Academic literature on the topic 'Actomyosine – Contraction'
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Journal articles on the topic "Actomyosine – Contraction"
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Murrell, Michael, and Margaret L. Gardel. "Actomyosin sliding is attenuated in contractile biomimetic cortices." Molecular Biology of the Cell 25, no. 12 (June 15, 2014): 1845–53. http://dx.doi.org/10.1091/mbc.e13-08-0450.
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Myosin II motors embedded within the actin cortex generate contractile forces to modulate cell shape in essential behaviors, including polarization, migration, and division. In sarcomeres, myosin II–mediated sliding of antiparallel F-actin is tightly coupled to myofibril contraction. By contrast, cortical F-actin is highly disordered in polarity, orientation, and length. How the disordered nature of the actin cortex affects actin and myosin movements and resultant contraction is unknown. Here we reconstitute a model cortex in vitro to monitor the relative movements of actin and myosin under conditions that promote or abrogate network contraction. In weakly contractile networks, myosin can translocate large distances across stationary F-actin. By contrast, the extent of relative actomyosin sliding is attenuated during contraction. Thus actomyosin sliding efficiently drives contraction in actomyosin networks despite the high degree of disorder. These results are consistent with the nominal degree of relative actomyosin movement observed in actomyosin assemblies in nonmuscle cells.
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Slabodnick, Mark M., Sophia C. Tintori, Mangal Prakash, Pu Zhang, Christopher D. Higgins, Alicia H. Chen, Timothy D. Cupp, et al. "Zyxin contributes to coupling between cell junctions and contractile actomyosin networks during apical constriction." PLOS Genetics 19, no. 3 (March 28, 2023): e1010319. http://dx.doi.org/10.1371/journal.pgen.1010319.
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One of the most common cell shape changes driving morphogenesis in diverse animals is the constriction of the apical cell surface. Apical constriction depends on contraction of an actomyosin network in the apical cell cortex, but such actomyosin networks have been shown to undergo continual, conveyor belt-like contractions before the shrinking of an apical surface begins. This finding suggests that apical constriction is not necessarily triggered by the contraction of actomyosin networks, but rather can be triggered by unidentified, temporally-regulated mechanical links between actomyosin and junctions. Here, we used C. elegans gastrulation as a model to seek genes that contribute to such dynamic linkage. We found that α-catenin and β-catenin initially failed to move centripetally with contracting cortical actomyosin networks, suggesting that linkage is regulated between intact cadherin-catenin complexes and actomyosin. We used proteomic and transcriptomic approaches to identify new players, including the candidate linkers AFD-1/afadin and ZYX-1/zyxin, as contributing to C. elegans gastrulation. We found that ZYX-1/zyxin is among a family of LIM domain proteins that have transcripts that become enriched in multiple cells just before they undergo apical constriction. We developed a semi-automated image analysis tool and used it to find that ZYX-1/zyxin contributes to cell-cell junctions’ centripetal movement in concert with contracting actomyosin networks. These results identify several new genes that contribute to C. elegans gastrulation, and they identify zyxin as a key protein important for actomyosin networks to effectively pull cell-cell junctions inward during apical constriction. The transcriptional upregulation of ZYX-1/zyxin in specific cells in C. elegans points to one way that developmental patterning spatiotemporally regulates cell biological mechanisms in vivo. Because zyxin and related proteins contribute to membrane-cytoskeleton linkage in other systems, we anticipate that its roles in regulating apical constriction in this manner may be conserved.
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Wirshing, Alison C. E., and Erin J. Cram. "Myosin activity drives actomyosin bundle formation and organization in contractile cells of the Caenorhabditis elegans spermatheca." Molecular Biology of the Cell 28, no. 14 (July 7, 2017): 1937–49. http://dx.doi.org/10.1091/mbc.e17-01-0029.
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Stress fibers—contractile actomyosin bundles—are important for cellular force production and adaptation to physical stress and have been well studied within the context of cell migration. However, less is known about actomyosin bundle formation and organization in vivo and in specialized contractile cells, such as smooth muscle and myoepithelial cells. The Caenorhabditis elegans spermatheca is a bag-like organ of 24 myoepithelial cells that houses the sperm and is the site of fertilization. During ovulation, spermathecal cells are stretched by oocyte entry and then coordinately contract to expel the fertilized embryo into the uterus. Here we use four-dimensional confocal microscopy of live animals to observe changes to spermathecal actomyosin network organization during cell stretch and contraction. Oocyte entry is required to trigger cell contraction and concomitant production of parallel actomyosin bundles. Actomyosin bundle size, connectivity, spacing, and orientation are regulated by myosin activity. We conclude that myosin drives actomyosin bundle production and that myosin activity is tightly regulated during ovulation to produce an optimally organized actomyosin network in C. elegans spermathecae.
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Krueger, Daniel, Theresa Quinkler, Simon Arnold Mortensen, Carsten Sachse, and Stefano De Renzis. "Cross-linker–mediated regulation of actin network organization controls tissue morphogenesis." Journal of Cell Biology 218, no. 8 (June 28, 2019): 2743–61. http://dx.doi.org/10.1083/jcb.201811127.
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Contraction of cortical actomyosin networks driven by myosin activation controls cell shape changes and tissue morphogenesis during animal development. In vitro studies suggest that contractility also depends on the geometrical organization of actin filaments. Here we analyze the function of actomyosin network topology in vivo using optogenetic stimulation of myosin-II in Drosophila embryos. We show that early during cellularization, hexagonally arrayed actomyosin fibers are resilient to myosin-II activation. Actomyosin fibers then acquire a ring-like conformation and become contractile and sensitive to myosin-II. This transition is controlled by Bottleneck, a Drosophila unique protein expressed for only a short time during early cellularization, which we show regulates actin bundling. In addition, it requires two opposing actin cross-linkers, Filamin and Fimbrin. Filamin acts synergistically with Bottleneck to facilitate hexagonal patterning, while Fimbrin controls remodeling of the hexagonal network into contractile rings. Thus, actin cross-linking regulates the spatio-temporal organization of actomyosin contraction in vivo, which is critical for tissue morphogenesis.
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Martin, Adam C., Michael Gelbart, Rodrigo Fernandez-Gonzalez, Matthias Kaschube, and Eric F. Wieschaus. "Integration of contractile forces during tissue invagination." Journal of Cell Biology 188, no. 5 (March 1, 2010): 735–49. http://dx.doi.org/10.1083/jcb.200910099.
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Contractile forces generated by the actomyosin cytoskeleton within individual cells collectively generate tissue-level force during epithelial morphogenesis. During Drosophila mesoderm invagination, pulsed actomyosin meshwork contractions and a ratchet-like stabilization of cell shape drive apical constriction. Here, we investigate how contractile forces are integrated across the tissue. Reducing adherens junction (AJ) levels or ablating actomyosin meshworks causes tissue-wide epithelial tears, which release tension that is predominantly oriented along the anterior–posterior (a-p) embryonic axis. Epithelial tears allow cells normally elongated along the a-p axis to constrict isotropically, which suggests that apical constriction generates anisotropic epithelial tension that feeds back to control cell shape. Epithelial tension requires the transcription factor Twist, which stabilizes apical myosin II, promoting the formation of a supracellular actomyosin meshwork in which radial actomyosin fibers are joined end-to-end at spot AJs. Thus, pulsed actomyosin contractions require a supracellular, tensile meshwork to transmit cellular forces to the tissue level during morphogenesis.
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Yi, Jason, Xufeng S. Wu, Travis Crites, and John A. Hammer. "Actin retrograde flow and actomyosin II arc contraction drive receptor cluster dynamics at the immunological synapse in Jurkat T cells." Molecular Biology of the Cell 23, no. 5 (March 2012): 834–52. http://dx.doi.org/10.1091/mbc.e11-08-0731.
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Actin retrograde flow and actomyosin II contraction have both been implicated in the inward movement of T cell receptor (TCR) microclusters and immunological synapse formation, but no study has integrated and quantified their relative contributions. Using Jurkat T cells expressing fluorescent myosin IIA heavy chain and F-tractin—a novel reporter for F-actin—we now provide direct evidence that the distal supramolecular activation cluster (dSMAC) and peripheral supramolecular activation cluster (pSMAC) correspond to lamellipodial (LP) and lamellar (LM) actin networks, respectively, as hypothesized previously. Our images reveal concentric and contracting actomyosin II arcs/rings at the LM/pSMAC. Moreover, the speeds of centripetally moving TCR microclusters correspond very closely to the rates of actin retrograde flow in the LP/dSMAC and actomyosin II arc contraction in the LM/pSMAC. Using cytochalasin D and jasplakinolide to selectively inhibit actin retrograde flow in the LP/dSMAC and blebbistatin to selectively inhibit actomyosin II arc contraction in the LM/pSMAC, we demonstrate that both forces are required for centripetal TCR microcluster transport. Finally, we show that leukocyte function–associated antigen 1 clusters accumulate over time at the inner aspect of the LM/pSMAC and that this accumulation depends on actomyosin II contraction. Thus actin retrograde flow and actomyosin II arc contraction coordinately drive receptor cluster dynamics at the immunological synapse.
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Lippincott, J., K. B. Shannon, W. Shou, R. J. Deshaies, and R. Li. "The Tem1 small GTPase controls actomyosin and septin dynamics during cytokinesis." Journal of Cell Science 114, no. 7 (April 1, 2001): 1379–86. http://dx.doi.org/10.1242/jcs.114.7.1379.
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Cytokinesis in budding yeast involves an actomyosin-based ring which assembles in a multistepped fashion during the cell cycle and constricts during cytokinesis. In this report, we have investigated the structural and regulatory events that occur at the onset of cytokinesis. The septins, which form an hour-glass like structure during early stages of the cell cycle, undergo dynamic rearrangements prior to cell division: the hourglass structure splits into two separate rings. The contractile ring, localized between the septin double rings, immediately undergoes contraction. Septin ring splitting is independent of actomyosin ring contraction as it still occurs in mutants where contraction fails. We hypothesize that septin ring splitting may remove a structural barrier for actomyosin ring to contract. Because the Tem1 small GTPase (Tem1p) is required for the completion of mitosis, we investigated its role in regulating septin and actomyosin ring dynamics in the background of the net1-1 mutation, which bypasses the anaphase cell cycle arrest in Tem1-deficient cells. We show that Tem1p plays a specific role in cytokinesis in addition to its function in cell cycle progression. Tem1p is not required for the assembly of the actomyosin ring but controls actomyosin and septin dynamics during cytokinesis.
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Szymanski, P. T., J. D. Strauss, G. Doerman, J. DiSalvo, and R. J. Paul. "Polylysine activates smooth muscle actin-myosin interaction without LC20 phosphorylation." American Journal of Physiology-Cell Physiology 262, no. 6 (June 1, 1992): C1446—C1455. http://dx.doi.org/10.1152/ajpcell.1992.262.6.c1446.
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Phosphorylation/dephosphorylation of the 20-kDa light chain of smooth muscle myosin is a major regulator of actin-myosin interaction. Phosphatase inhibitors have thus been shown to enhance contraction in smooth muscle. The activity of type II phosphatase against phosphorylated myosin light chains is inhibited by polylysine. Thus we studied the effects of polylysine (10-13 kDa) on actin-myosin interaction in permeabilized guinea pig taenia coli fibers and in bovine aortic actomyosin. Addition of polylysine (10-20 microM) to Ca-ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid buffered solution ([Ca2+] less than 0.01 microM) elicited a contraction in fibers of 40 +/- 8% (n = 6) of maximally stimulated contractions ([Ca2+] congruent to 1.5 microM). Untreated fibers did not generate any significant force in parallel control experiments. Similarly, polylysine stimulated the ATPase activity both in fibers and actomyosin in a dose-dependent manner. This stimulation could be completely inhibited and abolished upon addition of heparin, a negatively charged heteropolysaccharide. In actomyosin previously phosphorylated with ATP gamma S, polylysine in a concentration range of 2-13 microM did not further stimulate enzyme activity. These increases in activity were not connected with significant changes in the phosphorylation of 20-kDa myosin light chain nor could any incorporation of 32P associated with polylysine stimulation be detected in both skinned fibers and actomyosin by autoradiography of SDS gels. Our data indicate that polylysine increases actin-myosin interaction in both smooth muscle model systems by directly influencing contractile proteins. As such, polylysine may be a useful probe for the mechanism of activation of smooth muscle.
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Chew, Ting Gang, Junqi Huang, Saravanan Palani, Ruth Sommese, Anton Kamnev, Tomoyuki Hatano, Ying Gu, Snezhana Oliferenko, Sivaraj Sivaramakrishnan, and Mohan K. Balasubramanian. "Actin turnover maintains actin filament homeostasis during cytokinetic ring contraction." Journal of Cell Biology 216, no. 9 (June 27, 2017): 2657–67. http://dx.doi.org/10.1083/jcb.201701104.
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Cytokinesis in many eukaryotes involves a tension-generating actomyosin-based contractile ring. Many components of actomyosin rings turn over during contraction, although the significance of this turnover has remained enigmatic. Here, using Schizosaccharomyces japonicus, we investigate the role of turnover of actin and myosin II in its contraction. Actomyosin ring components self-organize into ∼1-µm-spaced clusters instead of undergoing full-ring contraction in the absence of continuous actin polymerization. This effect is reversed when actin filaments are stabilized. We tested the idea that the function of turnover is to ensure actin filament homeostasis in a synthetic system, in which we abolished turnover by fixing rings in cell ghosts with formaldehyde. We found that these rings contracted fully upon exogenous addition of a vertebrate myosin. We conclude that actin turnover is required to maintain actin filament homeostasis during ring contraction and that the requirement for turnover can be bypassed if homeostasis is achieved artificially.
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VerPlank, Lynn, and Rong Li. "Cell Cycle-regulated Trafficking of Chs2 Controls Actomyosin Ring Stability during Cytokinesis." Molecular Biology of the Cell 16, no. 5 (May 2005): 2529–43. http://dx.doi.org/10.1091/mbc.e04-12-1090.
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Cytokinesis requires the coordination of many cellular complexes, particularly those involved in the constriction and reconstruction of the plasma membrane in the cleavage furrow. We have investigated the regulation and function of vesicle transport and fusion during cytokinesis in budding yeast. By using time-lapse confocal microscopy, we show that post-Golgi vesicles, as well as the exocyst, a complex required for the tethering and fusion of these vesicles, localize to the bud neck at a precise time just before spindle disassembly and actomyosin ring contraction. Using mutants affecting cyclin degradation and the mitotic exit network, we found that targeted secretion, in contrast to contractile ring activation, requires cyclin degradation but not the mitotic exit network. Analysis of cells in late anaphase bearing exocyst and myosin V mutations show that both vesicle transport and fusion machineries are required for the completion of cytokinesis, but this is not due to a delay in mitotic exit or assembly of the contractile ring. Further investigation of the dynamics of contractile rings in exocyst mutants shows these cells may be able to initiate contraction but often fail to complete the contraction due to premature disassembly during the contraction phase. This phenotype led us to identify Chs2, a transmembrane protein targeted to the bud neck through the exocytic pathway, as necessary for actomyosin ring stability during contraction. Chs2, as the chitin synthase that produces the primary septum, thus couples the assembly of the extracellular matrix with the dynamics of the contractile ring during cytokinesis.
Dissertations / Theses on the topic "Actomyosine – Contraction"
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Özgüç, Özge. "Mechanical and Molecular Regulation of Periodic Cortical Waves of Contraction." Electronic Thesis or Diss., Sorbonne université, 2021. http://www.theses.fr/2021SORUS482.
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Au cours du développement préimplantatoire, l'embryon de mammifère forme le blastocyste, qui est la structure fixant l'embryon dans l'utérus. La formation du blastocyste repose en grande partie sur les forces contractiles générées par le cortex d'actomyosine. Chez la souris, sur des échelles de temps de quelques secondes, nous observons des impulsions de contractions d'actomyosine voyageant périodiquement autour du périmètre cellulaire. Nous appelons ce phénomène vagues de contraction corticale périodique (PeCoWaCo), une manifestation fascinante et mal comprise de la contractilité. Dans cette étude, nous profitons du développement lent de l'embryon de souris pour étudier des milliers d'impulsions de contraction. Nous mettons également à profit la robustesse de ce développement pour explorer les propriétés biophysiques des PeCoWaCo pendant les étapes de clivage précédant la morphogenèse précoce des mammifères.Nous constatons que, lors des étapes de clivage, des mouvements périodiques apparaissent occasionnellement au stade zygote et 2-cellules puis deviennent systématiques après le 2ème cycle de divisions de clivage. Fait intéressant, la période des oscillations diminue progressivement de 200s au stade zygote à 80s au stade 8-cellules. Étant donné que les cellules deviennent de plus en plus petites avec des divisions de clivage successives, la taille des cellules pourrait être un déterminant important dans l'initiation et la régulation des PeCoWaCo. Nous manipulons la taille des cellules sur une large gamme de rayons cellulaires (10-40 µm) en utilisant la fragmentation et la fusion des cellules et constatons que l'initiation, la persistance ou les propriétés des PeCoWaCo ne dépendent pas de la taille des cellules. Après la période des PeCoWaCo, on découvre que les tensions de surface des blastomères diminuent progressivement jusqu'au stade de 8-cellules et que l’assouplissement artificiel des cellules augmente prématurément les PeCoWaCo. Par conséquent, lors des étapes de clivage, l’assouplissement cortical réveille la contractilité zygotique avant la morphogenèse préimplantatoire. En plus, en manipulant la contractilité de l'actomyosine à l'aide de mutants et des drogues, nous avons montré que la période des PeCoWaCo peut être contrôlée par la régulation du taux de polymérisation de l'actine filamenteuse et de l'activité motrice de la myosine.Dans l'ensemble, nos résultats sur les aspects biophysiques et moléculaires du PeCoWaCo nous aident à comprendre comment la contractilité de l'actomyosine s'éveille avant la morphogenèse préimplantatoire et comment elle est régulée au niveau mécanique et moléculaireDuring pre-implantation development, the mammalian embryo forms the blastocyst, which is the structure embedding the embryo into the uterus. The shaping of the blastocyst relies in large part on contractile forces generated by the actomyosin cortex. In the mouse, on timescales of seconds, we observe pulses of actomyosin contractions traveling periodically around the cell perimeter. We call this phenomenon periodic cortical waves of contraction (PeCoWaCo), a fascinating and poorly understood manifestation of contractility. In this study, we take advantage of the slow development of the mouse embryo to study thousands of contraction pulses and of the robustness of the mouse embryo to size manipulation to explore the biophysical properties of PeCoWaCo during the cleavage stages preceding early mammalian morphogenesis. We find that, during cleavage stages, periodic movements appear occasionally at the zygote and the 2-cell stage and become systematic after the 2nd round of cleavage divisions. Interestingly, the period of oscillations progressively decreases from 200 s at the zygote stage to 80 s at the 8-cell stage. Since cells becomes successively smaller with successive cleavage divisions, cell size could be an important determinant in the initiation and regulation of PeCoWaCo. We manipulate cell size on a broad range of cell radii (10-40 µm) using fragmentation and fusion of cells and find that the initiation, persistence or properties of PeCoWaCo do not depend on cell size. Following the period of PeCoWaCo, we discover that blastomeres gradually decrease their surface tensions until the 8-cell stage and that artificially softening cells enhances PeCoWaCo prematurely. Therefore, during cleavage stages, cortical softening awakens zygotic contractility before preimplantation morphogenesis. In addition, by manipulating actomyosin contractility using mutants and drugs, we showed that the period of PeCoWaCo can be tuned by F-actin polymerization rate and myosin motor activity. Altogether our results on biophysical and molecular aspects of PeCoWaCo help us understand how actomyosin contractility awakens before preimplantation morphogenesis and how it is regulated both mechanically and molecularly
İmplantasyon öncesi gelişim sırasında, memeli embriyosu, embriyoyu rahim içineyerleştiren yapı olan blastosisti oluşturur. Blastosistin şekillendirilmesi büyük ölçüdeaktomiyozin korteks tarafından oluşturulan kasılma kuvvetlerine dayanır. Farede, saniyelikzaman ölçeklerinde, hücre çevresinde periyodik olarak dolaşan aktomiyozin kasılmalarınındarbeleri gözlemlenebilir. Bu fenomene, kasılmanın büyüleyici ve yeterince anlaşılmamış birtezahürü olan periyodik kortikal kasılma dalgaları (periodic cortical waves of contraction:PeCoWaCo) diyoruz. Bu çalışmada, erken memeli morfogenezinden önceki bölünmeaşamaları sırasında PeCoWaCo'nun biyofiziksel özelliklerini keşfetmek ve binlerce kasılmadarbesini inceleyebilmek için fare embriyosunun yavaş gelişiminden ve fare embriyosununboyut manipülasyonuna dayanıklılığından faydalandık.Bölünme aşamaları sırasında, zigotta ve 2 hücreli aşamada periyodik hareketlerinzaman zaman ortaya çıktığını ve ikinci tur bölünmeden sonra bu hareketlerin sistematik halegeldiğini bulduk. İlginç bir şekilde, salınım periyodunun zigot aşamasında 200 saniyeden, 8hücreli aşamada 80 saniyeye sistematik olarak azaldığını gözlemledik. Hücreler ardışıkbölünmeleriyle sürekli küçüldüğünden, hücre boyutu PeCoWaCo'nun başlatılmasında vedüzenlenmesinde önemli bir belirleyici olabilir. Hücreleri geniş bir hücre yarıçapı aralığında(10-40 μm) küçük parçalara bölerek veya birbirleriyle birleştirerek PeCoWaCo'nunbaşlatılmasının, kalıcılığının veya genel özelliklerinin hücre boyutuna bağlı olmadığını bulduk.PeCoWaCo periyodunu takiben, embriyo hücrelerinin zigottan 8 hücreli aşamaya kadar yüzeygerilimini kademeli olarak azalttığını ve yapay olarak korteksleri yumuşatılan hücrelerinPeCoWaCo'yu zamanından önce geliştirdiğini keşfettik. Bu sonuçlarla bölünme aşamalarısırasında, kortikal yumuşama, ilke implantasyon öncesi morfogenezinden önce zigotikkasılmaları uyandırdığını gösterdik. Ayrıca, genetik mutantlar ve kimyasallar kullanarakaktomiyozin kasılmasını manipüle ederek, PeCoWaCo periyodunun F-aktin polimerizasyonhızı ve miyozin motor aktivitesinin düzenlenmesi ile ayarlanabileceğini gösterdik.Sonuç olarak, PeCoWaCo'nun biyofiziksel ve moleküler yönleriyle ilgili bulgularımız,aktomiyosin kontraktilitesinin implantasyon öncesi morfogenezinden önce nasıl uyandığını,ayrıca hem mekanik hem de moleküler olarak nasıl düzenlendiğini anlamamıza yardımcı olur
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Elmezgueldi, Mohammed. "Régulation de la contraction du muscle lisse par les protéines associées au filament fin : caractérisation des interfaces actine-calponine et actine-caldesmone." Montpellier 1, 1994. http://www.theses.fr/1994MON13525.
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Chaussepied, Patrick. "Transduction de l'énergie par le complexe actomyosine dans le muscle squelettique : intercommunication entre le site ATPasique et les sites de reconnaissance de l'actine." Montpellier 2, 1986. http://www.theses.fr/1986MON20042.
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L'etude utilise principalement trois techniques differentes: premierement, la proteolyse specifique suivie de la purification et de la caracterisation des fragments peptiques obtenus; deuxiemement, l'introduction de pontages intra et inter-moleculaires et finalement, des etudes en cinetique rapide. Nous avons pu ainsi identifier une region de la tete de myosine contenant un site de liaison de la partie polyphosphate de l'atp et un site d'interaction de l7actine. La liaison des deux ligants (actine et atp) a ce peptide induisent une mobiite interne. Ces mouvements intramoleculaires reveles egalement dans d'autres regions de la tete de myosine fut mise en evidence grace a des experiences de resonance magnetique nucleaire du proton.
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Ennomani, Hajer. "Contractile response of biomimetic actomyosin systems." Thesis, Université Grenoble Alpes (ComUE), 2015. http://www.theses.fr/2015GREAY054/document.
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La contractilité cellulaire, un phénomène orchestrée par le système d'actomyosine, est un régulateur critique d'une large gamme de processus cellulaires, y compris l'établissement de la polarité cellulaire, la migration cellulaire, l'intégrité des tissus au cours de la morphogenèse ou du développement. Une simple perturbation de la génération de la force et des propriétés mécaniques des cellules peut affecter leurs fonctions physiologiques et par conséquent peut conduire à des défauts pathologiques y compris le cancer.Cependant, les mécanismes qui contrôlent la production de la force par le système acto-myosine et leurs modes de régulation dans les cellules ne sont pas pleinement compris. Au cours de ma thèse, j'ai utilisé un système biomimétique fait d'un ensemble minimal de protéines purifiées pour étudier les propriétés contractiles du système actomyosin.L'objectif était de comprendre comment l'architecture des filaments d'actine peut modifier la réponse contractile. A cet effet, j'étais d'abord intéressée par la construction d'une variété d'organisation de l'actine qui servira après comme substrat pour les moteurs moléculaires (la myosine) lors de la contraction.Afin de comprendre les principes généraux qui dictent l'assemblage de l'actine, nous avons développé un modèle numérique qui nous a permis d'identifier les paramètres clés, y compris l'interaction entre les filaments d'actine, les propriétés mécaniques de ces filaments et l'activation par contact entre une région de nucléation et les filaments d'actine qui poussent à partir d'un motif adjacent. Ce modèle a été utilisé en premier lieu pour implémenter les propriétés reliées à l'actine et en second lieu pour évaluer la réponse contractile des structures d'actine induite par la myosine.Durant ma thèse, j'ai pu démontrer que le niveau de connectivité module la déformation du réseau d'actine induite par la myosine, selon leur architecture. J'ai montré aussi que les protéines de pontages des filaments d'actine sont nécessaires pour effectuer une déformation et générer des forces au niveau des réseaux d'actine dynamiques en présence de la myosine. De plus, nous avons développé les simulations numériques dans le but de relier la déformation macroscopique des structures d'actines due à la myosine avec le mécanisme microscopique sous-jacent.Ce travail a révélé comment la variété des réseaux d'actine contracte d'une façon différente même en respectant les mêmes conditions biochimiques et a démontré l'importance de l'effet du réarrangement dynamique des structures d'actine sur la modulation de sa contractilitéCellular contractility – the internal generation of force by a cell orchestrated by theactomyosin machinery – is a critical regulator of a wide range of cellular processes includingthe establishment of cell polarity, cell migration, tissue integrity or morphogenesis duringdevelopment. Disruptions of the force generation and of mechanical properties of living cellsaffect their physiological functions and consequently can lead to pathological defectsincluding cancer. However, the parameters or mechanisms that drive force production by theactin-myosin system and their mode of regulation in cells are not fully understood. During myPhD, I used biomimetic system made of a minimum set of proteins to study the properties ofactomyosin contractile systems. The goal was to understand how/if the actin architecture canmediate the contractile response. For this purpose, I was first interested in building a varietyof actin organization that will serve next as substrate for myosin during contraction. Tounderstand the general principles that dictate geometrically-controlled actin assembly, wedeveloped a model that allowed us to identify key parameters including filaments/filamentsinteraction, filament mechanical property and contact activation between actin filamentsgrowing from the adjacent pattern and the nucleation area. These actin templates were usedthen to evaluate the response of oriented actin structures to myosin-induced contractility. Idemonstrated that crosslinking level modulates the myosin-induced deformation of actinnetworks according to their architecture. I showed also that crosslinkers are necessary tosustain myosin-driven deformation and force production of dynamic actin networks. Inaddition, we developed numerical simulation in order to relate the observed myosin-drivenactin deformation with the underlying microscopic mechanism. This work revealed howdiverse cellular actin networks contract differently to a define set of biochemical conditionsand hence how dynamic rearrangements can modulate network contractility
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Venkova, Larisa. "Régulation du volume cellulaire en réponse aux déformations." Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS396/document.
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Dans les tissus, les cellules génèrent et sont soumises en permanence à des forces mécaniques. Les perturbations biochimiques à l'intérieur des cellules, ainsi que les altérations de leur environnement mécanique peuvent modifier l'équilibre physiologique et mener à des pathologies, comme le cancer. Bien que les propriétés mécaniques puissent être modifiées à l'échelle du tissus, la compréhension de la mécanique au niveau de la cellule unique demeure importante. En particulier, la différenciation, la migration des cellules immunitaires et le caractère invasif d'un cancer dépendent fortement des propriétés mécaniques des cellules uniques. Les déformations mécaniques peuvent induire un changement de la surface et du volume cellulaires. Nous nous intéressons particulièrement à la régulation du volume cellulaire chez les cellules mammifères dans le contexte de déformations à différentes échelles de temps. Jusqu'à présent, la régulation du volume dans ce contexte n'a été que très peu étudiée, en raison de la difficulté d'obtention de mesures précises, et du fait que le volume de la cellule est généralement considéré comme constant. Nous avons développé une méthode de mesure du volume cellulaire reposant sur l'exclusion de fluorescence, qui nous permet d'effectuer des mesures de volume précise au niveau de la cellule unique. Dans cette étude, nous nous sommes concentrés sur la régulation du volume cellulaire au cours de l'étalement dynamique sur un substrat (échelle de temps : minutes). Nous avons démontré qu'il existe différents régimes de régulation du volume lors de l'étalement : les cellules réduisent, augmentent ou ne modifient pas leur volume, en fonction de l'état du cortex d'actomyosine et de la vitesse d'étalement. Nous avons constaté que les cellules s'étalant plus vite ont tendance à perdre davantage de volume. Notre hypothèse est que lors d'une extension rapide de lamellipode dépendante d'Arp2/3, l'actine tire sur la membrane et génère une tension et l'activation de transport ionique, s'accompagnant d'une perte de volume compensatoire. L'inhibition de la polymérisation de l'actine ou de sa ramification dépendante d'Arp2/3 réduit la vitesse d'étalement et ainsi la perte de volume. Nous avons ensuite montré que l'inhibition de la contractilité augmente la vitesse d'étalement et la perte de volume. Cependant, l'inhibition d'Arp2/3 dans des cellules à faible contractilité conduit à un étalement rapide sans perte de volume. En effet, l'inhibition d'Arp2/3 induit des bulles de membranes, une déformation rapide n'induirait donc pas de perte de volume car la cellule peut relâcher la tension en dépliant la membrane. Nous avons également montré que la régulation du volume en réponse à une compression mécanique rapide (échelle de temps : millisecondes) indépendante de l'adhérence dépend également de l'état du cortex d'actomyosine. Les cellules perdent jusqu'à 30% de leur volume lorsqu'elles sont confinées, car la membrane plasmique est attachée au cortex et ne peux pas être dépliée en réponse à l'augmentation de la tension. La perturbation du cortex d'actine induit le détachement de la membrane et limite la perte de volume. Enfin, nous avons montré que la réponse du volume à un choc osmotique (échelle de temps : secondes) est plus que complexe que décrite dans la littérature. Nos données indiquent qu'au niveau de la cellule unique, la réponse initiale du volume au changement de l'osmolarité extérieure n'est pas un processus passif uniforme. En utilisant la technique du choc osmotique, nous avons également confirmé que les cellules ont un large excès de membrane repliée dans des réservoirs. Nos résultats montrent que le volume et l'aire cellulaires sont couplés par l'homéostasie de la tension de surface, et, étant donné que les déformations induisent une augmentation de la tension de surface, elles conduisent à des modifications du volume et de l'aire de la celluleThe field of biomechanics significantly progressed in the last two decades. The importance of the feedback between biochemical signaling and physical properties was revealed in many studies. Cells within tissues constantly generate and experience mechanical forces. Biochemical perturbations inside the cells as well as alterations in the mechanical environment can shift the tiny balance of normal physiological state and lead to pathologies, e.g. cancer. Although the mechanical properties of individual cells can alter when they are within the tissues, the understanding of single cell mechanics is still important. Differentiation, immune cell migration, and cancer invasion strongly depend on the mechanical properties of individual cells. Mechanical deformations can lead to a change in cell surface area and volume. We are particularly interested in single mammalian cell volume regulation in the context of deformations of different timescales. For the moment, volume regulation in this context was out from the research interest, probably due to the difficulties of accurate measurements, and cell volume often considered as a constant parameter. We developed a method for cell volume measurements based on a fluorescent exclusion that allowed us to perform precise volume measurements of individual live cells. In the present study, we mainly focused on cell volume regulation while dynamic spreading on a substrate (timescale – minutes). We demonstrated that there are different regimes for volume regulation while spreading: cells decrease, increase or do not change volume, and a type of the regime depends on the state of the actomyosin cortex and spreading speed. We obtained that faster-spreading cells tend to lose more volume. Our hypothesis is that during fast Arp2/3-driven lamellipodia extension actin pull on the membrane that generates tension and activation of ion transport and regulatory volume loss. Inhibition of actin polymerization or Arp2/3-dependent actin branching decreases spreading speed and volume loss. Next, we showed that inhibition of contractility increases spreading speed and volume loss. However, inhibition of Arp2/3 complex in cells with low contractility leads to fast spreading without volume loss. Our explanation is that inhibition of Arp2/3 induces cell blebbing and even fast deformation does not lead to volume loss as a cell can relax tension by membrane unfolding. We also showed that volume regulation in response to fast mechanical compression (timescale – milliseconds) independent of adhesion also depends on the actomyosin cortex state. Control cells lose up to 30% of volume under confinement, as the cell membrane is attached to the cortex and cannot be unfolded in response to the tension increase. Disruption of actin cortex leads to membrane detachment and prevents volume loss under confinement. Additionally, we showed that cell volume response to the osmotic shock (timescale – seconds) is more complex than it used to be known in the literature. For instance, our data indicate that at the level of individual cells initial volume response to the change of external osmolarity is not a uniform passive process. Using osmotic shock technique, we also confirmed that cells have a large excess of membrane folded in reservoirs. Taken together, our data show that cell volume and surface area are coupled through surface tension homeostasis and as deformations induce surface tension increase, they lead to change volume and surface area
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Mendes, Pinto Inês. "Spatiotemporal mechanisms for actomyosin ring assembly and contraction in budding yeast cell division." Doctoral thesis, Universidade Nova de Lisboa. Instituto de Tecnologia Química e Biológica, 2012. http://hdl.handle.net/10362/8571.
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Dissertation presented to obtain the Ph.D degree in Molecular MedicineAnimal and yeast cells use a contractile ring that is attached to the plasma membrane to create a cleavage furrow that partitions a cell into two in the latest step of cell division. The contractile ring is a network of actin and myosin-II motor filaments embedded in a complex and compact protein core structure at the cell division site. In the absence of myosin-II, cells fail to assemble the contractile ring pursuing death or rapidly evolving divergent pathways to restore growth and cytokinesis, an event associated to aneuploidy, a common trait in cancer development and progression. The molecular mechanisms underlying myosin-II localization and function at the cell division site with actin ring assembly and contraction remain poorly understood. Based on analogy to the striated muscle, it has been classically proposed that contractile stress in the actomyosin ring is generated via a “sliding filament” mechanism in which bipolar myosin-II motor filaments walk along actin filaments, within organized sarcomere-like arrays. However, ultra-structural and genetic studies in different cellular systems have shown that contractile rings are more complex than striated muscles, and in some examples the motor activity can actually be dispensable for the contractibility of the cytokinetic ring.(...)
PhD fellowship awarded by the Rong Li laboratory and a previous awarded fellow of the GABBA PhD program at the Faculty of Medicine, University of Porto, Portugal and the Portuguese Foundation for Science and Technology, Portugal. Apoio financeiro da Fundação para a Ciência e Tecnologia e do Fundo Social Europeu no âmbito do Quadro Comunitário de Apoio, BD n°SFRH/BD/11760/2003.
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Redwood, Charles Stuart. "Identification of the functional domains of smooth muscle caldesmon." Thesis, Imperial College London, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.243858.
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Krüger, Daniel [Verfasser], and Ulrich [Akademischer Betreuer] Schwarz. "Regulation of Actomyosin Contraction during Tissue Morphogenesis: Genes and Mechanics / Daniel Krüger ; Betreuer: Ulrich Schwarz." Heidelberg : Universitätsbibliothek Heidelberg, 2019. http://d-nb.info/1196097712/34.
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Krüger, Daniel [Verfasser], and Ulrich S. [Akademischer Betreuer] Schwarz. "Regulation of Actomyosin Contraction during Tissue Morphogenesis: Genes and Mechanics / Daniel Krüger ; Betreuer: Ulrich Schwarz." Heidelberg : Universitätsbibliothek Heidelberg, 2019. http://nbn-resolving.de/urn:nbn:de:bsz:16-heidok-271886.
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Sumi, Angughali Aheto 1986. "On contractile actomyosin waves and their role in junctional remodeling during epithelial constriction." Doctoral thesis, Universitat Pompeu Fabra, 2017. http://hdl.handle.net/10803/565600.
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Epithelial tissues undergo extensive remodeling during embryonic development. Recent studies have revealed that, in a number of developmental processes, epithelial remodeling is associated with pulsations of individual cell surface areas and cortical actomyosin flows.
During Drosophila dorsal closure, the amnioserosa (AS), a contractile tissue covering the dorsal region of the embryo, shows contractile pulsations and regular actomyosin flows during the reduction of its apical surface area. The biophysical mechanism driving these shape pulsations as well as the role of contractile actomyosin waves in epithelial contraction and dorsal closure still remains unclear.
In this project, we developed a biophysical model for cell shape oscillations that is based on intrinsic properties of the cell: cortex turnover, active contractility by force producing molecules and cell elasticity. We show that coupling these three key ingredients is sufficient for generating stable oscillations. Further, within this framework we were also able to generate waves by coupling the oscillating units and introducing a diffusion term to account for exchange of force producing molecules between the units.
Next, we investigated the role for these contractile actomyosin waves in tissue remodeling. We developed a novel technique that allowed us to apply mechanical stretch on the AS tissue and study the response of cells to such stress. With this method, we were able to arrest the pulsatile contractions and actomyosin flows in AS cells. We show that this arrest is associated with the relocalisation of actin and myosin from the medial region of the cells towards the adherens junctions to maintain junction integrity upon stretch. This relocalisation of myosin directly correlates with the junctional strain and does not occur in cells that have excessive membrane material as a consequence of endocytosis inhibition. In the latter case, cells continue pulsing and seem to be “insensitive” to stretch.
Upon stretch release, myosin relocalises to the medial area of the cell and pulsations resume. This indicates that cells can switch between two states depending on tension: one in which cells exhibit shape oscillations associated with contractile actomyosin pulses and waves, and the other where cell shape is stabilised with myosin preferentially localised at the cell junctions. Further, following release from long duration ( >10mins ) stretch application, cell junctions were highly wrinkled. Strong and consistent localisation of myosin waves at these regions led to straightening and reduction of junctional lengths. Moreover, during dorsal closure, AS cells constantly reduce their areas while maintaining junctions of consistent thickness and length relative to area. This is not the case where endocytosis is blocked or myosin activity is down-regulated.
Our results not only shed light on fundamental physical properties of the actomyosin cortex, in particular they also indicate a role of myosin contractile waves in junctional remodeling during AS cell constriction.Los tejidos epiteliales llevan a cabo una remodelación extensiva durante el desarrollo embrionario. Estudios recientes han revelada que, en un sinnumero de procesos de desarrollo embrionario, la remodelación epitelial se asocia con pulsaciones de áreas en células individuales y con flujos corticales de actomiosina. Durante el cierre dorsal de Drosophila, la amnioserosa (AS), un tejido contractil que cubre la región dorsal del embrión, se observan pulsaciones contráctiles en células individuales y flujos regulares de actomiosina durante la reducción de la superficial apical celular. Al día de hoy, no se conoce el mecanismo biofísico que produce estas pulsaciones celulares ni y el papel que tienen las oscilaciones contráctiles de actomiosina en el epitelio del cierre dorsal embrionario. En este proyecto, se desarrolló un modelo biofísico para entender estas oscilaciones celulares. El modelo se basa en propiedades intrínsecas de la célula como la rotación de la corteza celular, la contractilidad activa mediante moléculas productoras de fuerza y la elasticidad celular. Utilizando éste modelo, se muestra que acoplando estas tres propiedades clave es suficiente para generar oscilaciones celulares estables. Además, dentro de este marco, se han generado oscilaciones mediante el acoplamiento de varias unidades oscilantes y la introducción de un término de difusión para considerar el intercambio de moléculas productoras de fuerza entre las unidades. A continuación, se investigó el papel de estas oscilaciones contráctiles de actomiosina en la remodelación de tejidos. Como resultado, se desarrolla una técnica innovadora que permite aplicar extensión mecánica al tejido de AS y estudiar la respuesta celular ante tal estrés. Con este método, se pueden detener las pulsaciones contráctiles y los flujos de actomiosina en células de la AS. Se muestra que este arresto celular está asociado con la relocalización de actina y miosina de la región central de las células hacia las uniones adherentes intercelulares para mantener su integridad durante la extension epitelial. Esta relocalización de miosina se correlaciona directamente con la tensión en uniones intercelulares y no ocurre en células en las que el reciclaje cellular a través de endocitosis se ha bloqueado. El resultado es un exceso en la acumulación de membrana plasmática en células oscilantes que no responden a la extension epitelial. Tras liberar al tejido de la extension epithelial, la miosina se relocaliza a la área central de las células y las pulsaciones continuan. Esto indica que las células pueden cambiar entre dos estados según la tension aplicada: uno dónde las células muestran oscilaciones asociadas con pulsaciones contráctiles de actomiosina, y otra donde la forma celular se establece con la localización preferente de miosina en las uniones intercelulares. Además, tras liberar el tejido de una extensión de alta duración (>10mins), las uniones intercelulares sufrieron corrugaciones. La localización consistente de oscilaciones de miosina en las regions corrugadas, resulta en una extension y reducción en la longitud de las uniones intercelulares. Además, durante el cierre dorsal, las células de la AS reducen sus areas constantemente, mientras mantienen uniones intercelulares de espesor consistente y longitud relativa a su área. Esto no es el caso cuando la endocitosis se bloquea o la actividad de miosina se reduce. Nuestros resultados no solo muestran las propiedades fundamentales de la corteza cellular de actomiosina, también indican el papel de oscilaciones contráctiles de miosina en la remodelación de uniones intercelulares durante la constricción de la AS.
Books on the topic "Actomyosine – Contraction"
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1933-, Sugi Haruo, Pollack Gerald H, International Union of Physiological Sciences., and Symposium on Mechanisms of Work Production and Work Absorption in Muscle (1997 : Hakone-machi, Japan), eds. Mechanisms of work production and work absorption in muscle. New York: Plenum Press, 1998.
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1945-, Squire John, ed. Molecular mechanisms in muscular contraction. London: Macmillan, 1989.
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1945-, Squire John, ed. Molecular mechanisms in muscular contraction. Boca Raton, Fla: CRC Press, 1990.
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1945-, Squire John, ed. Molecular mechanisms in muscular contraction. Boca Raton, Fla: CRC Press, 1989.
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E, Alia Emmanuele, Arena Nicolò, Russo Matteo A, and University of Asssare. Institute of Histology and General Embryology., eds. Contractile proteins in muscle and non-muscle cell systems: Biochemistry, physiology, and pathology. New York: Praeger, 1985.
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Kurskiĭ, Mikhail Dmitrievich. Reguli͡a︡t͡s︡ii͡a︡ vnutrikletochnoĭ kont͡s︡entrat͡s︡ii kalʹt͡s︡ii͡a︡ v mysht͡s︡akh. Kiev: Nauk. dumka, 1987.
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E, Alia Emanuele, Arena Nicolò, Russo Matteo A, Università degli studi di Sassari. Institute of Histology and General Embryology., and Symposium on Biochemistry, Physiology, and Pathology of Contractile Proteins in Muscle and Nonmuscle Cell Systems (1st : 1983 : Sassari, Italy), eds. Contractile proteins in muscle and non-muscle cell systems: Biochemistry, physiology, and pathology. New York: Praeger, 1985.
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(Editor), Haruo Sugi, and Gerald H. Pollack (Editor), eds. Mechanisms of Work Production and Work Absorption in Muscle (Advances in Experimental Medicine and Biology). Springer, 1999.
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1945-, Squire John, ed. Molecular mechanisms in muscular contraction. Basingstoke: Macmillan, 1990.
Find full textBook chapters on the topic "Actomyosine – Contraction"
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Rall, Jack A. "Setting the Stage: Myosin, Actin, Actomyosin and ATP." In Mechanism of Muscular Contraction, 1–27. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-2007-5_1.
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Curtin, N. A., T. G. West, M. A. Ferenczi, Z. H. He, Y. B. Sun, M. Irving, and R. C. Woledge. "Rate of Actomyosin ATP Hydrolysis Diminishes During Isometric Contraction." In Advances in Experimental Medicine and Biology, 613–26. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9029-7_54.
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Yanagida, Toshio, Akihiko Ishijima, Kiwamu Saito, and Yoshie Harada. "Coupling Between Atpase and Force-Generating Attachment-Detachment Cycles of Actomyosin In Vitro." In Mechanism of Myofilament Sliding in Muscle Contraction, 339–49. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2872-2_33.
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"Contractile Actomyosin Ring (CAR)." In Encyclopedia of Systems Biology, 498. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_100278.
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Murrell, Michael, Todd Thoresen, and Margaret Gardel. "Reconstitution of Contractile Actomyosin Arrays." In Methods in Enzymology, 265–82. Elsevier, 2014. http://dx.doi.org/10.1016/b978-0-12-397924-7.00015-7.
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Röper, Katja. "Integration of Cell–Cell Adhesion and Contractile Actomyosin Activity During Morphogenesis." In Current Topics in Developmental Biology, 103–27. Elsevier, 2015. http://dx.doi.org/10.1016/bs.ctdb.2014.11.017.
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Goldberg, Michael L., Kristin C. Gunsalus, Roger E. Karess, and Fred Chang. "Cytokinesis." In Dynamics of Cell Division, 270–316. Oxford University PressOxford, 1998. http://dx.doi.org/10.1093/oso/9780199636839.003.0009.
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Abstract Cytokinesis is a multi-step process that proceeds linearly with time according to the following general framework. It begins with a signal from the mitotic apparatus that must be transmitted to the cellular cortex at the cleavage site. Receipt of the signal at the cortex sets off a complex set of reactions that transduce the signal into changes in the actin cytoskeleton and lead to formation of an actomyosin-based contractile ring. Mechanical processes in the ring and its interaction with the cortex result in cytokinesis. The distinctions between these steps are probably largely artificial. It is not clear, for example, whether some of the molecules we describe as transducing a cytokinetic signal are in fact part of the signal itself. Even this seemingly innocuous (though admittedly simplified) view of cytokinesis is not free of controversy, and some kinds of cytokinesis almost certainly do not conform to this pattern. Many questions remain unanswered and are addressed in the following sections.
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Zacheus Cande, W. "[45] Preparation of N-ethylmaleimide-modified heavy meromyosin and its use as a functional probe of actomyosin-based motility." In Structural and Contractile Proteins Part C: The Contractile Apparatus and the Cytoskeleton, 473–77. Elsevier, 1986. http://dx.doi.org/10.1016/0076-6879(86)34113-2.
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Matsuda, Miho, and Sergei Y. Sokol. "Xenopus neural tube closure: A vertebrate model linking planar cell polarity to actomyosin contractions." In Current Topics in Developmental Biology, 41–60. Elsevier, 2021. http://dx.doi.org/10.1016/bs.ctdb.2021.04.001.
Full textConference papers on the topic "Actomyosine – Contraction"
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Owen, Drew, and Evan Zamir. "The Role of Actomyosin Contractility During Early Avian Gastrulation." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19574.
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Actin-myosin contraction has been shown to play a major role in early morphogenetic movements in Drosophila (fly) and Xenopus (frog) [1,2]. However, the specific role of actomyosin contractility in amniote embryos (reptiles, birds, and mammals) during primitive streak (PS) formation, the “organizing center” for gastrulation (formation of three primary germ layers), is not known. Current theories regarding primitive streak formation in higher order amniotes center around cell-cell intercalation or chemotactic cell movement [3,4]. We hypothesize that contraction via actin-myosin (AM) filaments is conserved from anamniotes and drives formation of the PS and the associated morphogenetic cell movements.
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Wang, Hailong, Alexander A. Svoronos, Thomas Boudou, Jeffrey R. Morgan, Christopher S. Chen, and Vivek B. Shenoy. "Necking and Failure of Constrained Contractile 3D Microtissues: Role of Geometry and Stiffness." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14091.
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We report the discovery of a fundamental morphological instability of constrained 3D microtissues induced by a positive chemomechanical feedback between actomyosindriven contraction and the mechanical stresses arising from the constraints. Using a 3D model for mechanotransduction we find that perturbations in the shape of contractile tissues grow in an unstable manner leading to formation of “necks” where tensile stresses are sufficiently large to lead to the failure of the tissue by narrowing and subsequent elongation. The origin of the failure mechanism driven by active forces we report is distinct from the seemingly similar and well studied necking phenomena observed in “passive” materials due to elastic softening. Here the instability is caused by the active contraction (extension) of the regions of the tissue where the mechanical stresses are smaller (greater) than the characteristic actomyosin stall stress of the tissue. The magnitude of the instability is shown to be determined by the level of active contractile strain, the stiffness of the ECM and the stiffness of the boundaries that constrain the tissue. A phase diagram that demarcates stable and unstable behavior of 3D tissues as a function of these material parameters is derived. The predictions of our model are verified by analyzing the necking and failure of normal human fibroblast (NHF) tissue constrained in a loopended dogbone geometry and cardiac microtissues constrained between microcantilevers. In the former case, the tissue fails first by necking of the connecting rod of the dogbone followed by failure of the toroidal loops in agreement with our 3D finite element simulations. In the latter case we find that cardiac tissue is stable against necking when the density of the extra cellular matrix is increased and when the stiffness of the supporting cantilevers is decreased, also in excellent agreement with the predictions of our model. By analyzing the time evolution of the morphology of the constrained tissues we have quantitatively determined the chemomechanical coupling parameters that characterize the generation of active stresses in these tissues. More generally, the analytical and numerical methods we have developed provide a quantitative framework to study the biomechanics of cell to cellinteractions in complex 3D environments such as morphogenesis and organogenisis.
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Zelenska, Kateryna S., Nataliya E. Nurishchenko, Tetyana V. Beregova, Olga V. Shelyuk, and Yuliya V. Tseysler. "Age-related deterioration of contractile activity of actomyosin complex in rat gastrointestinal smooth muscle." In 14th International Conference on Global Research and Education, Inter-Academia 2015. Japan Society of Applied Physics, 2016. http://dx.doi.org/10.7567/jjapcp.4.011302.
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Aprodu, Iuliana, Alberto Redaelli, Franco Maria Montevecchi, and Monica Soncini. "Mechanical Characterization of Myosin II, Actin and Their Complexes by Molecular Mechanics Approach." In ASME 8th Biennial Conference on Engineering Systems Design and Analysis. ASMEDC, 2006. http://dx.doi.org/10.1115/esda2006-95670.
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The knowledge of the mechanical properties of myosin and actin is of a crucial importance in order to better understand the molecular mechanism of sliding force generation in muscle contraction. The aim of our work was to realize a mechanical characterization of myosin II and actin monomer using the molecular mechanics approach, by assessing the elastic properties of the two proteins, and by establishing the interaction forces between the two monomers of the actomyosin complex, and between myosin’s scissure and adenine nucleotides (ATP and ADP). A restraining method was used in order to modify the axial length of the proteins or the intermolecular distances. The interaction force and the stiffness were calculated as first and second order derivative of the potential energy with respect to the applied elongation and intermolecular distance respectively. According to our results, the values of elastic modulus of myosin motor domain and actin are 0.48 GPa, and 0.13 GPa respectively, and myosin-ATP complex is characterized by an attraction force of 130 pN which is twofold greater than the interaction force between myosin and ADP. As for the actomyosin complex, the interaction force has a maximum value of 180 pN. The results of our simulations comply with theoretical and experimental remarks about mechanical properties of myosin II, actin, and their complex.
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McGarry, J. P., C. S. Chen, V. S. Deshpande, R. M. McMeeking, and A. G. Evans. "Cells on a Bed of Micro-Needles: Modeling of the Scaling of the Response." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176593.
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The behavior of a cell attached to a bed of micro-needles is investigated using a bio-chemo-mechanical model. In experiments, the cell is spread on the tips of the micro-needles to which it is attached by focal adhesions bonded to ligands in the fibronectin on the posts. Actin stress-fibers form and attach to the focal adhesion plaques and exert contractile force on the micro-needles. As a result, the posts deflect and their displacements are measured and used to calculate the applied forces. This step is straightforward, because the cells do not adhere to the flanks of the micro-needles, and Euler-Bernoulli beam theory can be used to convert the bending displacements to applied loads. The bio-chemo-mechanical model for the cytoskeleton incorporates a signal, the tension-stabilized formation of actomyosin stress fibers, and their myosin motor driven contractility. In conjunction, the focal adhesions are modeled to account for their mechanosensitivity, in which loads transmitted to them from the stress-fibers encourage the development of plaques attached to the fibronectin on the micro-needle tips. These features have been programmed into a finite element code (ABAQUS) and used to simulate the behavior of cells attached to a bed of micro-posts. The micro-needles themselves are modeled as elastic structures and, consequently, the contractile force applied by the cells causes them to bend. The model of a cell on micro-needles successfully reproduces the characteristics of the data from the experiments. The scaling of the behavior in terms of micro-needle height, diameter, spacing, and elastic stiffness is investigated. In addition, the parameters of the bio-chemo-mechanical model of the cytoskeleton and the focal adhesions are varied (contractile tension, rate of stress-fiber contraction, persistence time for the signal and the effective stiffness of the focal adhesions) and their effect on scaling of the response also investigated. The results provide insight into the bio-chemo-mechanical response of cells to biological stimuli. The scaling simulations also give guidance on how experiments utilizing cells on micro-needles can be designed to extend the understanding of the mechanosensitivity of cells.
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Hsu, Hui-Ju, Andrea Locke, Susan Q. Vanderzyl, and Roland Kaunas. "Stretch-Induced Stress Fiber Remodeling and MAPK Activations Depend on Mechanical Strain Rate." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53464.
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Actin stress fibers (SFs), bundles of actin filaments crosslinked by α-actinin and myosin II in non-muscle cells, are mechanosensitive structural elements that respond to applied stress and strain to regulate cell morphology, signal transduction and cell function. Results from various studies indicate that myosin-generated contraction extends SFs beyond their unloaded lengths and cells maintain fiber strain at an optimal level that depends on actomyosin activity (Lu et al., 2008). Stretching the matrix upon which cells adhere perturbs the cell-matrix traction forces and cells respond by actively re-establishing the preexisting level of force (Brown et al., 1998; Gavara et al., 2008). We have developed a sarcomeric model of SF networks (Kaunas et al., 2011) to predict the effects of stretch on SF reorganization depending on the rates of matrix stretching, SF turnover, and SF stress relaxation.
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Cohen, I., and J. G. White. "DIFFERENT SITES FOR FIBRINOGEN AND FIBRIN RECEPTORS ON PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643521.
Full textAbstract:
Platelet stickiness and aggregation depend on availability of surface membrane glycoprotein Ilb-IIIa complex to bind fibrinogen. The development of isometric tension in platelet-rich clots is a manifestation of fibrin binding to the cells as well as platelet contractile activity. The possibility that fibrinogen and fibrin may bind to different portions of the GPIIb-IIIa complex has apparently not been considered. In order to determine whether the receptors for the fibrinogen and fibrin on the GPIIb-IIIa complex are identical, we investigated the effect of various monoclonal antibodies to the Ilb-IIIa complex and the tetrapeptide Arg-Gly-Asp-Ser (RGDS), a recognition site on fibrinogen for IIb-IIIa, on the development of isometric tension and ultrastructure of platelet-fibrin clots. Monoclonal antibodies A2A6 and 7E3 decreased the maximal tension, as well as the rate of tension development. Platelets and fibrin were oriented longitudinally in antibody treated clots, but the concentrations of fibrin and platelet aggregates determined by morphometry were significantly reduced. T10 and 10E5 increased tension, while AP2 and PAC1 had no substantial effect. Increasing concentrations of RGDS from 62.5 pM to 500 pM resulted in greater maximal tension and rate of tension development, reaching a five-fold increase when 500 pM RGDS was used. RGDS did not affect the Mg-stimulated platelet actomyosin ATPase activity. Morphometry revealed increased concentrations of oriented fibrin and platelet aggregates in RGDS-treated clots. Results of this study confirm the different topography of the epitopes on the Ilb-IIIa complex and provide evidence for different receptor sites for fibrinogen and fibrin on the IIb-IIIa complex