Дисертації з теми "Non muscle myosin II A"
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Frei, Ryan. "Regulatory Elements of Drosophila Non-Muscle Myosin II." Thesis, University of Oregon, 2013. http://hdl.handle.net/1794/12954.
Повний текст джерела2015-07-11
Swailes, Nathan. "Actin and non-muscle myosin II in pre-fusion myoblasts." Thesis, University of Leeds, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.416842.
Повний текст джерелаPicariello, Hannah Stubbs. "The Diverse Roles of Non-muscle Myosin II in Tumorigenesis." Case Western Reserve University School of Graduate Studies / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=case1562680454131993.
Повний текст джерелаKhan, Protiti. "The Role of Myosin Light Chain Kinase and Non Muscle Myosin II In Ras Signaling to ERK." Scholarly Repository, 2008. http://scholarlyrepository.miami.edu/oa_theses/177.
Повний текст джерелаSankara, Narayana Gautham Hari Narayana. "Role of non-muscle myosin-II isoforms in adherens junction biogenesis and collective migration." Thesis, Université de Paris (2019-....), 2019. https://theses.md.univ-paris-diderot.fr/SANKARA_NARAYANA_Gautham_Hari_Naryana_va.pdf.
Повний текст джерелаAdherens junction formation and remodeling is essential for many biological processes like embryo compaction, tissue morphogenesis and wound healing. It is now well described that non-muscle myosin II (NMII) acts as a mechanical support and force-generator for E-cadherin junctions during collective migration and morphogenesis. However, the contribution of NMII during early steps of junction formation remains obscure, probably because of the technical difficulty to catch such a transient event. In this work, we investigate the role of non-muscle myosin II isoforms (NMIIA and NMIIB) during adherens junction biogenesis in MDCK cells, using an in vitro reductionist approach. This system, based on chemically switchable micropatterns allows a spatio-temporal control of adherens junction formation. Our observations on MDCK cells show that the cells form irreversible E-cadherin based contacts, junction elongation is accompanied by the repolarization of actin cytoskeleton and nucleus-centrosome axis. Using isoform-specific ShRNA for NMIIA and IIB, we show that they have distinct contributions to junction formation and dynamics. NMIIA and NMIIB differentially regulate biogenesis of AJ through association with distinct actin networks. Analysis of junction dynamics, actin organization, and mechanical forces of control and knockdown cells for myosins revealed that NMIIA provides the mechanical tugging force necessary for cell-cell junction reinforcement and maintenance. NMIIB is involved in E-cadherin clustering, maintenance of a branched actin layer connecting E-cadherin complexes and perijunctional actin fibres leading to the building-up of anisotropic stress. These data reveal unanticipated complementary functions of NMIIA and NMIIB in the biogenesis and integrity of AJ
Ricketson, Derek Lee. "Drosophila non-muscle myosin II bipolar filament formation : importance of charged residues and specific domains for self-assembly /." Connect to title online (Scholars' Bank) Connect to title online (ProQuest), 2009. http://hdl.handle.net/1794/10285.
Повний текст джерелаDing, Siyu Serena. "Elucidating the role of non-muscle myosin II in Caenorhabditis elegans stem-like seam cell divisions." Thesis, University of Oxford, 2015. https://ora.ox.ac.uk/objects/uuid:5b5cb805-327a-4a58-b3db-3787f5264efc.
Повний текст джерелаRicketson, Derek Lee 1980. "Drosophila non-muscle myosin II bipolar filament formation: Importance of charged residues and specific domains for self-assembly." Thesis, University of Oregon, 2009. http://hdl.handle.net/1794/10285.
Повний текст джерелаNon-muscle myosin II generates contractile forces for processes such as cytokinesis, motility, and polarity. Contractility requires assembly of myosin molecules into bipolar mini-filaments through electrostatic interactions between coiled-coil tail domains of the heavy chains. Analyses of myosin II from various organisms have revealed "assembly domains" within the C-terminal portion of the tail domain that mediate filament formation. However, it has been unclear precisely how assembly domains interact with one another, or otherwise contribute to tail-tail interactions, to form the bipolar mini-filament structure. To understand tail domain interactions, we first identified a 90-residue region (1849-1940) of the Drosophila non-muscle myosin II tail domain that was necessary and sufficient for filament formation, using salt-dependent solubility and a novel fluorescence energy transfer assay. We identified residues within this "assembly domain" that were critical for filament assembly by analyzing the effect of point mutations. We found that single point mutations in specific positively charged regions completely disrupt filament assembly. Surprisingly, none of the negatively charged regions within the assembly domain are required for assembly. Most of the mutations in positively charged residues that disrupted filament assembly clustered within a 15-residue segment (1880-1894) that appears to form a critical interaction surface. Using this information, along with known geometrical constraints and electrostatic calculations, we constructed a structural model of the bipolar mini-filament. This model features one favored anti-parallel tail overlap and multiple slightly less stable alternative overlaps. The ability of the positive segment to interact with multiple negative regions explains the lack of required negatively charged residues in the assembly domain. To our knowledge, this structural model of the non- muscle myosin II bipolar filament is consistent with all physical observations and provides a framework for understanding the detailed mechanism by which this fundamental cellular structure is generated. This dissertation contains previously published and unpublished co-authored material.
Committee in charge: Tom Stevens, Chairperson, Chemistry; Kenneth Prehoda, Advisor, Chemistry; J. Andrew Berglund, Member, Chemistry; Christopher Doe, Member, Biology; Karen Guillemin, Outside Member, Biology
Sarkar, Saheli. "Combined Experimental and Mathematical Approach for Development of a Microfabrication-Based Model to Investigate Cell-Cell Interaction during Migration." Case Western Reserve University School of Graduate Studies / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=case1301420667.
Повний текст джерелаMessineo, Stefania. "Development of a gene targeting strategy (Recombinase-Mediated CAssette Exchange) to generate cellular models of MYH9-related disease." Doctoral thesis, Università degli studi di Trieste, 2011. http://hdl.handle.net/10077/4603.
Повний текст джерелаLa malattia MYH9-correlata (MYH9-RD) è una malattia autosomica dominante, caratterizzata da trombocitopenia congenita con piastrine di grandi dimensioni, aggregati nei neutrofili, sordità progressiva, cataratta e nefropatia. La MYH9-RD è causata da mutazioni nel gene MYH9 che codifica per la catena pesante della miosina non muscolare di classe II (miosina-9). I meccanismi patogenetici che causano questa malattia non sono ancora stati chiaramente identificati e il loro studio è complicato dalla mancanza di adeguati modelli cellulari e animali. Lo scopo di questo progetto è stato di generare un modello in vitro per studiare la funzione della miosina-9 e il ruolo di due mutazioni che incorrono nel gene MYH9: la R702C e la R1933X, che correlano rispettivamente con un fenotipo grave e lieve. Per questo motivo abbiamo deciso di manipolare le cellule staminali embrionali murine (ES), che sono pluripotenti e possono essere differenziate in diversi linee cellulari, compresa la linea megacariocitica. Per ingegnerizzare queste cellule ad alta efficienza abbiamo messo a punto una strategia nota come "scambio di cassette mediato da ricombinasi" (RMCE). Dopo l'integrazione di una cassetta fiancheggiata da siti FRT (sequenze di riconoscimento per l'enzima flippasi), il sistema ci ha permesso di scambiare diverse sequenze di DNA in presenza dell'enzima flippasi. Quindi il primo esone codificante del gene Myh9 è stato distrutto dall'inserimento, mediante ricombinazione omologa, di una cassetta fiancheggiata da due siti FRT contenente il gene reporter Beta-galattosidasi. Successivamente abbiamo scambiato questa cassetta con altre tre contenenti il cDNA Myh9 murino wild-type e i due mutati, generando i cloni ES che esprimono queste sequenze esogene sotto il controllo del promotore Myh9 endogeno. La caratterizzazione a livello dell'RNA e delle proteine di questi cloni ci ha portato a stabilire che gli alleli mutati e wild-type sono espressi allo stesso livello, suggerendo che le manipolazioni genetiche non interferiscono con i corretti meccanismi fisiologici di trascrizione e traduzione del gene Myh9. Tuttavia, mediante Western Blot abbiamo mostrato che la proteina miosina-9 è espressa a livello inferiore nei cloni mutati rispetto ai wild-type. Le analisi di immunofluorescenza per indagare la presenza di aggregati di miosina-9, che sono sempre presenti nei neutrofili di pazienti, non hanno rilevato alcuna variazione nella distribuzione della miosina-9, fatta eccezione per un segnale di intensità minore. Questi risultati indicano che, nonostante l'espressione dell'allele ingegnerizzato sia normale, la proteina mutata sembra essere degradata, almeno nelle cellule ES murine, determinando un effetto di aploinsufficienza delle mutazioni R702C e R1933X. Per accertare la loro pluripotenza, abbiamo differenziato dei cloni ES in corpi embrioidi e cardiomiociti, senza rivelare alcuna differenza tra i cloni mutanti e i wild-type. Dal momento che una caratteristica congenita dei pazienti MYH9-RD è la macrotrombocitopenia, abbiamo sviluppato un protocollo per differenziare i cloni mutati ES in megacariociti per indagare come le mutazioni in MYH9 portino a una impropria produzione di piastrine. In conclusione, per studiare la MYH9-RD abbiamo sviluppato una strategia che ci ha permesso di esprimere sequenze di interesse in cellule ES di topo sotto il controllo del promotore Myh9 endogeno. La differenziazione in vitro di queste cellule ci permetterà di studiare l'effetto delle mutazioni nel corso della megacariocitopoiesi. Inoltre, poiché le cellule ES possono anche essere usate per generare modelli animali, questa strategia ci permetterà di testare diverse ipotesi patogenetiche in vitro, prima di passare a studi in vivo.
XXIII Ciclo
1982
Adamek, Nancy. "Kinetic properties of slow isoforms of mammalian muscle and non-muscle myosin." Thesis, University of Kent, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.516203.
Повний текст джерелаHawthorne, Alicia Lynn. "The Development and Regeneration of the Serotonergic System." Case Western Reserve University School of Graduate Studies / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=case1264027000.
Повний текст джерелаThomas, Dustin G. "ROLE OF NON-MUSCLE MYOSIN IIB IN BREAST CANCER INVASION." Case Western Reserve University School of Graduate Studies / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=case1449156792.
Повний текст джерелаFlynn, Patrick G. "Activation of Non-Muscle Myosin IIB Helps Mediate TNF-Alpha Cell Death Signaling." Scholarly Repository, 2010. http://scholarlyrepository.miami.edu/oa_dissertations/369.
Повний текст джерелаIrvine, Andrew Francis. "Characterising the interaction between metastasis-associated protein S100A4 and non-muscle myosin IIA in vitro and in vivo." Thesis, University of Leicester, 2012. http://hdl.handle.net/2381/27622.
Повний текст джерелаPersson, Malin. "Characterization and optimization of the in vitro motility assay for fundamental studies of myosin II." Doctoral thesis, Linnéuniversitetet, Institutionen för kemi och biomedicin (KOB), 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-25241.
Повний текст джерелаZepter, Valeria Lamounier. "Analyse der Funktion der nichtmuskulären schweren Myosinketten in glatten Muskelzellen." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2003. http://dx.doi.org/10.18452/14837.
Повний текст джерелаThe aim of the present study was to investigate the involvement of non-muscle myosin heavy chain in smooth muscle contraction under physiological conditions. As an experimental model urinary bladder from neonatal wild-type mice as well as from neonatal mice with disrupted smooth muscle myosin heavy chain expression was used. This animal model was established through gene targeting technology, resulting in complete elimination of the expression of smooth muscle myosin heavy chains. The lack of expression of smooth muscle myosin heavy chains was confirmed by electrophoresis and immunoblotting. On the other hand, non-muscle myosin heavy chain expression remained normal, as verified by Western blot analysis. The mechanical analysis of smooth muscle was performed with intact urinary bladder preparations, stimulated using prolonged KCl depolarization or with phorbol ester. Prolonged activation by KCl depolarization of intact bladder preparations from wild-type neonatal mice produced an initial transient state (phase 1) of high force generation and maximal shortening velocity, followed by a sustained state (phase 2) with lower force generation and maximal shortening velocity. In contrast, bladder preparations from homozygous knockout neonatal mice did not exhibit phase 1, but phase 2 could be observed, i.e. a similar isometric force and maximal shortening velocity, compared to wild-type phase 2. Thus, non-muscle myosin appears to be recruited in the sustained phase of smooth muscle contraction during prolonged KCl depolarization in the animal model used. Upon stimulation with phorbol ester a similar sustained contraction was observed in both wild-type and knockout smooth muscle preparations. Therefore, non-muscle myosin may also be recruited during phorbol ester stimulation in both wild-type and knockout muscle preparations. The participation of non-muscle myosin in smooth muscle contraction was further supported by the finding of longitudinally arranged intracellular filaments in cultivated smooth muscle cells from both wild-type and knockout mice by immunofluorescence microscopy, using a specific antibody raised against non-muscle myosin heavy chain. In a similar way, smooth muscle myosin heavy chain structures were investigated in cultivated smooth muscle cells. As expected, longitudinally arranged intracellular filamentous structures of smooth muscle myosin were observed in wild-type smooth muscle cells, but not in smooth muscle cells from knockout mice. In conclusion, in neonatal smooth muscle the initial phase of contraction elicited by KCl depolarization is generated by smooth muscle myosin heavy chain recruitment. Upon prolonged KCl depolarization non-muscle myosin is recruited in the sustained phase of contraction, as well as upon stimulation with phorbol ester. Thus, it was possible, for the first time, to verify the involvement of the non-muscle myosin in smooth muscle contraction in vivo. The results of the present study contribute to the understanding of the regulatory mechanisms of smooth muscle contraction.
Höök, Peter. "A novel single skeletal muscle cell in vitro motility assay : effects of aging and non-enzymatic glycosylation on myosin function /." Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4688-4/.
Повний текст джерелаZehrer, Annette [Verfasser], and Barbara [Akademischer Betreuer] Walzog. "The non-muscle myosin heavy chain Myh9 is essential for neutrophil migration during acute inflammation / Annette Zehrer ; Betreuer: Barbara Walzog." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2020. http://d-nb.info/1206878126/34.
Повний текст джерелаMatsunaga, Erika Midoli. "Distribuição do tipo de fibras musculares e sua correlação genotípica na doença de Pompe." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/5/5138/tde-29042009-102848/.
Повний текст джерелаThe glycogen storage disease type II (GSDII), autosomal recessive disorder, is caused by the deficiency of GAA (acid -glucosidase) a lysossomal enzyme that degrades the glycogen. The clinical findings are in accordance to great variability of age onset, degree of disease progression and extent of tissue involvement: predominantly cardiac and skeletal muscle in the infantile form (I) and more restricted to the skeletal muscle in the late-onset form (LO). The average survival time of the infantile form is 9-12 months. With advances of the histological, histochemical and imunohistochemical methods structural and functional analysis of muscle fiber types were intensified. The study of the capillary density is also important for nutritional and functional aspects. The objective of the present work is to analyze the correlations of the fiber type distribution to clinical presentation, genotype and residual GAA enzymatic activity. We analyzed 10 muscle biopsies of infantile and 09 of late-onset patients and compared to age and gender matched controls. The patients were selected according to clinical and laboratorial data, molecular diagnosis by full gene sequencing, and Western Blotting (WB) with monoclonal antibody 15362-157, courtesy Genzyme Science Group (primary 1:200 and secondary 1:10.000). Diagnostic confirmation was made by GAA enzymatic measurement in DBS, presence of vacuolar myopathy in muscle biopsy, and presence of mutation in GAA gene. The imunohistochemical study was carried out by detection of type I (slow), type II (fast) fibers and capillaries, using monoclonal antibodies, respectively: anti-slow myosin (1:80), anti-fast myosin (1:40) (Novocastra) and ulex (1:800) (Vector). Morphometry was performed by 2 observers using a half-automatized program. Type II fiber predominance was observed in both gender in the infantile form, type I fiber predominance in women and type II predominance in men with LO. Increase of the capillary density, in comparison to controls was noticed in both forms. 90% of vacuolated fibers with complete distortion of fiber architecture were demonstrated in I cases, while in LO, the percentage of vacuolated fibers ranged from 0 to 88%. As some constitutive gene, like ACE, influence muscle fiber distribution, its polymorphisms I/I, D/D and I/D gene were analyzed. Absence of agreement was observed between ACE genotype and fiber type distribution in 60% of I and LO cases, which was attributed as consequence of Pompe disease pathology itself. The disease severity varied inversely to the amount of residual GAA enzymatic activity, being compatible with the patient clinical findings. The presence of deleterious mutation in both alleles was observed in 3/10 infantile cases, and all 3 presented total enzyme absence at WB. A greater fiber type II involvement was observed in GSDII, without decrease in muscle capillary density. Recent studies demonstrated that glycogen deposit removal occurs distinctively in different fiber types, being less efficient in type II fibers. The present findings might have implications in the reply to the recent proposed enzyme replacement therapy.
Streppa, Laura. "Characterizing mechanical properties of living C2C12 myoblasts with single cell indentation experiments : application to Duchenne muscular dystrophy." Thesis, Lyon, 2017. http://www.theses.fr/2017LYSEN008/document.
Повний текст джерелаThis interdisciplinary thesis was dedicated to the atomic force microscopy (AFM) characterization of the mechanical properties of myoblasts (murine and human) and myotubes (murine). We reported that the mechanical properties of these cells were modified when their actin cytoskeleton (CSK) dynamics was inhibited or altered. Recording single AFM force indentation curves, we showed that adherent layers of myoblasts and myotubes introduced on the AFM cantilever an extra hydrodynamic drag as compared to a solid wall. This phenomenon was dependent on the cantilever scan speed and not negligible even at low scan velocities (1μm/s). We observed that the mechanical properties of the muscle precursor cells became non-linear (plastic behaviour) for large local deformations (>1μm) and that they varied depending on the state, type and environment of the cells. Combining AFM experiments, viscoelastic modeling and multi-scale analyzing methods based on the wavelet transform, we illustrated the variability of the mechanical responses of these cells (from viscoelastic to viscoplastic). Through AFM force indentation curves analysis, morpho-structural imaging (DIC, fluorescence microscopy) and pharmacological treatments, we enlightened the important role of active (ATP-dependent) processes in myoblast mechanics, focusing especially on those related to the molecular motors (myosin II) coupled to the actin filaments. In particular, we showed that the perinuclear actin stress fibers could exhibit some abrupt remodelling events (ruptures), which are characteristic of the ability of these cells to tense their CSK. Finally, we showed that this approach can be generalized to some human clinical cases, namely primary human myoblasts from healthy donors and patients affected by Duchenne muscular dystrophy, paving the way for broader studies on different cell types and diseases
Borges, Ricardo Moraes. "Constrição celular apical durante a invaginação do placóide do cristalino em galinhas." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/42/42134/tde-24032009-100332/.
Повний текст джерелаVertebrate lens derives from invagination of the ectoderm that overlies optic vesicles. Epithelial invagination in many model systems is driven by apical cell constriction, mediated by actin and myosin II contraction regulated by GTPase RhoA. Here we investigate the possibility that chick lens placode invagination could also be driven by apical cell constriction and controlled by RhoA. We show that actin and myosin II are expressed at lens apical side during lens invagination. Actin polymerization inhibition by in ovo Cytochalasin D treatment prevents lens placode invagination, suggesting that lens placode invagination could be driven by apical cell constriction. RhoA GTPase is also expressed at apical portion of lens placode and during lens invagination. However, when we overexpressed by electroporation the dominant-negative RhoA in the pre-lens ectoderm invagination was not affected. Furthermore, dominant-negative RhoA didnt affect myosin II apical localization nor myosin II phosphorilation, indicating that in lens invagination this process is not regulated by GTPase RhoA.
Schulz, Cathrin. "Tumour-selective apoptosis : identification of NMHCIIa as novel death receptor interactor regulating the response to TRAIL." Phd thesis, Université de Strasbourg, 2012. http://tel.archives-ouvertes.fr/tel-01069133.
Повний текст джерелаRao, Yanhua. "An Atat1/Mec-17-Myosin II axis controls ciliogenesis." Diss., 2013. http://hdl.handle.net/10161/7224.
Повний текст джерелаPrimary cilia are evolutionarily conserved, acetylated microtubule-based organelles that transduce mechanical and chemical signals. Primary cilium assembly is tightly controlled and its deregulation causes a spectrum of human diseases. Formation of primary cilium is a collaborative effort of multiple cellular machineries, including microtubule, actin network and membrane trafficking. How cells coordinate these components to construct the primary cilia remains unclear. In this dissertation research, we utilized a combination of cell biology, biochemistry and light microscopy technologies to tackle the enigma of primary cilia formation, with particular focus on isoform-specific roles of non-muscle myosin II family members. We found that myosin IIB (Myh10) is required for cilium formation. In contrast, myosin IIA (Myh9) suppresses cilium formation. In Myh10 deficient cells, Myh9 inactivation significantly restores cilia formation. Myh10 antagonizes Myh9 and increases actin dynamics, permitting pericentrosomal preciliary complex formation required for cilium assembly. Importantly, Myh10 is upregulated upon serum starvation-induced ciliogenesis and this induction requires Atat1/Mec-17, the microtubule acetyltransferase. Our findings suggest that Atat1/Mec17-mediated microtubule acetylation is coupled to Myh10 induction, whose accumulation overcomes the Myh9-dependent actin cytoskeleton, thereby activating cilium formation. Thus, Atat1/Mec17 and myosin II coordinate microtubules and the actin cytoskeleton to control primary cilium biogenesis.
Dissertation
Patino, Descovich Carlos. "Characterizing cortical myosin mini-filament regulation, length and its macroscopic implications in cytokinetic dynamics." Thèse, 2013. http://hdl.handle.net/1866/11328.
Повний текст джерелаPERCARIO, VALENTINA. "A study of the mechano-kinetic parameters of different isoforms of muscle myosin II in vivo." Doctoral thesis, 2017. http://hdl.handle.net/2158/1079340.
Повний текст джерелаSantos, Marina Patrícia Fonseca. "Identification of novel non-muscle myosin IIA (NMIIA) interacting partners." Master's thesis, 2013. https://repositorio-aberto.up.pt/handle/10216/70448.
Повний текст джерелаSantos, Marina Patrícia Fonseca. "Identification of novel non-muscle myosin IIA (NMIIA) interacting partners." Dissertação, 2013. https://repositorio-aberto.up.pt/handle/10216/70448.
Повний текст джерелаVaqueirinho, Daniela Helena da Ascenção Loureiro Geraldo. "The role of Arl13b and the non-muscle myosin IIA in cancer cell migration." Master's thesis, 2017. http://hdl.handle.net/10362/26412.
Повний текст джерелаTsai, Hsiao-Chu, and 蔡効矩. "Using an optogenetic platform (CRY2/CIB1) to study the interaction between non-muscle myosin MYH9 and microtubules." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/hkgbda.
Повний текст джерела國立交通大學
分子醫學與生物工程研究所
107
Growth cone is a highly motile structure in developing neuron. It detects different axon guidance cues, which is known to attract or repel axons growth. These guidance molecules accomplish this by changing the structure of neuronal cytoskeleton, which leads to neurite extension or retraction. Migrating cells exist similar structure called leading edge. It responds to extracellular cues to polarize and extend protrusions in the direction of migration. While the protein molecules involved in these processes have been identified, the precise mechanism remains unknown. MYH9 is an ubiquitously expressed non-muscle myosin that localizes to the leading edge and affect neurite outgrowth and cell migration. It has been shown that microtubules and F-actin transiently interact with each other in the growth cone. However, the protein mediating such interaction remains elusive. Our recent observation that MYH9 and microtubules interact with each other prompts us to investigate whether MYH9 is mediating such interaction and whether this interaction is the mechanism of neurite retraction and cell migration. To test this hypothesis, we set up a system that can artificially induce the interaction between microtubules and MYH9, and use this system to investigate whether microtubule-MYH9 interaction can affect neurite retraction and cell migration. However, we did not observe a stronger interaction between MYH9 and microtubules during neurite retraction, and the data in migration cells did not show any effect about cell migration after artificially induce the interaction between microtubules and MYH9.
Goloborodko, Alexander. "Molecular Mechanisms of Germ Plasm Anchoring in the Early Zebrafish Embryo." Doctoral thesis, 2019. http://hdl.handle.net/21.11130/00-1735-0000-0005-145A-0.
Повний текст джерелаSolinet, Sara. "Les rôles distincts des isoformes de myosine II non-musculaire dans des processus cellulaires impliquant le cytosquelette d'actine." Thèse, 2008. http://hdl.handle.net/1866/2852.
Повний текст джерелаWe are interested in studying the modulation of the actomyosin complex which is involved in different cellular processes such as cell locomotion and apoptosis. The actomyosin complex is formed by the association of actin filaments and myosin II. The non-muscle myosin II is a hexamer formed by one pair of heavy chains (MHCs) and two pairs of light chain (MLC20 and MLC17). The actomyosin activity is dependent on MLC20 and MHCs phosphorylation. There are three isoforms of MHCs (MHCIIA, MHCIIB and MHCIIC) which have common but also distinctive roles in several cellular processes. Our aim is to clarify the structural and contractile functions of each isoforme of myosin II in different cellular processes, in particular, cell contraction and cell morphology. First, we studied the implication of myosin II isoforms in cell shrinkage and detachment during apoptosis which are both dependent on actomyosin contractility. We treated four different cell lines with TNFα in combination with cycloheximide (CHX) to trigger apoptosis. We confirmed that TNFα induced caspase-3 activation, ROCK1 cleavage and increased MLC20 phosphorylation. We showed that TNFα/CHX induced the caspase-dependent MHCIIA degradation, whereas MHCIIB levels and association with the actin cytoskeleton remained virtually unchanged. Cell shrinkage and detachment were blocked by caspase and ROCK1 inhibitors. Using the MHCIIB (-/-) cell line, we observed that the absence of MHCIIB did not affect cell death rate. However, MHCIIB (-/-) fibroblasts showed more resistance to TNFα-induced actin disassembly, cell shrinkage and detachment than wild type (Wt) fibroblasts, indicating the participation of MHCIIB in these events. PKCζ, which only phosphorylates MHCIIB, was cleaved during apoptosis, co-immunoprecipitated preferentially with MHCIIB and, interestedly, PKCζ inhibition blocked TNFα-induced shrinkage and detachment. Our results demonstrate that MHCIIB, together with MLC phosphorylation and actin, constitute the actomyosin cytoskeleton that mediates contractility during apoptosis. Second, we studied the involvement of myosin II isoforms in cell shape modulation. Fibroblasts MHCIIB (-/-) spontaneously formed lamellipodia whereas Wt fibroblasts presented a stellate shape. Cortactin was associated with the leading edge of lamellipodia in MHCIIB (-/-) fibroblasts, but it localised diffusely in the cytoplasm or at the end of fine cellular projections in Wt fibroblasts. The levels of cortactin and cortactin phosphorylated in Tyr421 associated with membrane in MHCIIB (-/-) fibroblasts were higher than in Wt fibroblasts. Confocal microscopy showed cortactin/MHCIIA colocalization in wild type but not in MHCIIB (-/-) fibroblasts. bFGF activates Erk1/2 in wild type and MHCIIB (-/-) fibroblasts and induces the formation of aberrant membrane projections in MHCIIB (-/-) fibroblasts. In conclusion, our results contribute to characterize the structural and contractile role of each myosin II isoforms in the physiology of the cell.