Relevant bibliographies by topics / Contractile Proteins

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  3. Books
  4. Book chapters
  5. Conference papers
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Academic literature on the topic 'Contractile Proteins'

Author: Grafiati
Published: 4 June 2021
Last updated: 29 January 2023

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Journal articles on the topic "Contractile Proteins"

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Ruff, R. L., and J. Weissman. "Iodoacetate-induced contracture in rat skeletal muscle: possible role of ADP." American Journal of Physiology-Cell Physiology 261, no. 5 (November 1, 1991): C828—C836. http://dx.doi.org/10.1152/ajpcell.1991.261.5.c828.

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The effects of iodoacetic acid (IAA) and ischemic contraction were studied in rat extensor digitorum longus muscles. Ischemic contraction of IAA-treated muscles produced contracture. The onset of contracture was not associated with a change in sarcolemmal electrical properties or reduction in intracellular [ATP]; however, [creatine phosphate] was reduced by 75% and free [ADP] was increased by 665%. Continued stimulation of IAA-treated fibers resulted in depolarization, loss of membrane excitability, further depletion of creatine phosphate, and reduction in [ATP]. The effects seen in IAA-treated muscle did not appear to result from a direct action of IAA on the surface membrane, contractile proteins, or excitation-contraction coupling. The contractures in IAA-treated muscle may have resulted from increased Ca sensitivity of the contractile proteins, increased myoplasmic [Ca], or both. Both effects may have resulted from increased [ADP]. In addition, the reduced acidification during ischemic contraction of IAA-treated fibers compared with control fibers may have further increased the Ca sensitivity of IAA-treated fibers compared with controls.
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Gros, Francois, and Margaret Buckingham. "Polymorphism of contractile proteins." Biopolymers 26, S0 (1987): S177—S192. http://dx.doi.org/10.1002/bip.360260016.

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Syrový, I. "Isoforms of contractile proteins." Progress in Biophysics and Molecular Biology 49, no. 1 (January 1987): 1–27. http://dx.doi.org/10.1016/0079-6107(87)90007-1.

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Ordway, George A., P. Darrell Neufer, Eva R. Chin, and George N. DeMartino. "Chronic contractile activity upregulates the proteasome system in rabbit skeletal muscle." Journal of Applied Physiology 88, no. 3 (March 1, 2000): 1134–41. http://dx.doi.org/10.1152/jappl.2000.88.3.1134.

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Remodeling of skeletal muscle in response to altered patterns of contractile activity is achieved, in part, by the regulated degradation of cellular proteins. The ubiquitin-proteasome system is a dominant pathway for protein degradation in eukaryotic cells. To test the role of this pathway in contraction-induced remodeling of skeletal muscle, we used a well-established model of continuous motor nerve stimulation to activate tibialis anterior (TA) muscles of New Zealand White rabbits for periods up to 28 days. Western blot analysis revealed marked and coordinated increases in protein levels of the 20S proteasome and two of its regulatory proteins, PA700 and PA28. mRNA of a representative proteasome subunit also increased coordinately in contracting muscles. Chronic contractile activity of TA also increased total proteasome activity in extracts, as measured by the hydrolysis of a proteasome-specific peptide substrate, and the total capacity of the ubiquitin-proteasome pathway, as measured by the ATP-dependent hydrolysis of an exogenous protein substrate. These results support the potential role of the ubiquitin-proteasome pathway of protein degradation in the contraction-induced remodeling of skeletal muscle.
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Yamaguchi, Osamu, Yoshinari Sakagami, Takayuki Suzuki, Masato Kobayashi, and Yasuo Shiraiwa. "CONTRACTILE PROTEINS IN THE KIDENY." Japanese Journal of Urology 79, no. 2 (1988): 326–31. http://dx.doi.org/10.5980/jpnjurol1928.79.2_326.

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Sakagami, Yoshinari. "CONTRACTILE PROTEINS IN THE KIDNEY." Japanese Journal of Urology 79, no. 2 (1988): 332–38. http://dx.doi.org/10.5980/jpnjurol1928.79.2_332.

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KIEHART, D. P., A. KETCHUM, P. YOUNG, D. LUTZ, M. R. ALFENITO, X. j. CHANG, M. AWOBULUYI, et al. "Contractile Proteins in Drosophila Development." Annals of the New York Academy of Sciences 582, no. 1 Cytokinesis (April 1990): 233–51. http://dx.doi.org/10.1111/j.1749-6632.1990.tb21683.x.

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Mehta, D., M. F. Wu, and S. J. Gunst. "Role of contractile protein activation in the length-dependent modulation of tracheal smooth muscle force." American Journal of Physiology-Cell Physiology 270, no. 1 (January 1, 1996): C243—C252. http://dx.doi.org/10.1152/ajpcell.1996.270.1.c243.

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The active isometric force developed by a muscle decreases at muscle lengths below an optimal length (Lo). However, when the length of an actively contracting muscle is abruptly decreased, a lower level of isometric force is reached during force redevelopment than when the contraction is initiated at the shorter length. This has been attributed to a deactivation of contractile proteins caused by shortening. In this study, intracellular Ca2+ and myosin light chain (MLC) phosphorylation were measured to assess the mechanisms for the modulation of isometric force caused by changing smooth muscle length before or during isometric contraction. The decline in isometric force between Lo and 0.5Lo was associated with decreases in MLC phosphorylation and intracellular Ca2+ during contractions elicited by acetylcholine or 60 mM KCl. Quick release of the muscle during contraction depressed force redevelopment at the shorter length but not MLC phosphorylation. We conclude that decreases in Ca(2+)-calmodulin-dependent MLC phosphorylation contribute significantly to the decline in isometric force at lengths below Lo, but the depression of contractility associated with the quick release of actively contracted smooth muscle is not caused by a shortening-induced deactivation of contractile proteins.
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Dou, Ying, Per Arlock, and Anders Arner. "Blebbistatin specifically inhibits actin-myosin interaction in mouse cardiac muscle." American Journal of Physiology-Cell Physiology 293, no. 3 (September 2007): C1148—C1153. http://dx.doi.org/10.1152/ajpcell.00551.2006.

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Blebbistatin is a powerful inhibitor of actin-myosin interaction in isolated contractile proteins. To examine whether blebbistatin acts in a similar manner in the organized contractile system of striated muscle, the effects of blebbistatin on contraction of cardiac tissue from mouse were studied. The contraction of paced intact papillary muscle preparations and shortening of isolated cardiomyocytes were inhibited by blebbistatin with inhibitory constants in the micromolar range (1.3–2.8 μM). The inhibition constants are similar to those previously reported for isolated cardiac myosin subfragments showing that blebbistatin action is similar in filamentous myosin of the cardiac contractile apparatus and isolated proteins. The inhibition was not associated with alterations in action potential duration or decreased influx through L-type Ca2+ channels. Experiments on permeabilized cardiac muscle preparations showed that the inhibition was not due to alterations in Ca2+ sensitivity of the contractile filaments. The maximal shortening velocity was not affected by 1 μM blebbistatin. In conclusion, we show that blebbistatin is an inhibitor of the actin-myosin interaction in the organized contractile system of cardiac muscle and that its action is not due to effects on the Ca2+ influx and activation systems.
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Pavalko, F. M., L. P. Adam, M. F. Wu, T. L. Walker, and S. J. Gunst. "Phosphorylation of dense-plaque proteins talin and paxillin during tracheal smooth muscle contraction." American Journal of Physiology-Cell Physiology 268, no. 3 (March 1, 1995): C563—C571. http://dx.doi.org/10.1152/ajpcell.1995.268.3.c563.

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Reorganization of cytoskeletal-membrane interactions during contractile stimulation may contribute to the regulation of airway smooth muscle contraction. We investigated the effect of contractile stimulation on the phosphorylation of the actin-membrane attachment proteins talin, vinculin, and paxillin. Stimulation of 32P-labeled canine tracheal smooth muscle strips with acetylcholine (ACh; 10(-3) M) resulted in a rapid 2.6-fold increase in phosphorylation of serine and/or threonine residues, compared with resting levels of 0.22 mol PO4(3-)/mol talin. After stimulation with ACh, phosphorylation of tyrosine residues on paxillin increased approximately threefold. Two-dimensional phosphopeptide mapping of in vivo labeled talin and paxillin indicated phosphorylation on a limited number of sites. Vinculin phosphorylation was undetectable in either resting or ACh-stimulated muscle. We conclude that phosphorylation of talin and paxillin occurs during ACh-stimulated contraction of tracheal smooth muscle and that distinct signaling pathways activate a serine/threonine kinase that phosphorylates talin and a tyrosine kinase that phosphorylates paxillin. The pharmacological activation of airway smooth muscle cells might involve the anchoring of contractile filaments to the membrane.
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Dissertations / Theses on the topic "Contractile Proteins"

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Bayliss, Christopher Richard. "Dysfunction of contractile proteins in hypertrophic cardiomyopathy." Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/9293.

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The contractility of human heart samples from patients diagnosed with hypertrophic cardiomyopathy were studied using a quantitative in vitro motility assay. The aim of this work was to investigate the molecular phenotype of thin filament proteins in the HCM heart. Three biopsy samples with thin filament mutations were studied alongside samples acquired from a subset of HCM patients classified with hypertrophic obstructive cardiomyopathy. The primary effect of thin filament mutations was investigated by reconstituting Factin with ACTC E99K into thin filament with donor troponin. The E99K actin filaments had a higher Ca2+-sensitivity then filaments composed of donor F-actin (with no mutation) (EC50 E99K/donor 0.78±0.14, p=0.02). A similar higher Ca2+- sensitivity was found when recombinant TnT K273N was incorporated into donor troponin and compared to native donor troponin (EC50 K273N/donor 0.54±0.17, p=0.006). Troponin was also purified from HOCM heart samples. This troponin did not contain a causative mutation but behaved abnormally in the response of thin filament Ca2+- sensitivity to changes in TnI phosphorylation (EC50 PKA-HOCM/HOCM 1.08±0.25, p=0.3) as mean TnI phosphorylation of PKA-HOCM was 1.56 molsPi/molsTnI and HOCM was 0.29 molsPi/molsTnI. Thus, thin filament Ca2+-sensitivity was uncoupled from TnI phosphorylation in thin filaments with HOCM troponin. When the native TnT subunits were replaced with recombinant TnT this coupling was restored (EC50 HOCM rTnT/HOCM 0.63±0.26, p=0.03). It would appear that the result of HCM-causing mutations are two-fold. The primary effect of the HCM-causing mutations is to increase thin filament Ca2+-sensitivity. However, the contraction machinery appears to be the target of secondary modifications, that occur due to the pathology of the disease. Resulting in further changes, such as changes in protein composition and post-translational modification. One major consequence of these modifications may be to uncouple the relatively labile regulation of thin filament Ca2+-sensitivity by TnI phosphorylation.
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Du, Fei. "A RabGAP protein and BEACH Family proteins regulate contractile vacuole formation and activity and chemotaxis in Dictyostelium." Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2007. http://wwwlib.umi.com/cr/ucsd/fullcit?p3274747.

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Thesis (Ph. D.)--University of California, San Diego, 2007.
Title from first page of PDF file (viewed Oct. 5, 2007). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 87-99).
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Stromme, Adrianna. "The characterization of the cytoskeleton and associated proteins in the formation of wound-induced contractile arrays /." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116078.

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The cytoskeleton is an intrinsic aspect of all cells, and is essential for many cellular events including cell motility, endocytosis, cell division and wound healing. Remodeling of the cytoskeleton in response to these cellular activities leads to significant alterations in the morphology of the cell. One such alteration is the formation of an actomyosin contractile array required for cytokinesis, wound healing and embryonic development.
Cellular structure and shape depends upon tensional prestress brought about by the organization of cytoskeletal components. Using the Xenopus laevis oocyte wound healing model, it is first described how diminished cellular tension affects the balance of the Rho family of GTPases, and subsequently prevents the formation of actomyosin contractile arrays. This suggests that cellular tension in the cell is not created at the level of the cytoskeletal elements but rather via the upstream signaling molecules: RhoA and Cdc42.
The role of N-WASP (Neural-Wiscott Aldrich Syndrome Protein), a mediator of Arp2/3 based actin polymerization, is next examined for its putative role in cellular wound healing. Xenopus laevis oocytes injected with mutant N-WASP constructs reveals in vivo evidence that functional N-WASP is required for appropriate contractile array formation and wound closure.
Lastly, it is revealed that the cellular structures involved with single cell wound healing in other model systems are also important for the initial repair of severed muscle cells. Actin, non-muscle myosin-II, microtubules, sarcomeric myosin and Cdc42 are all recruited and reorganized at the edge of damaged C2C12 myotubes. This data promotes the possibility that an actomyosin array may be established in injured muscle cells as well.
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Bexis, Sotiria. "The relationship between vascular structure, contractile proteins, vascular reactivity and blood pressure in animal models of hypertension /." Title page, contents and abstract only, 1997. http://web4.library.adelaide.edu.au/theses/09PH/09phb572.pdf.

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Llinares, Elisa. "Function, regulation and intracellular trafficking of the vacuolaryeast pq-loop (Ypq) proteins." Doctoral thesis, Universite Libre de Bruxelles, 2012. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209704.

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The cytoplasm of eukaryotic cells contains several membrane-delimited compartments of specific molecular compositions and functions. Among those, the vacuole of fungal cells is often described as an organelle equivalent to the lysosomes of animal cells and the vacuoles of plant cells. These compartments indeed share two similar features: they contain a wide variety of hydrolases and are the most acidic compartments of the cell, which accounts for their key role in the intracellular degradation of macromolecules. In humans, dysfunctions of the lysosomes often give rise to lysosomal related diseases, such as lysosomal storage disorders. These are a class of metabolic disorders caused by the accumulation of non-degraded macromolecules or impaired export of hydrolytic degradation products. Cystinosis is an autosomal recessive disorder (1/200 000 incidence) generally associated with renal dysfunctions. It is caused by the accumulation and crystallization of cystine, the disulfide of cysteine, into the lumen of lysosomes. Cystinosin, the causative gene product of cystinosis, is present at the lysosomal membrane and catalyses the export of cystine from this compartment. The human cystinosin is a member of the Lysosomal Cystine Transporter (LCT) family. LCT proteins are conserved in all eukaryotic species and are defined by the presence of highly conserved PQ-loop motifs.

During this thesis work, we have studied three LCT proteins of the yeast Saccharomyces cerevisiae, named Ypq1, Ypq2 and Ypq3 (Yeast PQ-loop proteins 1, 2 and 3). We first showed that these proteins localize to the vacuolar membrane. We next studied the roles of these proteins, the regulation of their genes and the mechanisms and signals implicated in their delivery to the vacuolar membrane. We also contributed to the functional characterization of a mammalian homologue of yeast Ypq proteins, named rPqlc2.

In the first part of this work, we report that the Ypq proteins are most probably implicated in the export of basic amino acids from the vacuole to the cytosol. More precisely, Ypq2 and Ypq3 behave like vacuolar arginine and lysine exporters, respectively. Interestingly, the mammalian rPqlc2 protein expressed in yeast reaches the vacuolar membrane and functions as an orthologue of the Ypq proteins. Our results also reveal that the expression of the YPQ3 gene is regulated by the Lys14 transcription factor, responsible for the transcriptional activation of the LYS genes encoding enzymes implicated in the biosynthesis of lysine. We have also noted that, in general, the expression of the expression of the YPQ genes is regulated according to the quality of the nitrogen source available in the extracellular medium, eg. YPQ3 is sensitive to the nitrogen catabolite repression regulatory mechanism.

In the last part of this thesis work, we investigated the intracellular trafficking of the Ypq proteins and show that these predominantly reach the vacuolar membrane via the ALP (alkaline phosphatase) pathway due to the presence of a dileucine-based sorting signal in their sequences. Interestingly, a similar mechanism seems responsible for targeting to the yeast vacuole of the mammalian rPqlc2 protein.

Une caractéristique des cellules eucaryotes est leur organisation en compartiment internes délimité par une membrane lipidique, appelé organelles. Ces compartiments intracellulaires présentent une composition lipidique et protéique particulaire conforme à leur identité et fonction. Les lysosomes de cellules de mammifères et la vacuole fongique jouent un rôle clé dans la digestion intracellulaire de macromolécules et de ce fait leurs lumières sont enrichis d’enzymes hydrolytiques nécessaires à cette action. Des disfonctionnements du lysosome peuvent être la conséquence de pathologie chez l’homme, regroupé sous le nom de maladie lysosomale, lié à un à une accumulation de macromolécules non digéré ou un default d’export des produits d’hydrolysé depuis la lumière du lysosome. La cystinose est une maladie autosomale récessive avec une faible fréquence d’incidence (1/200 000) qui regroupe trois formes cliniques :deux formes rénales graves et une forme extra-rénale. Cette maladie est due à une accumulation et cristallisation de cystine dans la lumière du lysosome qui est corrélé à des mutations ponctuelles dans le gène CTNS qui code pour l’exporteur de cystine, la cystinosine. Cette protéine est un membre de la famille LCT (Lysosomal Cystine Transporter) qui possède des représentants chez les cellules animales, végétales et fongiques. Les protéines de la famille possèdent une taille et une topologie prédite similaire (7 segments transmembranaires) et on retrouve aussi au sein de ces protéines deux exemplaires de motifs PQ. Lors de ce travail de thèse nous nous sommes intéressés à trois membres de la famille LCT chez Saccharomyces cerevisiae que nous avons nommé Ypq1, Ypq2 et Ypq3 pour Yeast PQ-loop proteins. Ces protéines n’ayant pas fait l’objet de nombreuses études, nous nous sommes orientés vers une analyse fonctionnelle et transcriptionnelle. De plus, nous avons également étudié les mécanismes et signaux impliqué dans leur adressage vers la vacuole. Finalement, nous avons également inclus dans notre étude un homologue mammalien de ces protéines, rPqlc2.

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Doctorat en Sciences
info:eu-repo/semantics/nonPublished

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Crampin, Helen. "The identification of a Spitzenkörper in 'C. albicans' and the partial characterisation of the contractile ring proteins." Thesis, University of Sheffield, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.425604.

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Willott, Ruth Heather. "Functional analyses of cardiomyopathic contractile proteins : mutations in troponin that cause familial hypertrophic cardiomyopathy and familial dilated cardiomyopathy." Thesis, University of Oxford, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.400293.

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Bengreed, Amal H. I. "Characterisation of P2Y receptor-mediated contractile signalling and its regulation by G protein coupled receptor kinases and arrestin proteins in a rat bladder smooth muscle." Thesis, University of Leicester, 2018. http://hdl.handle.net/2381/42795.

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ATP released from parasympathetic nerves can mediated bladder contraction, can activate purinergic P2Y/Gq/11-coupled G protein-coupled receptors (GPCR) expressed on detrusor (bladder) smooth muscle cells (DSMC). P2Y/Gq/11 signalling activates phospholipase C (PLC) and increases intracellular calcium concentrations to induce contraction. DSMC contractile GPCR activity is tightly regulated to prevent inappropriate contraction/incontinence. Additionally, GPCRs activity is regulated by G protein-coupled receptor kinase (GRK) and arrestin proteins, it is likely that they play a similar role in DSMC, and may help to maintain continence. Combining confocal imaging, calcium-sensitive dyes and selective P2X and P2Y receptor agonists/antagonists, showed that after 3-4 days in culture DSMC calcium signals were mediated by P2Y1 and P2Y2, but not P2X, P2Y4 or P2Y6 receptors. Repeated agonist additions indicated a desensitization of P2Y1 and P2Y2 activated phospholipase C (PLC)/Ca2+ signals, which was restored when the washout period between agonist challenges was increased. Transfection of DSMC with dominant-negative, catalytically inactive GRK mutants, which block endogenous GRK function, showed that P2Y1 and P2Y2 receptor stimulated calcium signalling was selectively regulated by GRK3 and GRK2, respectively. Furthermore, desensitization of P2Y1 and P2Y2 receptor PLC/Ca2+ was attenuated following RNAi-mediated knockdown of arrestin2 or arrestin3, suggesting both arrestins were able to regulate P2Y1/2 receptor signalling. To mimic the effects of obstructive bladder, DSMC were mechanically stretched which resulted in increased GRK2, and decreased GRK3/5/6 expression. These data show that DSMC express functional P2Y1/P2Y2 receptors which mediate purinergic agonist PLC/Ca2+ signalling, implying roles for P2Y1 and P2Y2 in bladder contraction and voiding. Furthermore, P2Y1 and P2Y2 receptor are selectively regulated by GRK and arrestin proteins, which suggests that GRK and arrestin proteins play an important role in the regulation of bladder tone. Furthermore, since GRK expression following mechanical stretch this may in turn affect GPCR signalling and produce dysregulation of DSMC contraction observed during incontinence.
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Johnsen, Lisa 1987. "Lipid droplet regulation by the differentially spliced proteins Osw5L and Osw5S." Doctoral thesis, Universitat Pompeu Fabra, 2016. http://hdl.handle.net/10803/565566.

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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.
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Sjuve, Rolf. "Function of contractile and cytoskeletal proteins in smooth muscle effects of hypertrophy and age and of desmin removal in a transgenic animal /." Lund : Dept. of Physiology and Neuroscience, Lund University, 1998. http://books.google.com/books?id=ccFqAAAAMAAJ.

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Books on the topic "Contractile Proteins"

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1952-, Johnson Robert G., Kranias Evangelia G, and New York Academy of Sciences., eds. Cardiac sarcoplasmic reticulum function and regulation of contractility. New York, N.Y: New York Academy of Sciences, 1998.

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R, Barton Paul J., ed. Molecular biology of cardiac development and growth. Austin: R.G. Landes Co., 1995.

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Sabry, Mohamed Abdalla. Development transitions of the contractile regulatory proteins, troponin I and troponin T, in striated muscles: An immunochemical study. Birmingham: University of Birmingham, 1992.

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Carrington, Charlotte A. The pressor response to isometric exercise in man: Its relationship to age, muscle contractile characteristics and contractile protein profile. Birmingham: University of Birmingham, 1993.

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McHale, James M. Contracting with the federal government: Awards, protests, and disputes. New York (235 E. 45th St., New York 10017): M. Bender, 1985.

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1933-, Pette Dirk, and Symposium "The Dynamic State of Muscle Fibers" (1989 : University of Konstanz), eds. The Dynamic state of muscle fibers: Proceedings of the international symposium, October 1-6, 1989, Konstanz, Federal Republic of Germany. Berlin: De Gruyter, 1990.

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Nature's versatile engine: Insect flight muscle inside and out. Georgetown, Tex: Landes Bioscience/Eurekah.com, 2006.

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1934-, Ozawa Eijirō, Masaki Tomoh, and Nabeshima Yoichi, eds. Frontiers in muscle research: Myogenesis, muscle contraction, and muscle dystrophy : proceedings of the Uehara Memorial Foundation Symposium on Frontiers in Muscle Research, Tokyo, 15-19 July 1990. Amsterdam: Excerpta Medica, 1991.

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B, Vallee Richard, ed. Structural and contractile proteins. Orlando: Academic Press, 1986.

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W, Cunningham Leon, ed. Structural and contractile proteins. Orlando: Academic Press, 1987.

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Book chapters on the topic "Contractile Proteins"

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Bagshaw, Clive R. "Contractile proteins." In Muscle Contraction, 33–57. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-015-6839-5_4.

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Schliwa, Manfred. "Cytoplasmic Contractile Proteins." In The Cytoskeleton, 5–47. Vienna: Springer Vienna, 1986. http://dx.doi.org/10.1007/978-3-7091-7667-2_2.

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Walsh, Michael P. "Contractile Proteins of Smooth Muscle." In Physiology and Pathophysiology of the Heart, 855–78. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0873-7_42.

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Winegrad, S., G. McClellan, L. E. R. Lin, and S. Weindling. "Modulation properties of myocardial contractile proteins." In Developments in Cardiovascular Medicine, 253–60. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3313-2_15.

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Fox, Joan E. B. "The Organization of Platelet Contractile Proteins." In Platelet Membrane Glycoproteins, 273–98. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4880-1_13.

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Izumi, Tohru, Haruo Hanawa, Makihiko Saeki, and Makoto Kodama. "Cardiac Contractile Proteins and Autoimmune Myocarditis." In Cellular Function and Metabolism, 67–71. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3078-7_10.

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Ebashi, S. "Contractile and Regulatory Proteins in Cardiovascular System." In Developments in Cardiovascular Medicine, 279–91. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2053-1_18.

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Roberts, Robert, Jeffrey Towbin, Thomas Parker, and Roger D. Bies. "Molecular Biology of Contractile and Cytoskeletal Proteins." In A Primer of Molecular Biology, 129–50. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4684-6680-5_5.

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Goldfine, S. M., I. Peng, and D. A. Fischman. "The Insertion and Release of Contractile Proteins." In The Dynamic State of Muscle Fibers, edited by Dirk Pette, 103–18. Berlin, Boston: De Gruyter, 1990. http://dx.doi.org/10.1515/9783110884784-011.

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Kaneko, Masanori, and Yuji Matsumoto. "Changes in Contractile Proteins under Oxidative Stress." In Developments in Cardiovascular Medicine, 139–47. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1235-2_10.

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Conference papers on the topic "Contractile Proteins"

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Saban, Melissa, Narayanan Venkatesan, Michelle L. D'Antoni, Stephanie Pasternyk, and Mara S. Ludwig. "Effect Of Decorin On Airway Smooth Muscle Cell Contractile Proteins." 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.a2074.

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Spangenberg, P., W. Lobche, and U. Till. "ALTERATIONS OP THE ACTIN STATUS OP PLATELETS APPECTS THE FUNCTIONAL BEHAVIOUR OP THE CELL." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644874.

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Many platelet responses to agonists involve contractile proteins. Particularly, the status of the most abundant protein actin is changed in motile and contractile events. We have studied the effects of SH-reagents on platelets and found significant effects of a SH-oxidizing agent on the actin organization which are neutralized following the addition of a disulfide-reducing compound. SH-oxidation of intact platelets was achieved by incubation with diamide (azodicarboxylic acid-bis-dimethylamide). The P-actin of those cells is increased and the filaments became centralized indicating a disturbance of the membrane-cytoskeleton interaction. Treatment of SH-oxidized platelets with 2-mercaptopropionylglycine which reduces disulfides resulted in a return of P-actin levels to those seen in untreated cells The actin organization of platelets is discussed with regard to the altered functional behaviour of diamide-treated cells.
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Ramirez, Angelica Maria, Begoña Calvo Calzada, and Jorge Grasa. "The Effect of the Fascia on the Stress Distribution in Skeletal Muscle." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19696.

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The human and vertebrate interaction with the environment is done primarily through the movement. This is possible due the skeletal muscle: anatomical structure able to contract voluntarily. The skeletal muscles are made up of contractile proteins which slide one over another allowing the muscle shortening and the body force generation. This protein structure of actin and myosin maintains its organization through the connective tissue that surrounds it (endomysium, perimysium and epimysium), creating arrays of myofibrils, fibre bundles, fascicles until conform the whole muscle. All this connective tissue extends to the ends of the muscle to form the tendon.
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Southern, B. D., H. Li, J. F. Crish, L. M. Grove, R. G. Scheraga, and M. A. Olman. "S100a4 Mediates Myofibroblast Differentiation and Experimental Pulmonary Fibrosis Through Subcellular Redistribution of Contractile Cytoskeleton Proteins." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a6391.

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Scott, Devon, Robin Shandas, and Wei Tan. "Effect of Vessel Stiffening and High Pulsatility Flow on Contractile Function and Proliferation of Small Arterial Cells." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19597.

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Recent studies have identified arterial stiffening as a predictor of some vascular diseases such as pulmonary hypertension, which is characterized by dysfunction of small arteries. Stiffening is shown to cause changes in blood flow, extending high pulsatile flow into small arteries that normally experience steady flow conditions (Chui 2004). However, few studies have investigated the mechanisms underlying the effects of arterial stiffening on vascular remodeling. We hypothesized that arterial stiffness effects dysfunction of downstream vascular endothelium and smooth muscle through changes in flow pulsatility. Previously we developed a flow system to study the influence of pulse flow waves, by modulating upstream stiffness, on downstream mimetic vascular cell co-culture. With this system, the present study examines contractile and proliferating protein expressions of smooth muscle cell (SMC) co-cultured with endothelial cell (EC). The endothelium, directly interfaces with the blood flow, and transduces mechanical signals to underlying SMC (Stegemann 2005). We recently showed that high pulsatile flow induced EC dysfunction. Therefore, we further asked whether high pulsatility flow would cause characteristic changes of small arterial SMC in the hypertension condition such as smooth muscle hyperplasia (increased cell proliferation) and hypertrophy (increased contractile proteins) (Voelkel 1997), and whether these changes would be mediated by EC dysfunction.
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Schen, Aaron, and Lisa X. Xu. "Preliminary Study of Vascular Endothelial Ca2+ Response to Elevated Temperature." In ASME 2000 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2000. http://dx.doi.org/10.1115/imece2000-2487.

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Abstract The thermal regulation of tissue is controlled by the sympathetically mediated redistribution of cardiac output and change in local flow resistance of arterioles. The diameter change of the vessel from its resting level is governed by the state of the contractile proteins in vascular smooth muscle which can be influenced by the concentration of free cytosolic calcium ([Ca2+]i) in the vascular endothelial cells (Falcone, 1995).
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Sewell-Loftin, M. K., and W. David Merryman. "The Role of SRC in Strain- and Ligand- Dependent Phenotypic Modulation of Mouse Embryonic Fibroblasts." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53604.

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Connective tissue fibrosis represents a significant portion of mortality and morbidity in our society. These diseases include many illnesses such as heart valve disease, atherosclerosis, macular degeneration, and cirrhosis, meaning that millions of lives are affected by these conditions each year. Fibrotic tissues form when quiescent fibroblasts activate becoming myofibroblasts, the phenotype of active tissue construction and fibrosis. During this process, the cells produce smooth muscle α-actin (αSMA), a contractile element considered to be the hallmark of cellular activation [1]. Following the production of αSMA, there is an increase in the synthesis of extracellular matrix (ECM) proteins, most notably type I collagen; this increase in ECM proteins causes the stiffening of the tissue characteristic of fibrotic disease. In non-disease states (such as wound healing or tissue development), the myofibroblasts will either deactivate, becoming fibroblasts again, or apoptose before tissue fibrosis occurs. However, when myofibroblasts persist, increased ECM protein deposition causes increased tissue stiffness and activates neighboring cells, causing the fibrosis to propagate. Currently there are no therapies to prevent or reverse fibrosis. Therefore a more thorough understanding of the dynamic mechanical environment and signaling pathways involved in the activation of fibroblasts is required to develop potential treatments.
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Southern, B. D., H. Li, J. F. Crish, L. Grove, R. G. Scheraga, A. I. Ivanov, and M. A. Olman. "Endogenous Fibroblast S100a4 Mediates Myofibroblast Differentiation and Pulmonary Fibrosis Through Matrix-Stiffness Dependent Redistribution of Contractile Proteins." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4416.

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Shikhaleva, E., T. Sulman, A. Dokuchaev, Larisa V. Nikitina, and Leonid B. Katsnelson. "Mathematical modeling of the role of cooperativity between contractile and regulatory proteins in the mechano-calcium feedbacks in myocardium." In 2015 Computing in Cardiology Conference (CinC). IEEE, 2015. http://dx.doi.org/10.1109/cic.2015.7408651.

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

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

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Rafaeli, Ada, and Russell Jurenka. Molecular Characterization of PBAN G-protein Coupled Receptors in Moth Pest Species: Design of Antagonists. United States Department of Agriculture, December 2012. http://dx.doi.org/10.32747/2012.7593390.bard.

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The proposed research was directed at determining the activation/binding domains and gene regulation of the PBAN-R’s thereby providing information for the design and screening of potential PBAN-R-blockers and to indicate possible ways of preventing the process from proceeding to its completion. Our specific aims included: (1) The identification of the PBAN-R binding domain by a combination of: (a) in silico modeling studies for identifying specific amino-acid side chains that are likely to be involved in binding PBAN with the receptor and; (b) bioassays to verify the modeling studies using mutant receptors, cell lines and pheromone glands (at tissue and organism levels) against selected, designed compounds to confirm if compounds are agonists or antagonists. (2) The elucidation ofthemolecular regulationmechanisms of PBAN-R by:(a) age-dependence of gene expression; (b) the effect of hormones and; (c) PBAN-R characterization in male hair-pencil complexes. Background to the topic Insects have several closely related G protein-coupled receptors (GPCRs) belonging to the pyrokinin/PBAN family, one with the ligand pheromone biosynthesis activating neuropeptide or pyrokinin-2 and another with diapause hormone or pyrokinin-1 as a ligand. We were unable to identify the diapause hormone receptor from Helicoverpa zea despite considerable effort. A third, related receptor is activated by a product of the capa gene, periviscerokinins. The pyrokinin/PBAN family of GPCRs and their ligands has been identified in various insects, such as Drosophila, several moth species, mosquitoes, Triboliumcastaneum, Apis mellifera, Nasoniavitripennis, and Acyrthosiphon pisum. Physiological functions of pyrokinin peptides include muscle contraction, whereas PBAN regulates pheromone production in moths plus other functions indicating the pleiotropic nature of these ligands. Based on the alignment of annotated genomic sequences, the primary and secondary structures of the pyrokinin/PBAN family of receptors have similarity with the corresponding structures of the capa or periviscerokinin receptors of insects and the neuromedin U receptors found in vertebrates. Major conclusions, solutions, achievements Evolutionary trace analysisof receptor extracellular domains exhibited several class-specific amino acid residues, which could indicate putative domains for activation of these receptors by ligand recognition and binding. Through site-directed point mutations, the 3rd extracellular domain of PBAN-R was shown to be critical for ligand selection. We identified three receptors that belong to the PBAN family of GPCRs and a partial sequence for the periviscerokinin receptor from the European corn borer, Ostrinianubilalis. Functional expression studies confirmed that only the C-variant of the PBAN-R is active. We identified a non-peptide agonist that will activate the PBAN-receptor from H. zea. We determined that there is transcriptional control of the PBAN-R in two moth species during the development of the pupa to adult, and we demonstrated that this transcriptional regulation is independent of juvenile hormone biosynthesis. This transcriptional control also occurs in male hair-pencil gland complexes of both moth species indicating a regulatory role for PBAN in males. Ultimate confirmation for PBAN's function in the male tissue was revealed through knockdown of the PBAN-R using RNAi-mediated gene-silencing. Implications, both scientific and agricultural The identification of a non-peptide agonist can be exploited in the future for the design of additional compounds that will activate the receptor and to elucidate the binding properties of this receptor. The increase in expression levels of the PBAN-R transcript was delineated to occur at a critical period of 5 hours post-eclosion and its regulation can now be studied. The mysterious role of PBAN in the males was elucidated by using a combination of physiological, biochemical and molecular genetics techniques.
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