Academic literature on the topic 'Myosin mechanics'
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Journal articles on the topic "Myosin mechanics"
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Surcel, Alexandra, Win Pin Ng, Hoku West-Foyle, Qingfeng Zhu, Yixin Ren, Lindsay B. Avery, Agata K. Krenc, et al. "Pharmacological activation of myosin II paralogs to correct cell mechanics defects." Proceedings of the National Academy of Sciences 112, no. 5 (January 20, 2015): 1428–33. http://dx.doi.org/10.1073/pnas.1412592112.
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Current approaches to cancer treatment focus on targeting signal transduction pathways. Here, we develop an alternative system for targeting cell mechanics for the discovery of novel therapeutics. We designed a live-cell, high-throughput chemical screen to identify mechanical modulators. We characterized 4-hydroxyacetophenone (4-HAP), which enhances the cortical localization of the mechanoenzyme myosin II, independent of myosin heavy-chain phosphorylation, thus increasing cellular cortical tension. To shift cell mechanics, 4-HAP requires myosin II, including its full power stroke, specifically activating human myosin IIB (MYH10) and human myosin IIC (MYH14), but not human myosin IIA (MYH9). We further demonstrated that invasive pancreatic cancer cells are more deformable than normal pancreatic ductal epithelial cells, a mechanical profile that was partially corrected with 4-HAP, which also decreased the invasion and migration of these cancer cells. Overall, 4-HAP modifies nonmuscle myosin II-based cell mechanics across phylogeny and disease states and provides proof of concept that cell mechanics offer a rich drug target space, allowing for possible corrective modulation of tumor cell behavior.
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Farman, Gerrie P., Priya Muthu, Katarzyna Kazmierczak, Danuta Szczesna-Cordary, and Jeffrey R. Moore. "Impact of familial hypertrophic cardiomyopathy-linked mutations in the NH2 terminus of the RLC on β-myosin cross-bridge mechanics." Journal of Applied Physiology 117, no. 12 (December 15, 2014): 1471–77. http://dx.doi.org/10.1152/japplphysiol.00798.2014.
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Familial hypertrophic cardiomyopathy (HCM) is associated with mutations in sarcomeric proteins, including the myosin regulatory light chain (RLC). Here we studied the impact of three HCM mutations located in the NH2 terminus of the RLC on the molecular mechanism of β-myosin heavy chain (MHC) cross-bridge mechanics using the in vitro motility assay. To generate mutant β-myosin, native RLC was depleted from porcine cardiac MHC and reconstituted with mutant (A13T, F18L, and E22K) or wild-type (WT) human cardiac RLC. We characterized the mutant myosin force and motion generation capability in the presence of a frictional load. Compared with WT, all three mutants exhibited reductions in maximal actin filament velocity when tested under low or no frictional load. The actin-activated ATPase showed no significant difference between WT and HCM-mutant-reconstituted myosins. The decrease in velocity has been attributed to a significantly increased duty cycle, as was measured by the dependence of actin sliding velocity on myosin surface density, for all three mutant myosins. These results demonstrate a mutation-induced alteration in acto-myosin interactions that may contribute to the pathogenesis of HCM.
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Hoh, Joseph F. Y. "`Superfast' or masticatory myosin and the evolution of jaw-closing muscles of vertebrates." Journal of Experimental Biology 205, no. 15 (August 1, 2002): 2203–10. http://dx.doi.org/10.1242/jeb.205.15.2203.
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SUMMARY There are four fibre types in mammalian limb muscles, each expressing a different myosin isoform that finely tunes fibre mechanics and energetics for locomotion. Functional demands on jaw-closer muscles are complex and varied,and jaw muscles show considerable phylogenetic plasticity, with a repertoire for myosin expression that includes limb, developmental, α-cardiac and masticatory myosins. Masticatory myosin is a phylogenetically ancient motor with distinct light chains and heavy chains. It confers high maximal muscle force and power. It is highly jaw-specific in expression and is found in several orders of eutherian and marsupial mammals including carnivores,chiropterans, primates, dasyurids and diprotodonts. In exceptional species among these orders, masticatory myosin is replaced by some other isoform. Masticatory myosin is also found in reptiles and fish. It is postulated that masticatory myosin diverged early during gnathostome evolution and is expressed in primitive mammals. During mammalian evolution, mastication of food became important, and in some taxa jaw closers replaced masticatory myosin with α-cardiac, developmental, slow or fast limb myosins to adapt to the variety of diets and eating habits. This occurred early in some taxa(rodents, ungulates) and later in others (macropods, lesser panda, humans). The cellular basis for the uniqueness of jaw-closing muscles lies in their developmental origin.
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Buttrick, P. M., A. Malhotra, and J. Scheuer. "Effects of systolic overload and swim training on cardiac mechanics and biochemistry in rats." Journal of Applied Physiology 64, no. 4 (April 1, 1988): 1466–71. http://dx.doi.org/10.1152/jappl.1988.64.4.1466.
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We have previously shown that swim conditioning corrects the depressed mechanical function and myosin adenosinetriphosphatase (ATPase) activities associated with renovascular hypertension (HTN) in the rat. The present study was designed to assess the effects of swim conditioning on another form of systolic overload, subdiaphragmatic suprarenal aortic stenosis. Cardiac mechanics in an isolated working heart apparatus and myosin enzymology were studied in four groups of rats: controls (C), animals with chronic systolic overload secondary to aortic constriction (St), swim-conditioning animals (Sw), and animals exposed to a combined load (St-Sw). Heart weight was increased by 23% in St, 27% in Sw, and 36% in St-Sw. In contrast to HTN, cardiac pump and muscle function were not depressed in St. Sw was associated with improved cardiac output, stroke work, and velocity of circumferential fiber shortening. St-Sw showed improved mechanical cardiac performance relative to both C and St. The percent of ventricular myosin of the V1 type and Ca2+-activated myosin ATPase activity relative to C was unchanged in Sw but was depressed in St and St-Sw. These data demonstrate that the salutory mechanical effects of Sw can be superimposed on the systolic overload of St. However, the dissociation between mechanics and myosin enzymology suggests that factors in excitation-contraction coupling other than myosin isoenzyme shifts are responsible for this finding.
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Lee, Stacey, and Sanjay Kumar. "Actomyosin stress fiber mechanosensing in 2D and 3D." F1000Research 5 (September 7, 2016): 2261. http://dx.doi.org/10.12688/f1000research.8800.1.
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Mechanotransduction is the process through which cells survey the mechanical properties of their environment, convert these mechanical inputs into biochemical signals, and modulate their phenotype in response. These mechanical inputs, which may be encoded in the form of extracellular matrix stiffness, dimensionality, and adhesion, all strongly influence cell morphology, migration, and fate decisions. One mechanism through which cells on planar or pseudo-planar matrices exert tensile forces and interrogate microenvironmental mechanics is through stress fibers, which are bundles composed of actin filaments and, in most cases, non-muscle myosin II filaments. Stress fibers form a continuous structural network that is mechanically coupled to the extracellular matrix through focal adhesions. Furthermore, myosin-driven contractility plays a central role in the ability of stress fibers to sense matrix mechanics and generate tension. Here, we review the distinct roles that non-muscle myosin II plays in driving mechanosensing and focus specifically on motility. In a closely related discussion, we also describe stress fiber classification schemes and the differing roles of various myosin isoforms in each category. Finally, we briefly highlight recent studies exploring mechanosensing in three-dimensional environments, in which matrix content, structure, and mechanics are often tightly interrelated. Stress fibers and the myosin motors therein represent an intriguing and functionally important biological system in which mechanics, biochemistry, and architecture all converge.
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Picariello, Hannah S., Rajappa S. Kenchappa, Vandana Rai, James F. Crish, Athanassios Dovas, Katarzyna Pogoda, Mariah McMahon, et al. "Myosin IIA suppresses glioblastoma development in a mechanically sensitive manner." Proceedings of the National Academy of Sciences 116, no. 31 (June 24, 2019): 15550–59. http://dx.doi.org/10.1073/pnas.1902847116.
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The ability of glioblastoma to disperse through the brain contributes to its lethality, and blocking this behavior has been an appealing therapeutic approach. Although a number of proinvasive signaling pathways are active in glioblastoma, many are redundant, so targeting one can be overcome by activating another. However, these pathways converge on nonredundant components of the cytoskeleton, and we have shown that inhibiting one of these—the myosin II family of cytoskeletal motors—blocks glioblastoma invasion even with simultaneous activation of multiple upstream promigratory pathways. Myosin IIA and IIB are the most prevalent isoforms of myosin II in glioblastoma, and we now show that codeleting these myosins markedly impairs tumorigenesis and significantly prolongs survival in a rodent model of this disease. However, while targeting just myosin IIA also impairs tumor invasion, it surprisingly increases tumor proliferation in a manner that depends on environmental mechanics. On soft surfaces myosin IIA deletion enhances ERK1/2 activity, while on stiff surfaces it enhances the activity of NFκB, not only in glioblastoma but in triple-negative breast carcinoma and normal keratinocytes as well. We conclude myosin IIA suppresses tumorigenesis in at least two ways that are modulated by the mechanics of the tumor and its stroma. Our results also suggest that inhibiting tumor invasion can enhance tumor proliferation and that effective therapy requires targeting cellular components that drive both proliferation and invasion simultaneously.
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Bates, Genevieve, Sara Sigurdardottir, Linda Kachmar, Nedjma B. Zitouni, Andrea Benedetti, Basil J. Petrof, Dilson Rassier, and Anne-Marie Lauzon. "Molecular, cellular, and muscle strip mechanics of the mdx mouse diaphragm." American Journal of Physiology-Cell Physiology 304, no. 9 (May 1, 2013): C873—C880. http://dx.doi.org/10.1152/ajpcell.00220.2012.
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Duchenne muscular dystrophy (DMD) is a lethal disorder caused by defects in the dystrophin gene, which leads to respiratory or cardiac muscle failure. Lack of dystrophin predisposes the muscle cell sarcolemmal membrane to mechanical damage. However, the role of myosin in this muscle weakness has been poorly addressed. In the current study, in addition to measuring the velocity of actin filament propulsion (υmax) of mdx myosin molecules purified from 3- and 12-mo-old control (C57Bl/10) and mdx (C57Bl/10 mdx) mouse diaphragms, we also measured myosin force production. Furthermore, we measured cellular and muscle strip force production at three mo of age. Stress (force/cross-sectional area) was smaller for mdx than control at the muscle strip level but was not different at the single fiber level. υmax of mdx myosin was not different from control at either 3 or 12 mo nor was their relative myosin force. The type I and IIb myosin heavy chain composition was not different between control and mdx diaphragms at 3 or 12 mo. These results suggest that the myosin function, as well as the single fiber mechanics, do not underlie the weakness of the mdx diaphragm. This weakness was only observed at the level of the intact muscle bundle and could not be narrowed down to a specific mechanical impairment of its individual fibers or myosin molecules.
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Alpert, Norman R., Christine Brosseau, Andrea Federico, Maike Krenz, Jeffrey Robbins, and David M. Warshaw. "Molecular mechanics of mouse cardiac myosin isoforms." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 4 (October 1, 2002): H1446—H1454. http://dx.doi.org/10.1152/ajpheart.00274.2002.
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Two myosin isoforms are expressed in myocardium, αα-homodimers (V1) and ββ-homodimers (V3). V1exhibits higher velocities and myofibrillar ATPase activities compared with V3. We also observed this for cardiac myosin from normal (V1) and propylthiouracil-treated (V3) mice. Actin velocity in a motility assay ( V actin) over V1 myosin was twice that of V3 as was the myofibrillar ATPase. Myosin's average force (Favg) was similar for V1 and V3. Comparing V actin and Favg across species for both V1 and V3, our laboratory showed previously (VanBuren P, Harris DE, Alpert NR, and Warshaw DM. Circ Res 77: 439–444, 1995) that mouse V1 has greater V actin and Favg compared with rabbit V1. Mouse V3 V actin was twice that of rabbit V actin. To understand myosin's molecular structure and function, we compared α- and β-cardiac myosin sequences from rodents and rabbits. The rabbit α- and β-cardiac myosin differed by eight and four amino acids, respectively, compared with rodents. These residues are localized to both the motor domain and the rod. These differences in sequence and mechanical performance may be an evolutionary attempt to match a myosin's mechanical behavior to the heart's power requirements.
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Veigel, Claudia, and James R. Sellers. "Mechanics of myosin V near stall." Biophysical Journal 96, no. 3 (February 2009): 138a. http://dx.doi.org/10.1016/j.bpj.2008.12.3865.
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Siththanandan, Verl B., Yasuharu Takagi, Yi Yang, Davin K. T. Hong, and James R. Sellers. "Characterization of drosophila myosin 7a mechanics." Biophysical Journal 96, no. 3 (February 2009): 141a. http://dx.doi.org/10.1016/j.bpj.2008.12.3878.
Full textDissertations / Theses on the topic "Myosin mechanics"
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Ökten, Zeynep. "Single molecule mechanics and the myosin family of molecular motors." [S.l.] : [s.n.], 2006. http://www.diss.fu-berlin.de/2006/6/index.html.
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Pertici, Irene. "The power output of a myosin II-based nanomachine mimicking the striated muscle." Doctoral thesis, Università di Siena, 2018. http://hdl.handle.net/11365/1041106.
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This thesis reports the realization and first application of a synthetic nanomachine, able to reproduce in vitro the performance emerging from the array arrangement of myosin II motors in the sarcomere of the striated muscle. The nanomachine consists of an ensemble of less than ten myosin dimers from fast skeletal muscle disposed on a functionalized support carried by a piezoelectric nanopositioner and brought to interact with an actin filament attached with the correct polarity via gelsolin to a bead (Bead Tailed Actin, BTA) trapped into the focus of a Dual Laser Optical Tweezers (DLOT). In solution with [ATP] = 2 mM the nanomachine is able to produce steady force and shortening, delivering a maximum power of 5 aW. The nanomachine performances are interpreted with a kinetic model based on mechanics and energetics of fast skeletal muscle. In this way it is possible to define the minimal conditions that allow an actomyosin system in vitro to produce force and power with the efficiency of the striated muscle, in the absence of the confusing contribution of the other sarcomeric proteins. In turn, since the system is assembled one piece at a time, it allows different degrees of reconstitution of the sarcomeric assembly. Therefore it will be possible to characterize the function of native and engineered contractile, regulatory and accessory proteins. For future investigations on the Ca2+-dependent thin filament activation, the preparation of BTA has been implemented using a Ca2+-independent gelsolin fragment and the procedure for thin filament reconstitution has been established during my visit to the Institute for Biophysical Chemistry, MHH, Germany.
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Erzberger, Anna. "Actomyosin mechanics at the cell level." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-197642.
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Almost all animal cells maintain a thin layer of actin filaments and associated proteins underneath the cell membrane. The actomyosin cortex is subject to internal stress patterns which result from the spatiotemporally regulated activity of non-muscle myosin II motors in the actin network. We study how these active stresses drive changes in cell shape and flows within the cortical layer, and how these cytoskeletal deformations and flows govern processes such as cell migration, cell division and organelle transport. Following a continuum mechanics approach, we develop theoretical descriptions for three different cellular processes, to obtain - in collaboration with experimental groups - a detailed and quantitative understanding of the underlying cytoskeletal mechanics.
We investigate the forces and cortex flows involved in adhesion-independent cell migration in confinement. Many types of cell migration rely on the extension of protrusions at the leading edge, where the cells attach to the substrate with specific focal adhesions, and pull themselves forward, exerting stresses in the kPa range. In confined environments however, cells exhibit migration modes which are independent of specific adhesions. Combining hydrodynamic theory, microfluidics and quantitative imaging of motile, non-adherent carcinosarcoma cells, we analyze the mechanical behavior of cells during adhesion-independent migration. We find that the accumulation of active myosin motors in the rear part of these cells results in a retrograde cortical flow as well as the contraction of the cell body in the rear and expansion in the front, and we describe how both processes contribute to the translocation of the cells, depending on the geometric and mechanical parameters of the system. Importantly, we find that the involved propulsive forces are several orders of magnitude lower than during adhesive motility while the achieved migration velocities are similar. Moreover, the distribution of forces on the substrate during non-adhesive migration is fundamentally different, giving rise to a positive force dipole. In contrast to adhesive migration modes, non-adhesive cells move by exerting pushing forces at the rear, acting to expand rather than contract their substrate as they move. These differences may strongly affect hydrodynamic and/or deformational interactions between collectively migrating cells.
In addition to the work outlined above, we study contractile ring formation in the actin cytoskeleton before and during cell division. While in disordered actin networks, myosin motor activity gives rise to isotropic stresses, the alignment of actin filaments in the cortex during cell division introduces a preferred direction for motor-filament interactions, resulting in anisotropies in the cortical stress. Actin filaments align in myosin-dependent shear flows, resulting in possible feedback between motor activity, cortical flows and actin organization. We investigate how the mechanical interplay of these different cortical properties gives rise to the formation of a cleavage furrow during cell division, describing the level of actin filament alignment at different points on the cortex with a nematic order parameter, in analogy to liquid crystal physics. We show that cortical anisotropies arising from shear-flow induced alignment patterns are sufficient to drive the ingression of cellular furrows, even in the absence of localized biochemical myosin up-regulation. This mechanism explains the characteristic appearance of pseudocleavage furrows in polarizing cells.
Finally, we study the characteristic nuclear movements in pseudostratified epithelia during development. These tissues consist of highly proliferative, tightly packed and elongated cells, with nuclei actively travelling to the apical side of the epithelium before each cell division. We explore how cytoskeletal properties act together with the mechanics of the surrounding tissue to control the shape of single cells embedded in the epithelium, and investigate potential mechanisms underlying the observed nuclear movements. These findings form a theoretical basis for a more detailed characterization of processes in pseudostratified epithelia.
Taken together, we present a continuum mechanics description of the actomyosin cell cortex, and successfully apply it to several different cell biological processes. Combining our theory with experimental work from collaborating groups, we provide new insights into different aspects of cell mechanics.
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Bates, Genevieve. "Molecular mechanics of diaphragmatic myosin from a mouse model of Duchenne muscular dystrophy." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=97145.
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Duchenne muscular dystrophy (DMD) is a genetic disorder characterized by the absence of dystrophin in the muscle cell membranes, rendering them susceptible to mechanical damage. DMD leads to respiratory or cardiac muscle failure and death. We hypothesized that alterations in contractile protein function contribute to DMD muscle weakness. We measured muscle strip stress, myosin heavy chain (MHC) isoform composition, velocity (ʋmax) of actin propulsion by myosin, and relative myosin force in control and mdx mouse (C57Bl/10) diaphragms. Stress was statistically smaller for mdx (0.23kg/cm2±0.11; mean±SE) than control (0.69kg/cm2±0.01) whereas the MHC isoform composition was not statistically different (type I: p=0.423, type IIa/IIx: p=0.804, type IIb: p=0.401). υmax of mdx myosin (1.24µm/s±0.07) was not statistically different from control (1.37µm/s±0.12; p=0.353). Relative myosin force was not statistically different between control and mdx myosin (p=0.932). Thus, alterations in myosin molecular function do not contribute to the weakness of the mdx mouse diaphragm.La dystrophie musculaire de Duchenne (DMD) est une maladie génétique caracterisée par un manque de dystrophine dans la membrane des cellules musculaires, les rendant susceptibles au dommage mécanique. La mort survient suite à l'insuffisance des muscles cardiaques ou respiratoires. Notre hypothèse est que des altérations au niveau des protéines contractiles jouent un rôle dans la faiblesse musculaire de la DMD. Dans cette étude, nous avons mesuré le stress généré par des faisceaux musculaires, la composition des isoformes de la chaîne lourde de myosine (MHC), la vélocité (υmax) de propulsion de l'actine par la myosine, et la force relative de la myosine de diaphragme de souris control et mdx (C57Bl/10). Nous avons observé que le stress est statistiquement plus petit pour la souris mdx (0.23±0.11; moyenne±SE) que pour le control (0.69±0.01), mais que la composition de MHC n'est pas statistiquement différente (type I: p=0.423, type IIa/IIx: p=0.804, type IIb: p=0.401). υmax de la myosine mdx (1.24µm/s±0.07) n'est pas statistiquement différente du control (1.37µm/s±0.12; p=0.353). La force relative n'est pas statistiquement différente entre la myosine control et mdx (p=0.932). Donc des altérations de la fonction moléculaire de la myosine ne contribuent pas à la faiblesse du diaphragme de la souris mdx.
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Iliffe, Cathryn Ann. "The kinetics and mechanics of myosin and subfragment-1 from insect flight muscle." Thesis, University of York, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251800.
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Léguillette, Renaud. "Expression of smooth muscle myosin heavy chain isoforms in asthma and their molecular mechanics." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103169.
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Two smooth muscle (SM) myosin heavy chain isoforms, generated by alternative mRNA splicing, differ by the presence (SM-B) or absence (SM-A) of a 7 amino acid insert in the motor domain. The rate of actin filament propulsion (nu max) of SM-B, as measured in the in vitro motility assay, is 2-fold greater than that of SM-A. I investigated the expression and function of these isoforms in healthy SM and in asthma. First, I determined the sequence of the SM-B isoform in human SM and quantified its expression at the mRNA and protein levels in several human organs. The SM-B isoform was mostly expressed in rapidly contracting phasic SM. I then purified myosin from multiple rat organs and found a rank correlation between SM-B content and numax.I then quantified the expression of SM-B and several other contractile protein genes in endobronchial biopsies from normal and asthmatic subjects. SM-B, myosin light chain kinase (MLCK), which is responsible for myosin activation, and transgelin, a ubiquitously expressed actin binding protein but whose function is unknown, were overexpressed in the asthmatic biopsies. The increased SM-B expression and myosin activation, due to the increased MLCK expression, both contribute to the increased rate of shortening of the asthmatic airway SM. In addition, I showed that beyond its enzymatic effects, MLCK mechanically enhances numax. The binding of SM22 to actin, however, did not alter numax.
Finally, I addressed the mechanisms behind the unique capacity of SM to maintain force at low energy cost, namely the latch-state. This property is mostly observed in SM-A containing, tonic muscle. Using a laser trap, I measured the binding force of unphosphorylated (non-active) SM-A and SM-B myosin isoforms and found that they can both attach to actin and maintain force. I also measured numax at different MgADP concentrations and found that SM-A has a greater affinity for MgADP. Because MgADP must be released before myosin can detach from actin, these results suggest that the SMA isoform remains attached longer to actin, allowing it to get into the latch-state. These findings explain the greater propensity of tonic muscle to get into the latch-state.
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Patel, Sejal. "Myosin regulatory light chain phosphorylation and its role in active mechanics and force generation of the heart." Diss., [La Jolla] : University of California, San Diego, 2009. http://wwwlib.umi.com/cr/ucsd/fullcit?p1462361.
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Thesis (M.S.)--University of California, San Diego, 2009.Title from first page of PDF file (viewed May 4, 2009). Available via ProQuest Digital Dissertations. Includes bibliographical references (p. 43-48).
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Düttmann, Markus [Verfasser], and Alexander S. [Akademischer Betreuer] Mikhailov. "Elastic Network Models of Proteins - Uncovering the Internal Mechanics of Actin and Myosin / Markus Düttmann. Betreuer: Alexander S. Mikhailov." Berlin : Universitätsbibliothek der Technischen Universität Berlin, 2012. http://d-nb.info/1028912919/34.
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Pontén, Eva. "Tendon transfer mechanics and donor muscle properties : implications in surgical correction of upper limb muscle imbalance." Doctoral thesis, Umeå universitet, Institutionen för integrativ medicinsk biologi (IMB), 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-167.
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Tendon transfer surgery is used to improve the hand function of patients with nerve injuries, spinal cord lesions, cerebral palsy (CP), stroke, or muscle injuries. The tendon of a muscle, usually with function opposite that of the lost muscle function, is transferred to the tendon of the deficient muscle. The aim is to balance the wrist and fingers to achieve better hand function. The position, function, and length at which the donor muscle is sutured is essential for the outcome for the procedure. In these studies the significance of the transferred muscle’s morphology, length and apillarization was investigated using both animal and human models. Immunohistochemical, biochemical, and laser diffraction techniques were used to examine muscle structure. In animal studies (rabbit), the effects of immobilization and of tendon transfers at different muscle lengths were analyzed. Immobilization of highly stretched muscles resulted in fibrosis and aberrant regeneration. A greater pull on the tendon while suturing a tendon transfer resulted in larger sarcomere lengths as measured in vivo. On examination of the number of sarcomeres per muscle fiber and the sarcomere lengths after 3 weeks of immobilization and healing time, we found a cut-off point up to which the sarcomerogenesis was optimal. Transfer at too long sarcomere lengths inhibited adaptation of the muscle to its new length, probably resulting in diminished function. In human studies we defined the sarcomere lengths of a normal human flexor carpi ulnaris muscle through the range of motion, and then again after a routinely performed tendon transfer to the finger extensor. A calculated model illustrated that after a transfer the largest force was predicted to occur with the wrist in extension. Morphological studies of spastic biceps brachii muscle showed, compared with control muscle, smaller fiber areas and higher variability in fiber size. Similar changes were also found in the more spastic wrist flexors comparing with wrist extensors in children with CP. In flexors, more type 2B fibers were found. These observations could all be due to the decreased use in the spastic limb, but might also represent a specific effect of the spasticity. In children and adults with spasticity very small fibers containing developmental myosin were present in all specimens, while none were found in controls. These fibers probably represent newly formed fibers originating from activated satellite cells. Impaired supraspinal control of active motion as well as of spinal reflexes, both typical of upper motor syndrome, could result in minor eccentric injuries of the muscle, causing activation of satellite cells. Spastic biceps muscles had fewer capillaries per cross-sectional area compared to age-matched controls, and also a smaller number of capillaries around each fiber. Nevertheless, the number of capillaries related to the specific fiber area was normal, and hence the spastic fibers are sufficiently supplied with capillaries. This study shows that the length of the muscle during tendon transfer is crucial for optimization of force output. Laser diffraction can be used for accurate measurement of sarcomere length during tendon transfer surgery. Wrist flexor muscles have more morphological alterations typical of spasticity compared to extensors.
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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.
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Cette thèse interdisciplinaire a été dédiée à la caractérisation des propriétés mécaniques de myoblastes (murins et humains) et de myotubes (murins) à l'aide de la microscopie à force atomique (AFM). En modifiant ou en inhibant la dynamique du cytosquelette (CSK) d’actine de ces cellules, nous avons pu montrer que ces propriétés mécaniques variaient. L’enregistrement de courbes de force indentation nous a permis de montrer que la présence de cellules adhérentes introduisait sur les leviers d’AFM un amortissement visqueux supplémentaire à celui d’une paroi solide, et que cet amortissement visqueux dépendait de sa vitesse d’approche et que celui-ci restait non négligeable pour les plus faibles vitesses (1μm/s). Nous avons observé que les propriétés mécaniques des précurseurs de muscles devenaient non linéaires (comportement plastiques) pour des grandes déformations (>1μm) et qu’elles dépendaient de l’état, du type de cellule et de leur environnement. En combinant des expériences d’AFM, des modèles visco-élastiques et des méthodes d'analyse multi-échelle basées sur la transformation en ondelettes, nous avons illustré la variabilité des réponses mécaniques de ces cellules (de visco-élastiques à visco-plastiques). À l'aide de courbes de force-indentation, de l’imagerie morpho-structurale (DIC, microscopie à fluorescence) et de traitements pharmacologiques, nous avons éclairé le rôle essentiel des processus actifs (dépendants de l’ATP) dans la mécanique de myoblastes, en discutant tout particulièrement ceux des moteurs moléculaires (myosine II) couplés aux filaments d’actine. En particulier, nous avons montré que les fibres de stress du cytosquelette d’actine situées autour du noyau pouvaient présenter des évènements de remodelage soudains (ruptures) et que ces ruptures étaient une mesure indirecte de l’aptitude de ces cellules à tendre leur CSK. Nous avons enfin montré qu’il était possible de généraliser cette approche à des cas cliniques humains, en l’occurrence des myoblastes primaires de porteurs sains et de patients atteints de dystrophie musculaire de Duchenne, ouvrant la voie à des études plus larges sur d’autres types cellulaires et pathologiesThis 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
Books on the topic "Myosin mechanics"
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J, Staiger C., ed. Actin: A dynamic framework for multiple plant cell functions. Dordrecht: Kluwer Academic Publishers, 2000.
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(Editor), C. J. Staiger, F. Baluska (Editor), D. Volkmann (Editor), and P. Barlow (Editor), eds. Actin: A Dynamic Framework for Multiple Plant Cell Functions (Developments in Plant and Soil Sciences). Springer, 2000.
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Arrigo, Mattia, and Alexandre Mebazaa. Positive inotropes. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0035.
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Inotropic agents are substances used to improve cardiac output and end-organ perfusion in severe forms of acute heart failure. However, inappropriate use of inotropic agents may be associated with severe adverse effects and death. Despite clear indications to restrict their use to acute heart failure patients presenting with signs of end-organ hypoperfusion, the current use of inotropes is very frequent and often unnecessary. This chapter reviews mechanisms of action of current and future inotropes (including catecholamines, phosphodiesterase-III inhibitors, calcium sensitizers, cardiac myosin activators, and istaroxime) and discusses their clinical use in acute heart failure.
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Sheehy-Skeffington, Jennifer. Decision-Making Up Against the Wall. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190492908.003.0005.
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This chapter provides an overview of research on the behavioral dimension of low socioeconomic status and a set of theoretical and empirical principles for better understanding it. In particular, the chapter focuses on those behaviors that are claimed to exacerbate a situation of poverty or deprivation, such as poor academic performance, myopic financial decisions, early child-bearing, consumption of unhealthy foods, and engaging in unhealthy lifestyle habits. Though such behavioral patterns have been used to make claims as to the defective values or motives of the poor, the chapter argues that studying them rigorously, aided by the experimental method, leads to a more nuanced and accurate picture, in which psychology is systematically shaped by socioeconomic position. After reviewing evidence from education, public health, and behavioral economics concerning the behavioral dimension of low socioeconomic status, the chapter suggests an organizing set of mechanisms that might structure a comprehensive explanatory account of it.
Book chapters on the topic "Myosin mechanics"
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Mehta, A. D., and J. A. Spudich. "Single Molecule Myosin Mechanics Measured Using Optical Trapping." In Interacting Protein Domains, 247–59. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60848-3_38.
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Rice, Sarah. "Regulatory Mechanisms of Kinesin and Myosin Motor Proteins: Inspiration for Improved Control of Nanomachines." In Nano and Cell Mechanics, 19–33. Chichester, UK: John Wiley & Sons, Ltd, 2012. http://dx.doi.org/10.1002/9781118482568.ch2.
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Altman, David. "Myosin Work and Motility: Mechanism." In Encyclopedia of Biophysics, 1671–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-16712-6_754.
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Garcia, Kristen, Marcus Hock, Vikrant Jaltare, Can Uysalel, Kimberly J. McCabe, Abigail Teitgen, and Daniela Valdez-Jasso. "Investigating the Multiscale Impact of Deoxyadenosine Triphosphate (dATP) on Pulmonary Arterial Hypertension (PAH) Induced Heart Failure." In Computational Physiology, 77–90. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-05164-7_7.
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Abstract2-deoxy-ATP (dATP) is a myosin activator known to improve cardiac contractile force [1]. In vitro studies have shown that dATP alters the calcium transient profile in addition to the kinetics of the cross-bridge cycle [2]. Furthermore, in vivo studies of transgenic mice with increased production of dATP show elevated left ventricular systolic function [3]. Pulmonary arterial hypertension (PAH) is a rare disease of the pulmonary vasculature in which pressure overload in the right ventricle results in reduced contractile function and right heart failure [4]. We hypothesize that dATP may have a therapeutic effect on PAH-induced heart failure, by improving contractile function and restoring cardiac output and ejection fraction. However, because the effects of dATP cannot easily be assessed experimentally, we propose using a computational multiscale modeling approach to predict cardiac function. By altering parameters in an existing multiscale biventricular cardiac model [5], we were able to reproduce end-systolic and end-diastolic pressures and volumes that reflect the PAH condition, as well as healthy hearts. dATP was simulated by adjusting parameters in the model at the molecular and cellular levels based on experimental data [1], allowing us to predict the effects of dATP on PAH at the organ level. Our results show that the molecular effects of dATP can increase cardiac output and restore ejection fraction in PAH conditions, though at the cost of elevated mean arterial pressure, and may provide a new approach to treating this disease. Our multiscale modeling approach paves the way for further studies mapping out cardiovascular mechanics. As novel therapeutics continue to be discovered, their application and mechanism can be further explored through these computational models.
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Altman, David. "Myosin Work and Motility, Mechanism of." In Encyclopedia of Biophysics, 1–12. Berlin, Heidelberg: Springer Berlin Heidelberg, 2021. http://dx.doi.org/10.1007/978-3-642-35943-9_754-1.
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Sutoh, Kazuo. "Identification of Actin Surface Interacting with Myosin During the Actin-Myosin Sliding." In Mechanism of Myofilament Sliding in Muscle Contraction, 241–45. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2872-2_23.
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Stone, Richard A. "Neural Mechanisms and Eye Growth Control." In Myopia Updates, 241–54. Tokyo: Springer Japan, 1998. http://dx.doi.org/10.1007/978-4-431-66959-3_47.
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Chakraborty, Ranjay, Scott A. Read, and Stephen J. Vincent. "Understanding Myopia: Pathogenesis and Mechanisms." In Updates on Myopia, 65–94. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-8491-2_4.
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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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Oette, Mark, Marvin J. Stone, Hendrik P. N. Scholl, Peter Charbel Issa, Monika Fleckenstein, Steffen Schmitz-Valckenberg, Frank G. Holz, et al. "Myosin Heavy Chain IIa Myopathy, Autosomal Dominant." In Encyclopedia of Molecular Mechanisms of Disease, 1421–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_1230.
Full textConference papers on the topic "Myosin mechanics"
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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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Egan, Paul F., Philip R. LeDuc, Jonathan Cagan, and Christian Schunn. "A Design Exploration of Genetically Engineered Myosin Motors." In ASME 2011 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2011. http://dx.doi.org/10.1115/detc2011-48568.
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As technology advances, there is an increasing need to reliably output mechanical work at smaller scales. At the nanoscale, one of the most promising routes is utilizing biomolecular motors such as myosin proteins commonly found in cells. Myosins convert chemical energy into mechanical energy and are strong candidates for use as components of artificial nanodevices and multi-scale systems. Isoforms of the myosin superfamily of proteins are fine-tuned for specific cellular tasks such as intracellular transport, cell division, and muscle contraction. The modular structure that all myosins share makes it possible to genetically engineer them for fine-tuned performance in specific applications. In this study, a parametric analysis is conducted in order to explore the design space of Myosin II isoforms. The crossbridge model for myosin mechanics is used as a basis for a parametric study. The study sweeps commonly manipulated myosin performance variables and explores novel ways of tuning their performance. The analysis demonstrates the extent that myosin designs are alterable. Additionally, the study informs the biological community of gaps in experimentally tabulated myosin design parameters. The study lays the foundation for further progressing the design and optimization of individual myosins, a pivotal step in the eventual utilization of custom-built biomotors for a broad range of innovative nanotechnological devices.
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Bidone, Tamara Carla, Haosu Tang, and Dimitrios Vavylonis. "Insights Into the Mechanics of Cytokinetic Ring Assembly Using 3D Modeling." In ASME 2014 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2014. http://dx.doi.org/10.1115/imece2014-39006.
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During fission yeast cytokinesis, actin filaments nucleated by cortical formin Cdc12 are captured by myosin motors bound to a band of cortical nodes. The myosin motors exert forces that pull nodes together into a contractile ring. Cross-linking interactions help align actin filaments and nodes into a single bundle. Mutations in the myosin motor domain and changes in the concentration of cross-linkers alpha-actinin and fimbrin alter the morphology of the condensing network, leading to clumps, rings or extended meshworks. How the contractile tension developing during ring formation depends on the interplay between network morphology, myosin motor activity, cross-linking and actin filament turnover remains to be elucidated. We addressed this question using a 3D computational model in which semiflexible actin filaments (represented as beads connected by springs) grow from formins, can be captured by myosin in neighboring nodes, and get cross-linked with one another through an attractive interaction. We identify regimes of tension generation between connected nodes under a wide set of conditions regarding myosin dynamics and strength of cross-linking between actin filaments. We find conditions that maximize circumferential tension, correlate them with network morphology and propose experiments to test these predictions. This work addresses “Morphogenesis of soft and living matter” using computational modeling to simulate cytokinetic ring assembly from the key molecular mechanisms of viscoelastic cross-linked actin networks that include active molecular motors.
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Bates, Genevieve, Anne-Marie Lauzon, and Basil J. Petrof. "Molecular Mechanics Of Myosin In Muscular Dystrophy: The MDX Mouse Diaphragm." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5048.
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Angstadt, Shantel M. "Abstract 169: Uncovering a myosin phosphatase regulator in pancreatic tumor cell mechanics and behavior." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-169.
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Angstadt, Shantel M. "Abstract 169: Uncovering a myosin phosphatase regulator in pancreatic tumor cell mechanics and behavior." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-169.
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Koppes, Ryan A., Douglas M. Swank, and David T. Corr. "Force Depression in the Drosophila Jump Muscle." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19436.
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The depression of isometric force after active shortening, termed force depression (FD), is a well-accepted characteristic of skeletal muscle that has been demonstrated in both whole muscle [1,3] and single-fiber preparations [1,2]. Although this history-dependent behavior has been observed experimentally for over 70 years, its underlying mechanism(s) remain unknown. Drosophila melangastor, commonly known as the fruit fly, is a well established, comprehensively understood, and genetically manipulable animal model. Furthermore, Drosophila have proved to be an accurate model species for studying muscle mechanics, and the Tergal Depressor of the Trochanter (TDT), or jump muscle, has most precisely resembled the mechanics of mammalian skeletal muscle [4]. Due to the structural and phenomenological similarities of the TDT muscle to skeletal muscle, in addition to the potential use of genetic mutations in fly models, it is extremely advantageous to investigate the presence of history dependent phenomenon in the TDT. If such phenomena are present, further investigation utilizing different myosin and actin isoforms to study the underlying mechanism(s) could produce new insight into this history-dependent phenomenon, otherwise impossible to elucidate using current experimental models. Thus, it is the goal of this study to determine the presence and degree of FD in the TDT muscle of wild type Drosophila.
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Daniel, J. L., and M. Rigmaiden. "Evidence for Ca2+-independent phosphorylation of human platelet myosin." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644527.
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Phosphorylation of platelet myosin is thought to be required for activation of the contractile events occurring during platelet activation. At present the only known mechanism for Onitiating myosin phosphorylation is through a Ca2+-calmodulin-dependent activation of myosin light chain kinase. However, our previous studies using the fluorescent Ca2+-indicator quin2 indicated that both platelet shape change and myosin phosphorylation could be induced in an EGTA-containing media in the absence of a measurable change in cytosolic free Ca2+ concentration (Hallam, Daniel, Kendrick-Jones & Rink. Biochem. J. 232 (1985) 373). In order to confirm this finding, we fyave investigated the regulation of myosin phosphorylation usin^+a preparation of electrically-permeabilized platelets and Ca2+ buffers to control the internal Ca2+ concentration. Fifty percent myosin phosphorylation was obtained at 700 nM Ca2+. When thrombin (5 U/ml) was added to this system, this curve shifted both to the left and upward; 50% myosin phosphorylation was obtained at 400 nM Ca2+.A synthetic inhibitor of protein kinase C, H7, had no effect on myosin phosphorylation in the absence of agonist but did inhibit the thrombin-induced shift to left suggesting that protein kinase C may modulate myosin phosphorylation. We also compared the effects of H7 agonist-induced myosin phosphorylation and shape change in control and an quin2 loaded platelets. Comparable inhibition of both phosphorylation and the rate of shape change was observed with both quin2 and H7. Addition of H7 to quin2-loaded platelets resulted in complete inhibition of both agonist-induced shape change and myosin phosphorylation. These results indicate that both protein kinase C and Ca2+-dependent reactions are involved in complete expression of myosin phosphorylation in human platelets.
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Merryman, W. David, and Joshua D. Hutcheson. "Controlling the Mechanical Myofibroblast via SRC: A Potential Drug Discovery Platform." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19187.
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Connective tissue makes up a large portion of our bodies, with collagen constituting ∼30% of the protein of connective tissue. Any tissue that undergoes fibrosis, either due to a genetic mutation or with age or use, typically falls into the ubiquitous category of ‘connective tissue fibrosis’. There are multiple potential contributors to connective tissue fibrosis; however, two dominate the literature — mechanical stress/strain and cytokines. Both stimuli lead to activation of fibroblast cells to a myofibroblast phenotype, the cellular hallmark of fibrotic disease. The myofibroblast phenotype is indicated by the expression of smooth muscle α-actin (αSMA), which associates with myosin to form actin-myosin contractile elements and generates intracellular force that is transduced to the ECM via cell membrane integrins.
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Tisdale, John, Hugh Durrant-Whyte, and J. Karl Hedrick. "Path Planning for Cooperative Sensing Using Unmanned Vehicles." In ASME 2007 International Mechanical Engineering Congress and Exposition. ASMEDC, 2007. http://dx.doi.org/10.1115/imece2007-43728.
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This work explores online path-planning for unmanned vehicles performing cooperative sensing. Much existing work employs receding-horizon optimization, where an objective function is repeatedly optimized over some short lookahead length. The use of receding horizon optimization often results in ad-hoc methods for dealing with the problem of myopic lookahead, where no value is visible in an agent’s planning horizon. This work examines the use of an algorithm for receding-horizon optimization that explicitly accounts for myopia by allowing for a variable lookahead length. Cooperation is maintained by ensuring that all agents plan to the same horizon, potentially with different strategies. This algorithm is used to develop trajectories for a team of unmanned vehicles searching for a target using a probabilistic framework. Simulation results are presented and discussed.
Reports on the topic "Myosin mechanics"
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Sadot, Einat, Christopher Staiger, and Mohamad Abu-Abied. Studies of Novel Cytoskeletal Regulatory Proteins that are Involved in Abiotic Stress Signaling. United States Department of Agriculture, September 2011. http://dx.doi.org/10.32747/2011.7592652.bard.
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In the original proposal we planned to focus on two proteins related to the actin cytoskeleton: TCH2, a touch-induced calmodulin-like protein which was found by us to interact with the IQ domain of myosin VIII, ATM1; and ERD10, a dehydrin which was found to associate with actin filaments. As reported previously, no other dehydrins were found to interact with actin filaments. In addition so far we were unsuccessful in confirming the interaction of TCH2 with myosin VIII using other methods. In addition, no other myosin light chain candidates were found in a yeast two hybrid survey. Nevertheless we have made a significant progress in our studies of the role of myosins in plant cells. Plant myosins have been implicated in various cellular activities, such as cytoplasmic streaming (1, 2), plasmodesmata function (3-5), organelle movement (6-10), cytokinesis (4, 11, 12), endocytosis (4, 5, 13-15) and targeted RNA transport (16). Plant myosins belong to two main groups of unconventional myosins: myosin XI and myosin VIII, both closely related to myosin V (17-19). The Arabidopsis myosin family contains 17 members: 13 myosin XI and four myosin VIII (19, 20). The data obtained from our research of myosins was published in two papers acknowledging BARD funding. To address whether specific myosins are involved with the motility of specific organelles, we cloned the cDNAs from neck to tail of all 17 Arabidopsis myosins. These were fused to GFP and used as dominant negative mutants that interact with their cargo but are unable to walk along actin filaments. Therefore arrested organelle movement in the presence of such a construct shows that a particular myosin is involved with the movement of that particular organelle. While no mutually exclusive connections between specific myosins and organelles were found, based on overexpression of dominant negative tail constructs, a group of six myosins (XIC, XIE, XIK, XI-I, MYA1 and MYA2) were found to be more important for the motility of Golgi bodies and mitochondria in Nicotiana benthamiana and Nicotiana tabacum (8). Further deep and thorough analysis of myosin XIK revealed a potential regulation by head and tail interaction (Avisar et al., 2011). A similar regulatory mechanism has been reported for animal myosin V and VIIa (21, 22). In was shown that myosin V in the inhibited state is in a folded conformation such that the tail domain interacts with the head domain, inhibiting its ATPase and actinbinding activities. Cargo binding, high Ca2+, and/or phosphorylation may reduce the interaction between the head and tail domains, thus restoring its activity (23). Our collaborative work focuses on the characterization of the head tail interaction of myosin XIK. For this purpose the Israeli group built yeast expression vectors encoding the myosin XIK head. In addition, GST fusions of the wild-type tail as well as a tail mutated in the amino acids that mediate head to tail interaction. These were sent to the US group who is working on the isolation of recombinant proteins and performing the in vitro assays. While stress signals involve changes in Ca2+ levels in plants cells, the cytoplasmic streaming is sensitive to Ca2+. Therefore plant myosin activity is possibly regulated by stress. This finding is directly related to the goal of the original proposal.
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Philosoph-Hadas, Sonia, Peter B. Kaufman, Shimon Meir, and Abraham H. Halevy. Inhibition of the Gravitropic Shoot Bending in Stored Cut Flowers Through Control of Their Graviperception: Involvement of the Cytoskeleton and Cytosolic Calcium. United States Department of Agriculture, December 2005. http://dx.doi.org/10.32747/2005.7586533.bard.
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Original objectives: The basic goal of the present project was to study the mechanism involved in shoot graviperception and early transduction, in order to determine the sequence of events operating in this process. This will enable to control the entire process of gravity-induced differential growth without affecting vertical growth processes essential for development. Thus, several new postulated interactions, operating at the perception and early transduction stages of the signaling cascade leading to auxin-mediated bending, were proposed to be examined in snapdragon spikes and oat shoot pulvini, according to the following research goals: 1) Establish the role of amyloplasts as gravireceptors in shoots; 2) Investigate gravity-induced changes in the integrity of shoot actin cytoskeleton (CK); 3) Study the cellular interactions among actin CK, statoliths and cell membranes (endoplasmic reticulum - ER, plasma membrane - PM) during shoot graviperception; 4) Examine mediation of graviperception by modulations of cytosolic calcium - [Ca2+]cyt, and other second messengers (protein phosphorylation, inositol 1,4,5-trisphosphate - IP3). Revisions: 1) Model system: in addition to snapdragon (Antirrhinum majus L.) spikes and oat (Avena sativa) shoot pulvini, the model system of maize (Zea mays) primary roots was targeted to confirm a more general mechanism for graviperception. 2) Research topic: brassinolide, which were not included in the original plan, were examined for their regulatory role in gravity perception and signal transduction in roots, in relation to auxin and ethylene. Background to the topic: The negative gravitropic response of shoots is a complex multi-step process that requires the participation of various cellular components acting in succession or in parallel. Most of the long-lasting studies regarding the link between graviperception and cellular components were focused mainly on roots, and there are relatively few reports on shoot graviperception. Our previous project has successfully characterized several key events occurring during shoot bending of cut flowers and oat pulvini, including amyloplast displacement, hormonal interactions and differential growth analysis. Based on this evidence, the present project has focused on studying the initial graviperception process in flowering stems and cereal shoots. Major conclusions and achievements: 1) The actin and not the microtubule (MT) CK is involved in the graviperception of snapdragon shoots. 2) Gravisensing, exhibited by amyloplast displacement, and early transduction events (auxin redistribution) in the gravitropic response of snapdragon spikes are mediated by the acto-myosin complex. 3) MTs are involved in stem directional growth, which occurs during gravitropism of cut snapdragon spikes, but they are not necessary for the gravity-induced differential growth. 4) The role of amyloplasts as gravisensors in the shoot endodermis was demonstrated for both plant systems. 5) A gravity-induced increase in IP.