD, I have been also involved in two other projects, in line with my thesis project, that have led to the publication of four articles. Two shorter chapters are therefore devoted to these projects. The second chapter of my thesis explores myosin VII activity regulation by its cellular partners. Finally, the third chapter is devoted to the allosteric regulation of myosins activity by small molecules
Planelles, Herrero Vicente José. „Bases mécanistiques et structurales de la régulation de l'activité des myosines“. Electronic Thesis or Diss., Paris 6, 2017. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2017PA066465.pdf.
Der volle Inhalt der QuelleMolecular motors are essential agents of force production in the cells: they convert the chemical energy released by the hydrolysis of ATP into mechanical work. This thesis focuses on myosins, a family of molecular motors responsible for actin-based motility. Myosin VI is unique among all of the myosin superfamily members in that it moves in the opposite direction of all other known myosins. Previous work revealed myosin VI tail ability to fold back, constituting a potential auto-inhibited state that prevents motor activity. Several myosin VI partners, binding to the C-terminal tail of the myosin, have been identified and shown to recruit the motor for different functions. In the first chapter of this thesis, the mechanism allowing the regulation of myosin VI activity has been studied using biochemical and biophysical analysis (SAXS, light scattering, microscopy, binding assays and mutagenesis). GIPC1, the most studied myosin VI partners, promotes myosin dimerization and activation. During my PhD, I have been also involved in two other projects, in line with my thesis project, that have led to the publication of four articles. Two shorter chapters are therefore devoted to these projects. The second chapter of my thesis explores myosin VII activity regulation by its cellular partners. Finally, the third chapter is devoted to the allosteric regulation of myosins activity by small molecules
Porquet, Nicolas. „Caractérisation du rôle non ciliaire de la Kinésine-2 dans l'établissement de l'axe droite/gauche chez Drosophila melanogaster“. Electronic Thesis or Diss., Nice, 2013. http://www.theses.fr/2013NICE4112.
Der volle Inhalt der QuelleIn nature most of the bilateralia are left/right (L/R) asymmetric. In Drosophila, asymmetry is apparent in the directional looping of gut and terminalia. Dextral orientation of organs is controlled by the activity of a single gene myosin ID (myoID) whose mutation induces a fully inverted L/R axis. To date little is known of how the initial L/R cue induced by MyoID is propagated and maintained through the rest of the architecture of the L/R organizer. Here we present the identification of klp64D and klp68D as new myoID interacting genes. These genes encodes the two motor sub-units of the Drosophila Kinesin-2 motor complex. Interestingly, this microtubule-based motor plays a ciliary function in vertebrate L/R morphogenesis. However, we show that in Drosophila cilia are not involved in L/R asymmetry. We demonstrate that Kinesin-2 acts during L/R determination in the dextral pathway. Furthermore Kinesin-2 is required for proper L/R patterning both of male genitalia and of adult hindgut. L/R activity of Kinesin-2 is restricted to cells that do not express MyoID suggesting a role for this motor in propagation of the L/R cue. Our findings show for the first time a non ciliary role for Kinesin-2 in L/R axis determination. Thus, these results shed light on an evolutionary conservation between Drosophila and vertebrate L/R determination
Cordonnier, Marie-Neige. „Etude du rôle de la Myosine I alpha dans l'endocytose“. Paris 6, 2001. http://www.theses.fr/2001PA066408.
Der volle Inhalt der QuelleLavie, Julie. „Approche des mécanismes de différenciation du muscle lisse vasculaire par l'étude de la régulation de la transcription des gènes VCAM-1 et sm-MHC“. Bordeaux 2, 1999. http://www.theses.fr/1999BOR28682.
Der volle Inhalt der QuelleAubry, Aurélie. „Recherche d'interacteurs de Myosine II au cours de l'intercalation cellulaire chez l'embryon de Drosophila melanogaster“. Thesis, Aix-Marseille 2, 2011. http://www.theses.fr/2011AIX22117/document.
Der volle Inhalt der QuelleEpithelial tissue is composed of polarized cells, which are closely attached to each other by adherens junctions. The loss of adherens junctions is often a key step in the development of cancer in epithelial tissues. It is therefore important to understand the mechanisms of attachment between the cells. To study such epithelial plasticity, we use the Drosophila embryo as a model system, where a fine regulation of adherens junctions is required for one of the early processes of development: germ band elongation. During this process, epithelial cells change their neighbors along the anterior-posterior axis (cell cell intercalation) without loss of cell adhesion. Polarized recruitment of the molecular motor Myosin II at the junctions, that disassemble and reassemble, underlies the intercalation process. In part, intercalation relies on the normal activity of the the JAK / STAT pathway that is crucial for the spatial control of Myosin II. During my PhD, I conducted a genetic screen, in a mutant for the ligand of the JAK / STAT pathway, designed to identify second site interactors for Myosin II control. I identified several genes that appear to be involved in the intercalation process. Among these candidates, I focused on one with the strongest phenotype: the gene CG13992. The functional characterization of this gene was the second stage of my thesis (because only the nucleotide and the protein sequences were known). Preliminary results highlight the involvement of this gene in the localization of Myosin II that remain to be confirmed
Mercadier, Jean-Jacques. „Expression des isomyosines cardiaques : modifications au cours des surcharges hémodynamiques chroniques du cœur de rat et du cœur humain“. Paris 11, 1985. http://www.theses.fr/1985PA112211.
Der volle Inhalt der QuelleOwing to its ability to hydrolyze ATP and to the associated conformational changes, myosin is the most important protein of muscle contraction. Pyrophosphate gel electrophoresis under non denaturing conditions separates rat ventricular myosin in three isoforms V1, V2 and V3 in order of decreasing electrophoretic mobility and ATPase activity, V1 being the predominant form in the adult animal. During chronic hemodynamic overload of the rat ventricle, a myosin isoenzymic redistribution is observed in parallel with ventricular hypertrophy, with an accumulation of the V3 isoform and a parallel decrease in the V1 isoform. This redistribution is, at least in part, responsible for the decrease in the speed of muscle shortening observed with hypertrophy. Moreover, improving the efficiency of muscle contraction, it can be regarded as a truly adaptational mechanism. The myosin isoenzymic redistribution is also observed in chronic overload of the human auricle, also predominantly composed of a “V1-like” isoform. By contrast, the human ventricle already almost exclusively composed of a “V3-like” isoform, is scarcely concerned by this phenomenon. Myosin isoenzymic redistribution observed with chronic hemodynamic overload represents the first example of the regulation of myocardial muscle contractility by differential expression of a family of multigenic proteins
Diagana, Thierry. „Analyse fonctionnelle de la région promotrice du gène murin codant pour la chaîne lourde de la myosine musculaire MyHC IIB“. Paris 5, 1995. http://www.theses.fr/1995PA05S033.
Der volle Inhalt der QuelleBertet, Claire. „Rôle et régulation du recrutement de la myosine-II au cours de la morphogénèse épithéliale chez l'embryon de drosophile“. Aix-Marseille 2, 2008. http://theses.univ-amu.fr.lama.univ-amu.fr/2008AIX22047.pdf.
Der volle Inhalt der QuelleDuring my PhD, I have used drosophila germband extension as a model to study epithelial morphogenesis. This process relies on epithelial cell intercalation during which cells exchange neighbors along the anteroposterior axis of the embryo. I have shown that to intercalate, cells rearrange their adherens junctions in a highly organized and polarized pattern within the plane of the tissue. The Myosin-II molecular motor orchestrates this polarized remodeling. Myo-II is specifically enriched at the level of disassembling junctions. A deletion genetic screen has allowed me to identify a new mechanism controlling Myo-II recruitment. This mechanism is based on regulating the actin network organization. Using this mechanism, the JAK/STAT signaling pathway and a still unknown planar polarity pathway control Myo-II recruitment during germband elongation
Tetaert, Daniel. „Structure et rôle de la chaîne légère dite alcaline de la myosine ventriculaire de coeur de porc“. Lille 1, 1988. http://www.theses.fr/1988LIL10017.
Der volle Inhalt der QuelleSpéder, Pauline. „Asymétrie droite-gauche chez la drosophile : étude d'un mutant Situs inversus“. Nice, 2007. http://www.theses.fr/2007NICE4038.
Der volle Inhalt der QuelleThe establishment of a fixed and invariant Left-Right (LR) asymmetry is crucial for both the structural organization of the body and for organ’s functions, like the heart. Studies led on deuterostomes have proposed elegant models for symmetry breaking, involving Nodal flow or ion flows. However, the molecular nature of the determinant(s) responsible for the LR orientation (situs choice) remains largely unknown, as well as the conservation of early mechanisms during evolution. Our study has identified the conserved type ID unconventional myosin gene (Myo31DF) as a Situs inversus gene in Drosophila. Myo31DF mutations reverse both the dextral looping of genitalia, a prominent LR marker in adult flies, and the positioning of embryonic gut. Genetic mosaic analysis identifies the A8 segment of the genital disc, the precursor of adult genitalia, as a LR organizer, and reveals an anterior–posterior compartmentalization of Myo ID function that directs dextral development (A8p) and represses a sinistral default asymmetry (A8a). As expected of a LR determinant, Myo ID has a trigger-like function, as well as an endogenous symmetric expression, and its symmetric overexpression doesn’t lead to LR defects. We also showed that Myo ID interacts and colocalizes with β-catenin, like the only other molecularly identified Situs inversus gene, the mouse Inversin. It suggests that Situs inversus genes could direct LR development through the adherens junction. We demonstrate here the existence of a LR axis in Drosophila, and identify an actin-dependant molecular motor, Myo ID, as a dextral determinant controlling situs choice, and thus establishment of an invariant asymmetry in a protostome
Ripoll, Léa. „Role of myosin VI and actin dynamics in membrane remodeling during pigmentation“. Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCB102.
Der volle Inhalt der QuelleIntracellular transport among organelles and the plasma membrane occurs through the formation and transport of vesicular and tubular membrane carriers. The formation of these carriers requires first the bending of membrane and the generation of a bud, followed by its elongation to form the tubule-vesicle. Lastly, the carrier is released from the membrane source by the scission of the membrane. Importantly, all these different steps need an accurate orchestration to properly deform the membrane. The actions exerted by molecular motors onto microtubule and actin cytoskeletons provide forces onto membrane that contribute to its remodeling during the biogenesis of carrier. Actin filaments (F-actin) and myosins are thought to participate in the initiation and the fission of carriers. However, the role of actin machinery during carrier biogenesis remains elusive. We thus decided to address the role of F-actin and the actin-based motor myosin VI in the formation of tubular intermediates at melanosome. Melanosomes are lysosome-related organelles of skin melanocytes and eye pigment cells that function in the synthesis and storage of the melanin pigment. Melanosomes originate from endosomes and progressively mature into fully pigmented compartments, which fate is to be secreted and transferred to neighboring keratinocytes. Melanosomes are dynamic organelles that constantly receive, but also recycle proteins such as the SNARE VAMP7 through the formation and release of tubular intermediates. Our work reveals that myosin VI, together with Arp2/3- and WASH-mediated branched actin localize at specific melanosomal subdomains where they promote the constriction and scission of tubular intermediates. This fission event allows the export of components such as VAMP7 from melanosomes and promotes their maturation and subsequent transfer to keratinocytes. Altogether, our results uncover a new role for myosin VI and F-actin in the constriction and scission of membrane tubules at melanosome that is required for organelle homeostasis and function
Marion, Sabrina. „Rôle de la myosine IB durant la phagocytose chez Entamoeba histolytica“. Paris 11, 2004. http://www.theses.fr/2004PA112142.
Der volle Inhalt der QuellePhagocytosis of human cells by the human parasite E. Histolytica is a crucial activity for the invasive process of the host tissues. Myosin IB, the unique unconventional myosin of E. Histolytica, is the molecular motor providing forces to deform the plasma membrane to engulf human cells. During my PHD, I characterized the biophysical properties of myosin IB in living parasites and showed that this molecule can cross-link actin filaments and thereby regulate the viscoelastic properties of the cortical actin gel. This property appeared important for the dynamics of the membrane deformation at the first step of the phagocytic process. Furthermore, I used a proteomic approach to dissect the early signaling events involved in the activity of the cytoskeleton during phagocytosis. I purified phagosome at different time point of the uptake process and identified the phagosomal proteins by mass spectroscopy. We identified 600 proteins involved in cytoskeleton activity, signaling pathways, lytic factors and new putative receptors. Furthermore, comparing the phagosomal proteins of early phagosomes purified from the wild type cells and parasites that overproduce myosin IB, we identified putative candidates, which the activity is linked to myosin IB function during the first steps of the phagocytic process in E. Histolytica
Chauca, Espinoza Karen Lorena. „Study of the dynamics of cortical myosin in the early embryo of the nematode C. elegans“. Electronic Thesis or Diss., Sorbonne université, 2023. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2023SORUS411.pdf.
Der volle Inhalt der QuelleNon-muscle myosin II is a key player in cell and tissue morphogenesis. The cortical dynamics Myosin as minifilaments in vivo however remain poorly understood. Here, we use SIM-TIRF microscopy in a developing embryo to gain further insights into the mechanisms and structure of bipolar minifilaments assembly. Combining SIM-TIRF and TIRF single-molecule microscopy, we first characterized the structure of minifilaments, specifically size and stoichiometry, at multiple stages in the early embryo. Using high temporal-resolution SIM- TIRF movies, we then characterized a diverse range of behaviors of myosin minifilaments, minifilament split events, alignments of multiple minifilaments over long distances (which we called protostress fibers), partial unbinding events and, surprisingly, events of sequential unbinding and rebinding to the cortex. Using mutants of the myosin motor domain, we tested how these behaviors relied on the myosin motor activity. Our data suggest that the functional unit of myosin assembly may be composed of one or multiple myosin bipolar minifilaments, but also that minifilaments do not fully disassemble upon unbinding and diffusing in the cytoplasm. To test the overall stability of bipolar assemblies, we thus used photoconversion experiments and show that the myosin minifilaments are indeed recycled over long distances and diffusion times in the cytoplasm as minifilamentous units, that do not dissolve upon unbinding. Our work thus sheds light on how myosin minifilaments interact with the cortex, but offers a new perspective on how they assemble, disassemble and are recycled during cell morphogenesis
Chougule, Anil Mahaveer. „Rôle des régulateurs de l'actine dans la mise en place de l'asymétrie gauche-droite chez la Drosophile : la formine DAAM est essentielle pour l’asymétrie gauche-droite“. Electronic Thesis or Diss., Université Côte d'Azur (ComUE), 2019. http://www.theses.fr/2019AZUR4007.
Der volle Inhalt der QuelleBesides their external bilateral symmetry, most of the animals display left-right (LR) asymmetry of their internal organs. The asymmetric shapes and positions of the visceral organs are regulated by LR asymmetry signaling pathways and their disturbance results in severe congenital disorders. LR patterning in vertebrates and in invertebrates is regulated by different cytoskeletal elements: vertebrates employ microtubules and cilia, while in invertebrates, including Drosophila, the actin cytoskeleton has a prominent role. The actin system has long been proposed to play important role in animal LR asymmetry. To date, the proteins that are directly involved in the regulation of actin dynamics in establishing LR asymmetry have not been identified. In Drosophila, dextral anatomical handedness is determined by a single gene, the conserved type 1D myosin (Myo1D), discovered by the Noselli laboratory. myo1D is a unique situs inversus gene and a key LR determinant. Loss of myo1D function leads to a totally inverted LR organ asymmetry in flies (Sinistral). The genetic and developmental basis of sinistral asymmetry is unknown. Studies in zebrafish and Xenopus have shown that the myo1D orthologs control LR asymmetry indicating its evolutionarily conserved function in LR patterning in Drosophila and vertebrates. Further recent work by the Noselli laboratory has discovered that Myo1D is not only necessary for establishing LR asymmetry in Drosophila but also sufficient to generate de novo LR asymmetries at multiscale levels. This de novo asymmetry is assumed to result from a chiral interaction of Myo1D and actin filaments based on noncell-based assays. Defining this mechanism in vivo is critical to understanding the role of actin and its regulators as a reinforcing link between Myo1D and the actin cytoskeleton in animal LR asymmetry. To characterize the role of actin cytoskeleton in LR asymmetric development, I performed an RNA interference-based genetic screen down-regulating the functions of cytoskeletal genes in both Dextral and Sinistral genetic backgrounds. My study identifies the main actin nucleator formin DAAM as an essential component for LR asymmetry determination in Drosophila. Flies lacking DAAM show symmetrical morphogenesis of LR organs indicating the loss of LR asymmetry. Notably, DAAM is required for both dextral and sinistral development in Drosophila. In addition, genetic analysis revealed that dextral development requires the F-actin network constructed by coordinated activities of the formins Diaphanous and DAAM. Moreover, DAAM is also required for de novo formation of LR asymmetry, suggesting that the DAAM nucleated F-actin network acts as an essential structural component required for chirality determination involving Myo1D activity. DAAM overexpression enhances these asymmetries further adding an extra chiral twist, reflecting that a pool of DAAM decorated actin filaments acts as limiting factor for organ looping in LR asymmetry. In this setting, DAAM molecularly interacts with the Drosophila homolog of Profilin, chickadee (chic) and silencing chic mimics the DAAM loss-of-function phenotype. I also uncovered roles for a subset of actin regulators fli, Lg(2)l, Tec29, Dizzy, βPS mys, rhea and Rap1 in LR asymmetry, indicating they functionally act in the same actin regulatory pathway. Altogether, these original findings clearly demonstrated the fundamental role of actin and its regulation by formins in LR asymmetry and provide insight into the molecular basis underlying animal asymmetry
Chen, Yolande. „Mécanismes de la thrombocytopénie chez les patients atteints de maladies liées au gène MYH9“. Sorbonne Paris Cité, 2015. http://www.theses.fr/2015USPCC107.
Der volle Inhalt der QuelleMutations in the MYH9 gene cause autosomal dominant MYH9-related diseases (MYH9-RD) that associate macrothrombocytopenia with various other clinical conditions. The mechanisms giving rise to giant platelets remain poorly understood. The aim was to study the proplatelet formation (PPF) derived from megakaryocytes (MKs) generated in vitro from 11 patients with MYH9-RD with different mutations, compared with controls. Proplatelet formation from cultured patients' MKs was evaluated with or without blebbistatin or the ROCK inhibitor Y27632. Myosin HA and actin distribution were studied in spreading MKs on different surfaces by immunoconfocal analysis. Kinetic studies of contractility were performed on spreading MKs and the impact of blebbistatin on the maturation of the patients' MKs was evaluated by electron microscopy. We show that in vitro MKs of 11 patients formed significantly fewer proplatelets than controls. MKs from MYH9-RD displayed an abnormal spreading on polylysine, fibronectin and collagen, with a disorganized actin network and a marked increase in stress fiber formation. Traction force microscopy studies demonstrated an elevated level of contractile forces in adherent mutated MKs. The myosin II inhibitor blebbistatin and the ROCK inhibitor Y27632 both rescued the proplatelet formation defect and normalized the ultrastructural characteristics of MYH9-RD MKs. Altogether, our results show that in MYH9-RD, mutations modify the overall MYH9 function and provoke a proplatelet defect through an excess of actomyosin contractility in spreading MKs. These results may promote new therapeutic strategies aimed at reducing this actomyosin contractility
Lepine, Priscilla. „Rôle de la myosine 1b dans la ségrégation cellulaire et le développement intestinal induits par la signalisation EphB/éphrineB“. Paris 6, 2013. http://www.theses.fr/2013PA066367.
Der volle Inhalt der QuelleInteraction of EphB transmembrane tyrosine kinase receptors with their ligands ephrinB triggers signaling that regulates cell migration and proliferation and contributes to the formation of tissues boundaries. Changes in cell morphology including cell contraction and formation of protrusions have been reported during this process. By controlling cell migration EphB/ephrinB signaling is also required to guide progenitor cells to an appropriate environment and indirectly regulates their proliferation. The mechanisms controlling cell migration induced by EphB/ephrinB signaling are not fully characterized. We aimed to understand the mechanism that couples plasma membrane to the cortical actin network upon EphB/ephrinB signaling. We found that the activated EphB2 receptors interact with myosin 1b (Myo1b) and promote its phosphorylation. Myo1b is required for cell segregation mediated by EphB2/ephrinB1 signaling and both ephb2 and myo1b proteins also control the intestinal epithelium development in zebrafish by regulating cell proliferation. Both cell segregation and proliferation rely on directed cell migration, actin cytoskeleton remodeling and coupling between the cortical actin network and the EphB2 receptors at the plasma membrane. Myosins 1 which mechanically couple membranes to actin cytoskeleton can fulfill this function. We observed that Myo1b motor activity and its phosphorylation are required for protrusions and actomyosine cables formation upon EphB/ephrinB signaling. These data suggest that by coupling the plasma membrane to the underlying cortical actin network Myo1b conveys EphB2 signaling and contributes to cell segregation and intestinal epithelium development
Petzoldt, Astrid G. „DE-cadherin regulates unconventional myosin ID through myosin IC in Drosophila melanogaster“. Nice, 2009. http://www.theses.fr/2009NICE4048.
Der volle Inhalt der QuelleThe accurate establishment of stereotyped L/R asymetry is subject to a strict genetic program and crucial for the functionality of the organism. It is only recently that the mechanism of L/R asymmetry establishment is exploited in the invertebrate species Drosphophila melanogaster (Hozumi et al. , 2006 ; Speder et al. , 2006). The unconventional type ID myosin (MyoID) has been characterised as a dextral determinant accountable for the clockwise (dextral) rotation of the male genital plate during pupae stage. In our attempt to isolate new components of the L/R mechanism, we first focussed on MyoIC, the closest homologue of genitalia, thus L/R axis inversion. We provide evidence that this situs inversus phenotype is du to an inhibition of MyoID function through MyoIC and consequently define MyoIC as an anti-dextral effector of MyoID. An interaction between MyoID and adherents junctions had been suggested by Speder et al. (2006) as the authors could show by two-hybrid screen and GST pull down that MyoID tail and beta-catenin cal physically interact. Our DE-cadherin loss and gain of function studies revealed a linear interaction between DE-cadherin zand the unconventional myosins MyoID and MyoIC. DE-cadherin controls MyoIC expression, acting as inhibitor of MyoIC. As MyoID functionality is regulated by MyoIC expression, myoIC functions as a mediator between DE-cadherin and myoID. In summary, we present in this study a new regulatory network of L/R asymmetry establishment, where DE-cadherin affects MyoID activity through regulation of MyoIC protein expression
Bouvagnet, Patrice. „Polymorphisme de la myosine et étude de la régulation de sa transcription“. Montpellier 2, 1989. http://www.theses.fr/1989MON20112.
Der volle Inhalt der QuelleBoyer, Cécile. „Etude de la gelification thermique de la myosine : incidence du polymorphisme musculaire“. Clermont-Ferrand 2, 1995. http://www.theses.fr/1995CLF21725.
Der volle Inhalt der QuelleNOZAIS, MURIEL. „Stabilite des tetes globulaires et de la queue fibreuse de la myosine“. Paris 11, 1993. http://www.theses.fr/1993PA112418.
Der volle Inhalt der QuelleBETTACHE, NADIR. „Interactions de la g-actine avec la tete globulaire de la myosine“. Paris 6, 1991. http://www.theses.fr/1991PA066418.
Der volle Inhalt der QuellePaduano, Vanessa. „Regulation of Myosin-II activation and planar polarity during epithelial morphogenesis in Drosophila embryo“. Thesis, Aix-Marseille, 2015. http://www.theses.fr/2015AIXM4102.
Der volle Inhalt der QuelleEpithelial build up strong mechanical and chemical barriers in Metazoans. Epithelia can be dramatically remodeled during embryogenesis. Tissue morphogenesis is driven by coordinated cellular deformations which are powered by intracellular contractile networks constituting actin and Myosin. Actomyosin networks can either be pulsatile or stable. One example is the elongation of the ventral-lateral ectoderm by cell intercalation, along antero-posterior (AP) axis of Drosophila embryo. Junctions parallel to the dorso-ventral (DV) axis shrink and form new junctions along AP axis. Medial apical Myosin-II (Myo-II) pulses flow anisotropically towards junctions aligned in DV axis, resulting in steps of junction shrinkage which are stabilized by a planar-polarized pool of Myo-II enriched at these junctions. Sequential deformation and stabilization drive irreversible tissue deformations akin to a ratchet. The cellular mechanisms that regulate Myo-II pulsatility, stability and polarity remained to be unfurled. During my PhD, I identified new regulators for Rho1-Rok-Myo-II pathway at junctions, and Myo-II planar polarity. On the one hand, I characterized the function of Misshapen kinase in polarized activation of Rho1 pathway at junctions. Misshapen acts downstream GPCR signaling to enhance Rho1 activation, and controls the polarization of this activation by transducing information from Toll receptors. Also, I identified Pebble as RhoGEF regulating Rho1 at junctions and Myo-II accumulation
Pochitaloff-Huvalé, Marie. „Auto-organisation de faisceaux d'actine oscillants dans un systeme minimal d'actomyosine“. Thesis, Sorbonne université, 2018. http://www.theses.fr/2018SORUS318/document.
Der volle Inhalt der QuelleThe emergent active behaviors of molecular motors assemblies and cytoskeletal filaments systems remain poorly understood, though individual molecules have been extensively characterized. By controlling the geometry of actin polymerization with surface micropatterns of a nucleation promoting factor, we were able to demonstrate in vitro the emergence of flagellar-like beating of bundles of parallel actin filaments in the presence of myosin motors. We worked with both myosin V and heavy-meromyosin II. The waveform of oscillation was similar for the two types of motors, but oscillations with myosin II were one order of magnitude faster than with myosin Va. In both cases, a bending wave traveled at a uniform speed from the anchored base of the actin bundle towards the tip. As polymerization occurred, the actin bundle elongated at a constant speed, resulting in an increase of the oscillation period, but the speed of the traveling bending wave remains constant. GFP-tagged myosin V revealed the presence of a myosin concentration peak within the actin bundle. Strikingly, myosin V motors were locally recruited within the actin bundle, before a concentration wave propagated towards the bundle’s tip in concert with the actin bending wave. These results revealed a novel form of coupling between the myosin affinity for actin and the actin bundle shape. Our work demonstrates that active flagellar-like beating emerges as an intrinsic property of polar bundles of filaments in interaction with molecular motors. Structural control over the self-assembly process provides key information to clarify the underlying physical principles of flagellar-like beating
Logé, Cédric. „Conception et synthèse d'inhibiteurs de la rho-kinase“. Lille 2, 2002. http://www.theses.fr/2002LIL2P007.
Der volle Inhalt der QuellePernelle, Jean-Jacques. „Expression de différentes protéines myofibrillaires au cours de la myogénèse in vitro de cellules musculaires humaines normales et dystrophiques“. Paris 11, 1989. http://www.theses.fr/1989PA112369.
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