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Laddada, Lilia. "Etude du développement des tendons et de leur interaction avec les précurseurs de muscles lors de la myogenèse appendiculaire chez la Drosophile." Thesis, Université Clermont Auvergne (2017-2020), 2018. http://www.theses.fr/2018CLFAC011/document.
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La mise en place du système musculo-(exo)squelettique de la drosophile est un modèle d’organisation particulièrement propice à l’étude des interactions tissulaires au cours du développement.Notre étude vise à, d’une part, comprendre la myogenèse appendiculaire à travers l’étude des interactions précoces entre les précurseurs de tendon et les myoblastes, et d’autre part, étudier les mécanismes de différenciation des précurseurs de tendons associés au disque de patte. Dans ce contexte nous avons adapté la méthode GRASP (GFP Reconstitution Across Synaptic Partners) ainsi que l’imagerie en temps réel à notre modèle pour démontrer l’existence des interactions cellulaires entre les précurseurs de tendons et les myoblastes, nous avons aussi mis au point une approche cellule-spécifique afin de trier les précurseurs de tendons et les myoblastes associés au disque de patte, ce qui nous a permis d’obtenir dans un premier temps les données transcriptomiques des précurseurs de tendons. J’ai également étudié l’impact de l’altération des précurseurs de tendon sur le comportement des myoblastes associés et inversement. Nos résultats montrent que l’altération du développement des tendons entraîne une désorganisation spatiale des myoblastes environnants. Dans la seconde partie de mon projet, je me suis intéressée à l’implication de la voie Notch et des gènes de la famille odd-skipped dans la différenciation et la morphogenèse des précurseurs de tendon. J’ai ainsi démontré que Notch est nécessaire et localement suffisant pour induire l’expression de stripe et que les gènes odd-skipped et stripe coopèrent en aval cette voie pour permettre l’invagination et l’élongation sous forme de tube des longs tendons internes de la patte<br>The formation of the musculo-(exo)skeletal system in drosophila is a remarkable example of tissue patterning making it a suitable model for studying multiple tissue interactions during development.The aim of our study is to better understand appendicular myogenesis through the identification of early interactions between tendon and muscle precursors, and by investigating the mechanisms governing the specification of tendon cell precursors of the leg disc. In order to characterize the interaction between these two tissues, we adapted the GRASP method (GFP Reconstitution Across Synaptic Partners) and set up live imaging experiments to reveal cellular interactions between tendon precursors and myoblasts. We have also conducted a genome wide cell-specific analysis using Fluorescence-activated cell sorting (FACS) on imaginal discs which allowed us to perform a tendon cell specific transcriptional analysis.To test whether reciprocal muscle-tendon interactions are necessary for correct muscle-tendon development, I performed experiments to specifically interfere with the development of tendon or muscle precursors. By altering tendon precursors formation during the early steps of leg development, we affect the spatial localization of the associated myoblasts. These findings provide the first evidence of the developmental impact of early interactions between muscle and tendon precursors in the leg disc.In the second part of my project, I investigated the role of Notch pathway and odd-skipped genes in the differentiation and morphogenesis of tendon precursors. Thus, I have demonstrated that Notch signalling pathway is necessary and locally sufficient for the initiation of stripe expression, and that both odd-skipped genes and stripe are required downstream of Notch to promote morphological changes associated with formation of long tubular tendons
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Orfanos, Zacharias. "Dynamics of sarcomere assembly in drosophila indirect flight muscles." Thesis, University of York, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.533510.
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Cripps, Richard Matthew. "Genetical and biochemical studies of Drosophila indirect flight muscles." Thesis, University of York, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.276490.
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Varshney, Gaurav. "Identification of downstream targets of ALK signaling in Drosophila melanogaster /." Doctoral thesis, Umeå : Umeå universitet, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1894.
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Yang, Hairu. "Drosophila skeletal muscles regulate the cellular immune response against wasp infection." Doctoral thesis, Umeå universitet, Institutionen för molekylärbiologi (Medicinska fakulteten), 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-125842.
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Drosophila melanogaster is widely used as a model organism to study the innate immune system because it lacks an adaptive immune response that could mask its innate immune response. The innate immune response of Drosophila primarily consists of humoral and cellular immune responses. The humoral immune response ismediated by antimicrobial peptides, and is induced by bacterial and fungal infections. The cellular immune response is mediated by blood cells (hemocytes), and is induced by bacterial and wasp infection. While the humoral immune response of Drosophila has been studied extensively, the cellular immune response is less well understood. In this work, I investigated the communication between different signaling pathways and tissues in Drosophila during infection by the parasitic wasp Leptopilina boulardi. I find that JAK/STAT signaling is strongly activated by wasp infection, in both hemocytes and (unexpectedly) larval skeletal muscles. This activation is mediated by the cytokines Upd2 and Upd3, which are secreted from circulating hemocytes. Deletion of upd2 or/and upd3 weakens the wasp-induced activation of JAK/STAT signaling in skeletal muscles and the cellular immune response to wasp infection, leading to reduced encapsulation of wasp eggs and a decrease in the number of circulating lamelloyctes. The suppression of JAK/STAT signaling also significantly weakens the cellular immune response in skeletal muscles, but not in fat bodies and hemocytes. However, the activation of this signaling in skeletal muscles has no obvious effect on the cellular immune response. Together, these results suggest that rather than being uninvolved bystanders, Drosophila skeletal musclesactively participate in cellular immune responses against wasp infection. To answer how Drosophila larval muscles participate cellular immune response, I min-screened the effects of several immune related signaling pathways in the muscles and the fat body on the cellular immune response. Interestingly, the cellular immune response was only significantly compromised by the suppression ofinsulin signaling in skeletal muscles, in a way that was veryreminiscent of the phenotypes induced by suppressing JAK/STAT signaling in muscles. While wasp infection activates JAK/STAT signaling in muscles, it has the opposite effect on insulin signaling. In addition, I find that insulin signaling in skeletal muscles can positively regulate JAK/STAT signaling. On the other hand, suppression of JAK/STAT signaling in muscles reduces insulin signaling locally in muscles and systemically in the fat body. Suppression of either insulin or JAK/STAT signaling in muscles leads to reductions in glycogen storage in muscles, the trehalose concentration in the hemolymph, and the frequency of feeding behavior. All these results indicate that JAK/STAT and insulin signaling in Drosophila skeletal muscles regulate cellular immune responses via their effects on carbohydrate metabolism. Our findings shed new light on the interactions between diabetes, metabolism, the immune system, and tissue communication.
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Shirinian, Margret. "Midgut and muscle development in Drosophila melanogaster." Doctoral thesis, Umeå universitet, Institutionen för molekylärbiologi (Medicinska fakulteten), 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-22137.
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The fully developed and functional Drosophila midgut comprises two layers, the visceral mesoderm and the endoderm. The visceral muscle of the midgut is formed by the fusion of founder cells with fusion competent cells to form the muscle syncytia. The specification of these cells and thus the fusion and the formation of the midgut muscle is dependent on the Receptor tyrosine kinase (RTK) Alk (Loren et al., 2003). The endoderm underlies the visceral muscle and is formed from cells that originate from the anterior and the posterior parts of the embryo. These cells use the visceral mesoderm as a substrate for their migration. Using Alk mutant animals, we have studied endoderm migration during embryonic development. While the initial migration of the endoderm is not affected in the absence of the visceral mesoderm, we observe that the later dorsal-ventral endodermal migration does not take place. The development of the visceral muscle and its dependence on the endoderm is poorly understood. We have analysed gürtelchen (gurt) mutant animals, originally identified in a genetic screen for mutations affecting visceral muscle formation. Gurt mutants are so named due to their belt-like phenotype of the visceral muscle (gürtelchen is German for belt). Mapping of the genomic locus identified gurt as a mutation in a previously described gene - huckebein (hkb) which is known to have an important function in endoderm development. Gurt (hkb) mutants were used to further study the interaction between the endoderm and the visceral muscle during development. The initial specification of founder cells and fusion competent myoblasts as well as fusion events are unaffected in gurt (hkb) mutants, however, the elongation and stretching of the visceral muscle does not proceed as normal. Moreover, ablation of the visceral mesoderm disrupts endoderm migration, while ablation of the endoderm results in a delayed disruption of visceral muscle formation. Signaling between the two tissues was investigated in detail. Since Alk is a critical player in visceral muscle development, we employed Alk mutant embryos for this task. In addition to the role of Alk in specifying the founder cells and initiating the visceral muscle fusion, we have shown that Alk mediated signaling has a role in the induction of the midgut constriction process by regulating dpp expression in the developing embryonic gut. Finally, we wished to identify genes in the founder cells/fusion competent myoblasts that might be regulated by Alk. C3G is a gunaine nucleotide exchange factor expressed in the visceral muscle founder cells. Deletion of the Drosophila C3G locus resulted in the generation of null mutants in C3G which are viable, but display decreased longevity, fitness and are semi-lethal. Further analysis of C3G mutants indicated that C3G is essential for normal larval musculature development, in part by regulating integrin localization at muscle attachment sites.
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Islam, Riswana. "The role of [beta]FTZ-F1 in the innervation of the abdominal and pharyngeal muscles in Drosophila /." Connect to online version, 2005. http://ada.mtholyoke.edu/setr/websrc/pdfs/www/2005/92.pdf.
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Soler, Cédric. "La formation des muscles de la patte chez Drosophila melanogaster : un nouveau modèle d'étude de la myogenèse appendiculaire." Clermont-Ferrand 1, 2005. http://www.theses.fr/2005CLF1MM20.
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Bernard, Frédéric. "Etude du rôle du gène vestigial au cours de la myogenèse adulte chez Drosophila Melanogaster." Paris 7, 2006. http://www.theses.fr/2006PA077073.
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Drosophila melanogaster est un système modèle particulièrement adapté à la génétique du développement. La facilité d'entretien et de stockage des différentes lignées, une large collection de lignées mutantes à disposition et de nombreux outils génétiques sont les plus gros avantages de ce système d'étude. Chez la drosophile, le thorax contient l'ensemble des muscles nécessaires au vol de la mouche. Parmi ceux-ci on distingue de petits muscles tubulaires qui sont directement attachés à l'aile : les muscles directs du vol (DFM : Direct Flight Muscles) et de plus grands muscles attachés à l'exosquelette cuticulaire qui forme le thorax : les muscles indirects du vol (IFM : Indirect Flight Muscles). La contraction des IFM entraîne des déformations du thorax nécessaires à la synchronisation du battement des ailes. Au laboratoire, il a été isolé un allèle nul du gène (vgnull) qui est associé à des dégénérescences spécifiques des IFM. Le but de ma thèse était « L'étude du rôle du gène vestigial au cours de la myogenèse adulte chez Drosophila melanogaster ». Des expériences de génétique et d'immunohistochimie ont permis de mettre en évidence plusieurs dérégulations génétiques indiquant un rôle de VG dans l'identité du développement des muscles indirects du vol (Indirect Flight Muscles, IFM). Ce rôle se fait en partie en inhibant une identité du développement de type DFM. De plus, j'ai pu montrer que VG est impliquée dans la différenciation musculaire en réprimant la voie Notch, Durant la dernière partie de ma thèse, j'ai étudié la régulation du gène vg au cours du processus myogénique, et j'ai pu identifier une séquence génomique responsable de l'expression musculaire de vg<br>Drosophila melanogaster is an attractive experimental model System because of its short generation time and the easy handling of the flies. This model also benefit from a wide range of methods for carrying out molecular genetic analysis ; these include transgenesis, controlled gene-overexpression System based on the yeast GAL4-UAS System, and a tool (the Flp-FRT System) for performing site-specific recombination. Flight muscles in Drosophila are located in the thorax and are subdivided into two distinct classes : the Direct Flight Muscles (DFMs) attached to the wing hinge and directly responsible for wing movement, and the Indirect Flight Muscles (IFMs) attached to the cuticule and contributing to flight by deformation of the thorax. The IFMs represent the majority of the thoracic muscles. During my PhD, I was interested in IFM development in Drosophila melanogaster. I focus my work on the function of a mammalian-confserved transcription factor Vestigial - Scalloped (VG-SD) during this process. I have shown that VG is necessary for developmental identity of IFM and that an absence of VG leads to IFM specific degeneration through an apoptotic process. I have also obtained some results involving VG in muscle differentiation through Notch pathway inhibition. Finally, I have studied the régulation of vg gene during this process and I have isolated a genomic sequence responsible for the muscular expression of this gene
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Caine, Charlotte. "Etude des interactions entre MEF2 et la voie de signalisation Notch au cours de la myogenèse adulte chez Drosophila melanogaster." Paris 7, 2012. http://www.theses.fr/2012PA077248.
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La myogenèse des muscles indirects du vol (IFM) chez Drosophila melanogaster suit un schéma développemental précis. Au cours de l'embryogenèse, un groupe de cellules, les Précurseurs adultes Musculaires (AMP) se spécifient. Ces cellules deviennent des myoblastes qui prolifèrent au cours des stades larvaires et donneront par la suite les IFM adultes. Nos travaux se sont concentrés sur les interactions requises lors de la transition de myoblastes qui prolifèrent au statut de myoblaste différencié prêt à fusionner à la fibre musculaire. Il a été montré que les myoblastes qui prolifèrent ont une voie Notch active et que cette voie est inhibée dans les fibres en cours de différenciation. De plus, il a également été montré que les facteurs de transcription Myocyte Enhancer Factor 2 (MEF2), Vestigial (VG) et Scalloped (SD) sont nécessaires pour le développement des IFM et que VG est requis pour la répression de la voie Notch dans les fibres. Cette étude porte sur les interactions entre la voie Notch et MEF2 et les mécanismes mis en jeu pour réprimer la voie au cours de la différenciation. Nous avons montré que MEF2 peut réprimer la voie Notch dans des contexgtes non-musculaires. En utilisant un crible récent pour identifier des cibles potentielles de MEF2, nous avons cherché ceux qui sont également des cibles de SD. Parmi les résultats, deux cibles ont présenté un intérêt particulier, Delta et neuralized, deux composants de la voie de signalisation Notch. Nos résultats montrent dans un contexte ex vivo que les séquences enhancers de DI et neur sont régulées par MEF2/SD et MEF2/NOTCH respectivement. In vivo ces enhancers sont actifs dans les fibres des IFM en cours de différenciation pour DI et au cours de la différentiation tardive pour neur. Au cours de ma thèse, j'ai pu étudier l'effet de MEF2 sur la régulation de ces cibles pour comprendre leur rôle au cours de la différentiation des IFM<br>Myogenesis of indirect flight muscles (IFM) in Drosophila melanogaster follows a well defined cellular developmental scheme. During embryogenesis, a subset of cells, the Adult Muscle Precursors (AMPs), are specified. These cells will become proliferating myoblasts during the larval stages which will then give rise to the adult IFM. Our work focused on the interactions required during the transition between proliferating myoblasts to differentiated myoblasts ready to fuse to the muscle fiber. It has been previously shown that proliferating myoblasts express the Notch pathway, and that this pathway is inhibited in developing muscle fibers. On the other hand, it has also been shown that the Myocyte Enhancing Factor 2 (MEF2), Vestigial (VG) and Scalloped (SD) transcription factors are necessary for IFM development and that VG is required for Notch pathway repression in differentiating fibers. Our study focuses on the interactions between Notch and MEF2 and mechanisms by which the Notch pathway is inhibited during differentiation. Here we show that MEF2 is capable of inhibiting the Notch pathway in non myogenic cells. A previous screen for MEF2 potential targets identified Delta and Neuralized, two components of the Notch pathway. Both are expressed in developing fibers where MEF2, SD and VG are expressed. Our preliminary results show that MEF2 is required for Delta expression in developing IFMs and that this regulation is potentially dependent on an enhancer to which MEF2 and SD bind. We have identified a similar neuralized enhancer that seems to be potentially regulated by MEF2 and NICD. During my thesis I studied the effect of MEF2 on these targets in vivo and in vitro to understand the rote they play during IFM differentiation
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Lavergne, Guillaume. "Caractérisation des précurseurs de muscles adultes et de leurs interactions au cours de l'embryogenèse chez Drosophila melanogaster." Thesis, Université Clermont Auvergne (2017-2020), 2018. http://www.theses.fr/2018CLFAC105.
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Les précurseurs de muscles adultes (ou AMPs) représentent une population transitoire de cellules souches musculaires chez la Drosophile. Ces cellules dérivent du mésoderme embryonnaire et sont caractérisées par l’activation de la voie Notch ainsi que par le maintien d’une forte expression du facteur de transcription Twist (de type basic helix loop helix). La répartition des AMPs chez la larve est établie au cours de l’embryogénèse de manière stéréotypée : on distingue 6 AMPs par hémisegment abdominal en position ventrale, latérale, dorso-latérale et dorsale. Après spécification et jusqu’au début du deuxième stade larvaire, les AMPs sont maintenues dans un état de quiescence, au cours duquel, les AMPs sont en contact étroit avec les fibres musculaires et les axones moteurs. L’objectif principal de mon projet de thèse a été de caractériser le rôle et le comportement de ces cellules AMPs au cours de l’embryogenèse. Dans un premier temps, j’ai pu montrer que les AMPs sont capables d’attirer les axones moteurs responsables de l’innervation des muscles. Cette attraction passe par l’établissement de contacts entre ces deux tissus via une forte dynamique filopodiale. De plus, une sous-population d’AMPs dans la région latérale est responsable de la formation d’une des branches nerveuses qui innervera le muscle de bordure de segment. La deuxième partie de ce projet s’est concentrée sur l’étude du comportement de ces cellules, ainsi que sur l’analyse du rôle des gènes exprimés dans les AMPs. J’ai ainsi pu mettre en évidence de nouvelles interactions entre les AMPs latérales et leur environnement musculaire. De plus, j’ai identifié de nouveaux marqueurs des AMPs tels que le récepteur Unc-5, la métalloprotéase MMP1 et la protéine de guidance Sidestep. L’une des contributions majeures de ce projet a été de pouvoir établir pour la première fois le rôle des cellules souches musculaires AMPs dans la mise en place du système nerveux moteur. L’ajout de ce nouvel acteur va permettre une meilleure compréhension des mécanismes de guidance des axones au cours de l’innervation musculaire<br>Adult muscle precursors (or AMPs) represent a transient muscle stem cell population in Drosophila. These cells arise from the embryonic mesoderm and are characterized by the activation of the Notch pathway as well as the maintenance of a high expression of the transcription factor Twist. The distribution of AMPs is established during embryogenesis in a stereotyped manner: we distinguish 6 AMPs per abdominal hemisegment in ventral, lateral, dorso-lateral and dorsal positions. After specification and until the beginning of the second larval instar, AMPs are maintained in a quiescent state where they stay in close contact with muscle fibers and motor axons. The main objective of my PhD project was the characterization of the role and the behavior of these AMP cells during embryogenesis. Firstly, I could demonstrate that AMPs are able to attract motor axons responsible for the innervation of embryonic muscles. This attraction goes through the establishment of contacts between these two tissues via a high filopodial dynamic. Moreover, a sub-population of AMPs in the lateral region in responsible of the formation of one of the nervous branches which will innervate the segmental border muscle. Secondly, this project focused on the behavior of these cells, as well as the analysis of the role of several genes expressed by AMPs. Thus, I could highlight new interactions between lateral AMPs and their muscle environment. Furthermore, I identified new markers of AMPs such as the receptor Unc-5, the metalloproteinase MMP1 and the guidance molecule Sidestep. One of the major contributions of this project was the establishment for the first time of the role of the muscle stem cells AMPs in the setup of the motor nervous system. The addition of this new actor will allow a better comprehension of the mechanisms behind the guidance of axons during muscle innervation
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Sevdali, Maria. "Drosophila indirect flight muscles as a model system for the study of human thin filament myopathies." Thesis, University of York, 2009. http://etheses.whiterose.ac.uk/21058/.
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Human thin filament myopathies are a group of skeletal muscle diseases caused by mutations in thin filament protein genes. Over 170 mutations within the human skeletal Cl-actin gene, ACTA1, cause congenital actin myopathies (CAM). These are dominant, often lethal mutations resulting in death at birth or shortly after. Several mutations have been identified in the genes encoding for Troponin I and Troponin T proteins, which cause arthrogryposis. The aim of this work was to see if the Drosophila Indirect Flight Muscles can be used as a genetic model system, with which to study the ACTA1 and arthrogryposis disorders and understand their aetiology. Six different mutations in the Drosophila Act88F gene, GI5R, I136M, DI54N, VI63L, VI63M and D292V, homologous to the human CAM actin mutations were transgenically expressed in Drosophila Indirect Flight Muscles (lFM) as wild type heterozygotes. All the mutants were dominant and with some myofibrillar defects similar to those seen in humans. Certain mutations resulted in intranuclear rods, similar to those found in humans and split Z-discs. The mutations varied in severity and matched that of the human mutations. An extra copy of wild type actin rescued the phenotype of all the heterozygote mutants, suggesting that upregulation of expression of the wild type actin gene might be a future prospect for therapy. Atypically, flies heterozygous for the R372H Act88F mutation complete normal IFM myogenesis and young flies can fly, but later become flightless and by day 7 show the Drosophila equivalent of the human nemaline phenotype. Electron microscopy revealed progressive loss of muscle structure. From the ultrastructure, the phenotypic requirement for muscle usage and the known α-actinin binding sites on the actin monomer, the R372H mutation is proposed to reduce the strength of F-actin/α-actinin binding, leading to muscle damage during use and breakdown of muscle structure. Binding studies confirmed a I3-fold reduction in u-actinin binding for R372H actin. The GAL4/UAS system was employed for the study of arthrogryposis mutations. The wild-type TnT and TnI IFM isoforms were transgenically expressed to rescue the TnT and TnI IFM nulls, respectively. Only the TnI null was rescued. The TnI arthrogryposis mutants were transgenically expressed and resulted in hypercontracted muscles.
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Franco-Cea, Omar Ari. "The role of microtubular motors and other cytoskeletal proteins in the development of Drosophila melanogaster indirect flight muscles." Thesis, University of York, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.444303.
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Wester, Jorge Victor Wilfredo Cachay. "Caracterização molecular do módulo regulador TT (Traqueia-Tórax) de >Drosophila melanogaster." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/17/17136/tde-06062017-163006/.
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Estudos funcionais anteriores identificaram um módulo cis-regulador (MCR) de 67 pb (-253/- 187) na região promotora do gene de pufe de DNA BhC4-1 que dirige a expressão do gene repórter na glândula anelar de Drosophila melanogaster. Uma análise bioinformática identificou 67 sequências de D. melanogaster que são similares a sequências contidas no MCR de glândula anelar. Uma das sequências identificadas reside em um fragmento genômico de 657 pb localizado aproximadamente 2500 pb à montante do CG13711, 400 pb à montante do CG12493, em uma região genômica que constitui um dos íntrons do CG32239 (Gef64C). A caracterização preliminar de três linhagens transformadas com a construção 657 pb-lacZ mostrou expressão do gene repórter no sistema traqueal de larvas e prépupas e no tórax de adultos. Baseado padrão de expressão promovido por este MCR, o mesmo foi denominado Traqueia-Tórax (TT). O principal objetivo do presente trabalho constituiu estender a caracterização molecular das linhagens da série TT-lacZ. Inicialmente embriões, larvas de primeiro, segundo e terceiro estádio, prépupas 0 h, 1 h e 2 h, pupas 24 h e adultos com 1, 3 e 5 dias foram investigados quanto ao padrão de expressão do repórter utilizando ensaio histoquímico que detecta atividade de ?-galactosidase. A expressão do gene repórter é inicialmente detectada no sistema traqueal durante o terceiro estádio larval e continua a ser detectada neste tecido em prépupas 0 h, 1 h e 2 h e pupas 24 h. Em adultos, a expressão do gene repórter é verificada nos músculos longitudinais dorsais em adultos de 3 e 5 dias. Uma vez que o MCR TT reside em uma região intergênica e a informação disponível sobre os CGs próximos ainda é escassa, não foi possível inferir qual dos CGs é regulado pelo MCR TT. Neste contexto, o padrão de expressão do RNAm do gene repórter lacZ e do CG13711, CG12493 e CG32239 foi investigado no sistema traqueal de larvas e prépupas e no tórax de adultos de uma das linhagens da série TT-lacZ utilizando RT-qPCR. Os níveis de expressão do RNAm lacZ aumentam cerca de 3 vezes em prépupas 0 horas, quando comparados com os níveis de expressão do RNAm lacZ presentes no sistema traqueal de larvas de terceiro estádio. Um padrão de expressão similar foi observado no caso do CG32239 e do CG13711. Nos tóraxes de adultos de 3 e 5 dias de idade os níveis de expressão do RNAm lacZ aumentam cerca de 37 vezes e 11 vezes, respectivamente, quando comparados aos níveis de expressão iv do RNAm lacZ presentes nos tóraxes de adultos de 1 dia. No tórax de adultos, o único CG que apresenta um padrão de expressão similar ao padrão de expressão de lacZ constitui o CG12493. Em conjunto, nós concluímos que o MCR TT promove um padrão dinâmico de expressão durante o desenvolvimento. Além disso, com base nos resultados de RT-qPCR, nós sugerimos que o MCR TT regula a expressão do RNAm do CG32239 no sistema traqueal durante a transição larva-prépupa e também a expressão do RNAm do CG12493 no tórax de adultos de 3 e 5 dias de idade. Além de estender a caracterização funcional de um novo MCR, nossos resultados também contribuem com novas informações acerca dos padrões de expressão no desenvolvimento de três CGs de D. melanogaster.<br>Previous functional studies identified in the DNA puff BhC4-1 promoter region a 67 bp (- 253/-187) cis-regulatory module (CRM) that drives reporter gene expression in the ring gland of D. melanogaster. A bioinformatics analysis identified 67 Drosophila melanogaster sequences that are similar to sequences contained in the ring gland CRM. One of the identified sequences resides in a 657 bp genomic fragment located about 2500 bp upstream CG13711, about 400 bp upstream CG12493, in a genomic region that constitutes one of the introns of CG32239 (Gef64C). The preliminary characterization of three transgenic lines transformed with a 657 bp-lacZ construct revealed reporter gene expression in the larval/prepupal tracheal system and in adult thorax. Based on the pattern of expression driven by this CRM we named it Trachea-Thorax (TT). The main goal of this work was to extend the molecular characterization of the lines of the TT-lacZ series. Initially ?-galactosidase histochemical assays were performed in embryos, first, second and third instar larvae, 0h, 1h and 2h prepupae, 24 h pupae and 1, 3 and 5 days old adults. Reporter gene expression is initially detected during the third larval instar in the tracheal system and continues to be detected in this tissue at 0 h, 1h and 2 h prepupa and, 24 h pupa. During the adult stage, reporter gene expression is verified in the dorsal longitudinal muscles of 3 and 5 days old adults. Since the TT CRM lies in an intergenic region and the available information about the nearby CGs is still scarce it was not possible to infer which of the CGs is regulated by the TT CRM. In this context, the mRNA pattern of expression of the lacZ reporter gene and of CG13711, CG12493 and CG32239 was investigated in the tracheal system of both larvae and prepupae and in adult thoraxes of one of the transgenic lines of the TT-lacZ series using RTqPCR. The lacZ mRNA expression levels increase about 3 times in 0 h prepupae when compared to the lacZ mRNA expression levels present in the tracheal system of third instar larvae. A similar pattern of expression was observed for both CG32239 and CG13711. In three and five days old adult thoraxes lacZ mRNA expression levels increase about 37 times and 11 times, respectively, when compared to lacZ mRNA expression levels present in one day old thoraxes. In the adult thorax, the only CG that presents a similar pattern of expression constitutes CG12493. Overall, we conclude that the TT CRM drives a dynamic pattern of ii expression throughout development. Additionally, based on RT-qPCR results, we suggest that the TT CRM regulates the expression of CG32239 mRNA in the tracheal system during the larvae to prepupae transition, as well as the expression of CG12493 mRNA in the thorax of 3 and 5 days old adults. Besides extending the functional characterization of a novel CRM our results also contribute new information about the developmental patterns of expression of three Drosophila melanogaster CGs.
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Chakravorty, Samya. "Role of the Drosophila Melanogaster Indirect Flight Muscles in Flight and Male Courtship Song: Studies on Flightin and Mydson Light Chain - 2." ScholarWorks @ UVM, 2013. http://scholarworks.uvm.edu/graddis/1.
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Complex behaviors using wings have facilitated the insect evolutionary success and diversification. The Drosophila indirect flight muscles (IFM) have evolved a highly ordered myofilament lattice structure and uses oscillatory contractions by pronounced stretch activation mechanism to drive the wings for high powered flight subject to natural selection. Moreover, the IFM is also utilized during small amplitude wing vibrations for species-specific male courtship song (sine and pulse), an important Drosophila mating behavior subject to sexual selection. Unlike flight, the contractile mechanism and contribution of any muscle gene in courtship song is not known. To gain insight into how separate selection regimes are manifested at the molecular level, we investigated the effect on flight and mating behaviors of mutations in two contractile proteins essential for IFM functions: an IFM-specific protein, flightin (FLN), known to be essential for structural and mechanical integrity of the IFM, and a ubiquitous muscle protein, myosin regulatory light chain (MLC2), known to enhance IFM stretch activation.
Comparison of FLN sequences across Drosophila spp., reveal a dual nature with the N-terminal region (63 aa) evolving faster (dN/dS=0.4) than the rest of the protein (dN/dS=0.08). A deletion of the N-terminal region (fln�N62) resulted in reduced IFM fiber stiffness, oscillatory work and power output leading to a decreased flight ability (flight score: 2.8±0.1 vs 4.2±0.4 for fln+ rescued control) despite a normal wing beat frequency. Interestingly, the FLN N-terminal deletion reduced myofilament lattice spacing and order suggesting that this region is required to improve IFM lattice for enhancing power output and flight performance. Moreover, fln�N62 males sing the pulse song abnormally with a longer interpulse interval (IPI, 56±2.5 vs 37±0.7 ms for fln+) and a reduced pulse duty cycle (PDC, 2.6±0.2 vs 7.3±0.2 % for fln+) resulting in a 92% reduction in their courtship success. This suggested that FLN N-terminal region fine-tunes sexually selected song parameters in D. melanogaster, possibly explaining its hypervariability under positive selection. That FLN N-terminal region is not essential but required to optimize IFM functions of both flight and song, indicate that FLN could be an evolutionary innovation for IFM-driven behaviors, possibly through its role in lattice improvement.
Mutations of the highly conserved MLC2 [N-terminal 46 aa deletion (Ext), disruption of myosin light chain kinase phosphorylations (Phos), and the two mutations put together (Dual)] are known to impair or abolish flight through severe reductions in acto-myosin contractile kinetics and magnitude of the stretch activation response. Unlike FLN, these MLC2 mutations do not show a pleitropic effect on flight and song. Flight abolished Phos and Dual mutants are capable of singing suggesting that these mutations affect song minimally compared to flight. Moreover, unlike FLN, none of these mutations affect interpulse interval, the most critical sexually selected song parameter in Drosophila. Also, in contrary to the known additive effects of Ext and Phos in the Dual mutant on flight wing beat frequency, a subtractive effect on sine song frequency is found in this study. That mutations in MLC2 are manifested differently for song and flight suggest that stretch activation plays a minimal or no role in song production.
The results in this study suggest that the conserved regions of FLN and MLC2 are essential to support underlying IFM contractile structure and function necessary for flight, whereas the fast evolving FLN N-terminal region optimizes IFM's biological performance in flight and species-specific song possibly under positive selection regime.
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Kasherov, Petar. "Etude de la régulation du gène vestigial au cours de la myogenèse adulte chez Drosophila melanogaster." Paris 7, 2010. http://www.theses.fr/2010PA077112.
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Chez la drosophile deux vagues de myogenèse ont lieu - la myogenèse larvaire et la myogenèse adulte. La première permet la formation de la musculature larvaire alors que la deuxième aboutit à la formation de l'ensemble des muscles adultes y compris les muscles du vol. Les muscles du vol se subdivisent en muscles directs du vol (Direct Flight Muscles - DFM) et muscles indirects du vol (Indirect Flight Muscles - IFM). Au cours de ma thèse je me suis focalisé sur la régulation d'un des facteurs myogéniques clé pour la formation des IFM - le gène vestigial (vg). Nous avons montré que sa régulation implique deux mécanismes distincts : un premier mécanisme dépendant de la voie Notch a lieu dans les myoblastes en prolifération et un deuxième mécanisme dans les fibres musculaires et certains myoblastes en différenciation indépendant de la voie Notch. Nous avons montré que ce deuxième mécanisme est mis en place grâce à une séquence régulatrice située dans l’intron 4 du gène vg que nous avons nommé vgAME (pour vg Adult Muscle Enhancer). L'activité de cette séquence est régulée par plusieurs facteurs myogéniques connus - positivement par Myocyte enhancer factor 2 (MEF2), Scalloped (SD) et VG et négativement par Twist (TWI) et N. L'étude de cette séquence nous a permis de mettre en évidence certaines interactions fonctionnelles (MEF2, SD et TWI) et physiques (MEF2-SD et MEF2-TWI) entre ces facteurs myogéniques. Par la suite nous avons continué à examiner la signification biologique de ces interactions et notamment celles entre VG, MEF2 et N. Nos résultats préliminaires montrent que l'activité de N peut être régulée négativement par MEF2<br>In Drosophila two waves of myogenesis occur - the larval myogenesis and the adult myogenesis. The first wave allows the formation of the larval muscles, while the second lead to the formation of all adult muscles including the flight muscles. The flight muscles are subdivided into Direct Flight Muscles (DFM) and Indirect Flight Muscles (IFM). During my thesis I have investigated the regulation of one of the key myogenic factors for IFM formation - the vestigial (vg) gene. We showed that its regulation involves two distinct mechanisms: one mechanism is dependent on the Notch pathway takes place in proliferating myoblasts and a second mechanism in muscle fibers and some differentiating myoblasts independent of the Notch pathway. We showed that this second mechanism requires a regulatory sequence located in intron 4 of vg gene that we named vgAME (for vg Adult Muscle Enhancer). The activity of this sequence is controlled by several known myogenic factors - positively by Myocyte enhancer factor 2 (MEF2), Scalloped (SD) and VG and negatively by Twist (TWI) and N. In vivo study of this sequence allowed us to highlight some functional (MEF2, SD and TWI) and physical (MEF2-SD and MEF2 -TWI) interactions between myogenic factors. Thereafter we continued to examine the biological significance of these interactions implicating VG, MEF2 and N. Our preliminary results show that the activity of N can be negatively regulated by MEF2
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Aradhya, Rajaguru. "Characterization of quiescent state and reactivation of adult muscle precursor cells in Drosophila melanogaster." Thesis, Clermont-Ferrand 1, 2013. http://www.theses.fr/2013CLF1MM16.
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Pas de résumé disponible<br>Use of stem cells in regenerative medicine has attracted great interest in the past decade. Muscle stem cells such as satellite cells were shown to regenerate skeletal muscle tissue after injury and to contribute to muscle growth. These properties have raised an enormous interest in using satellite cells for the therapy of skeletal muscle wasting disorders where the intrinsic stem cell population is unable to repair muscle tissue. However, better understanding of the mechanisms controlling satellite cell lineage progression and self-renewal is crucial to exploit the power of these cells in combating myopathic conditions. In the studies described here, the mechanisms regulating the in vivo behavior and maintenance of quiescence of Drosophila Adult Muscle Precursors (AMPs) that share several properties with the vertebrate satellite cells are analyzed. We show that undifferentiated embryonic AMPs display homing behavior and that their survival depends on the somatic muscles. We observe that AMPs establish direct contact with muscle fibers by sending thin filopodia and that this AMP-muscle interaction is crucial for AMPs spatial positioning. Larval muscles also play an important role in promoting the AMP cell proliferation. They achieve this by secreting Drosophila Insulin like peptide 6 (dIlp6) that activate the AMPs from their quiescent state and induce proliferation during the end of the second larval instar. We also demonstrate that Notch acts downstream of Insulin pathway and positively regulates proliferation of AMPs via dMyc. In the second part of the thesis manuscript we report that the affected formation ofadult muscles impacts on persisting abdominal larval templates. In this section role of the Notch signaling pathway in specification of the Adult founder cells is also demonstrated. Finally, we report generation of new tools for the cell type specific genome wide approaches that can be applied to identify global gene expression profiles in quiescent versus activated AMPs. Together these studies identified several new features of AMPs and enhance our understanding on the processes regulating stem cells homing, quiescence and reactivation
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Maity, Chaitali. "Determining the role of a candidate gene in Drososphila muscle development." Oxford, Ohio : Miami University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=miami1145459719.
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Hancock, Daniel H. "Role of Mef2 in Drosophila muscle development." Thesis, Cardiff University, 2009. http://orca.cf.ac.uk/55033/.
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Muscle differentiation is a complex process involving the transition from undifferentiated mesoderm to a final functional musculature. Mef2 is an essential positive regulator central to the co-ordination of this process. It targets a plethora of key genes both early and late in the differentiation program and its activity must be tightly controlled (Pothoff and Olson, 2007). The aim of my research was to investigate the role of Mef2 in orchestrating Drosophila muscle differentiation. I did this by analysing the formation of the larval somatic musculature under conditions that either increased or decreased Mef2 activity using gain and loss-of -function of either Mef2 itself, Him, a repressor of Mef2 activity (Liotta et al, 2007) or of Zfhl, a potential regulator of Mef2 expression (Postigo et al, 1999). Part of this investigation involved the generation and characterisation of Mef2 dominant negative proteins and isolation of a Him mutant. Detailed analysis revealed a distinct subset of somatic muscles that are missing when Mef2 activity is reduced and another subset of muscles that are duplicated when Mef2 activity is increased. This suggests a role for Mef2 in patterning of the musculature that has not been established previously. In addition, I identified a role for Mef2 in the regulation of Him expression, revealing a mechanism whereby Mef2 could be involved in its own repression. I also investigated the role of mesol8E in muscle differentiation a previously uncharacterised novel gene identified as an early target of Mef2 (Taylor, 2000). I found this to be a Myb-like domain containing protein that is a direct target of Mef2. Over-expression caused a severe disruption to the somatic musculature, revealing a potential role for mesol8E in muscle guidance. Generation of mesol8E mutant alleles by FRT element mediated recombination showed the gene to be essential for development.
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Liotta, David. "Dmeso17A : a novel inhibitor of Drosophila muscle differentiation." Thesis, Cardiff University, 2005. http://orca.cf.ac.uk/56020/.
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Muscle differentiation is a complex process finely tuned by the interplay of positive and negative factors. Although key positive regulators have been identified, there is rather little evidence of restraining molecules that can control the time and place of muscle differentiation. Identification of such molecules and analysis of their function during muscle differentiation is therefore necessary to gain new insight into the molecular events that regulate this process. My work centred on a gene, Dmeso17A that was identified in the Taylor laboratory in a screen to isolate novel genes specifically expressed in muscle progenitors in Drosophila (Taylor, 2000). Its pattern of expression suggested it could be an inhibitor of muscle development. My aim was to analyse both the role and mechanism of action of Dmeso17A. Dmeso17A expression rapidly declines as muscle differentiation starts, but persists in the adult muscle precursors that remain undifferentiated at this stage. Using the GAL4/UAS system (Brand and Perrimon, 1993) to both mis-express and over-express either full-length or modified proteins, I show that Dmeso17A is a novel co-repressor that inhibits muscle progenitor differentiation. Dmef2, the key promoter of muscle differentiation, can suppress Dmeso17A inhibitory effect on muscle development. This was quantitated by a hatching and survival assay. Moreover, I show that Dmeso17A can down-regulate DMef2 activity. Dmeso17A protein contains a WRPW motif. I show that this motif is functionally important and is required for the interaction of Dmesol7A with the co-repressor Groucho. Finally, I show that Dmeso17A genetically interacts with Histone Deacetylases (HDACs), which are known to bind and down-regulate Mef2 in vertebrates. My model is that Dmeso17A down-regulates DMef2 activity through interactions with Groucho and HDACs, and therefore is a component of an inhibitory complex that holds muscle precursors in an undifferentiated state until cues trigger their differentiation.
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Schönbauer, Cornelia. "Genetic analysis of Drosophila adult muscle type specification." Diss., Ludwig-Maximilians-Universität München, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-170130.
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Muscles of all higher animals comprise different muscle types adapted to perform distinct functions in the body. These express different sets of genes controlled by distinct combinations of transcriptional programs and extracellular signals, and thus differ in their myofibrillar organization and contractile properties. Despite major progress in our understanding of myogenesis, the genetic pathways controlling the formation and function of different muscle types are still largely uncharacterized.
Flying insects possess specialized flight muscles enabling wing oscillations with frequencies of up to 1000 Hz together with high power outputs of 80 W per kg muscle. To achieve these parameters, flight muscles contain stretch-activated myofibrils with a unique fibrillar organization, whereas all other, more slowly contracting muscles, such as leg muscles, display a tubular morphology.
To delineate the genetic regulation of muscle development and function, and, in particular, muscle type specification, we performed a genome-wide RNA interference (RNAi) screen in Drosophila, in which we systematically inactivate genes exclusively in muscle tissue. We uncovered more than 2000 genes with putative roles in muscles, many of which we were able to assign to specific functions in muscle, myofibril or sarcomere organization by phenotypic characterization. Muscle-specific knockdown of 315 genes resulted in viable, but completely flightless animals, indicating a specific function of those genes in fibrillar flight muscles.
Detailed morphological analysis of these 315 genes revealed a striking phenotype upon knockdown of the zinc finger transcription factor spalt major (salm): the fibrillar flight muscles are switched to tubular muscles, whereas tubular leg muscles are wild type, demonstrating that salm is a key determinant of fibrillar muscle fate. We could show that the transcription factor vestigial (vg) acts upstream of salm to induce its expression specifically in fibrillar flight muscles. Importantly, salm is not only required but also sufficient to induce the fibrillar muscle fate upon ectopic expression in other muscle types. Microarray analysis, comparing mRNA expression from adult wild-type flight and leg muscles to salm knockdown flight muscles, indicates that salm instructs most features of fibrillar muscles by regulating both gene expression as well as alternative splicing. Remarkably, we could show that spalt’s function in programming stretch-activated fibrillar muscles is conserved in insect species separated by 280 million years of evolution. Interestingly, in mouse two of the four spalt-like (sall) genes are expressed in heart, a stretch-activated muscle, sharing some features with insect fibrillar flight muscles. Since heart abnormalities observed in patients suffering from the Towns-Brocks syndrome are caused by a mutation in SALL1, it is possible that Spalt’s function to determine a fibrillar, stretch-modulated muscle type is conserved to vertebrates.
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Weitkunat, Manuela. "Mechanistic dissection of adult muscle formation in Drosophila." Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-178864.
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Vishal, Kumar. "EGF signaling regulates adult muscle patterning in Drosophila." Miami University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=miami1416505009.
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Frei, Ryan. "Regulatory Elements of Drosophila Non-Muscle Myosin II." Thesis, University of Oregon, 2013. http://hdl.handle.net/1794/12954.
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Non-muscle myosin II (NM-II) is present in every cell type and moves actin filaments to provide contraction within the cell. NM-II has a motor domain, a neck domain that binds two light chains, a long coiled-coil tail domain, and a carboxyl-terminal tailpiece. NM-II forms bipolar filaments by associating near the carboxyl-terminus of the tail. It has long been known that both the formation of bipolar filaments and enzymatic activity of the motor domain are regulated by phosphorylation of one of the neck-binding light chains, known as the regulatory light chain (RLC). This phosphorylation causes a large-scale conformational shift of both the motor domains and the tail domain. However, the mechanism of this regulation and the elements that mediate the autoinhibition remain unknown.
We have taken a deletional approach to finding the elements necessary for autoinhibition and regulation of filament assembly. We have used salt- dependent pelleting assays, cell culture, and analytical ultracentrifugation to identify two small regions in the IQ motifs of the neck and the carboxyl-terminal tailpiece that are essential for autoinhibition.
Another necessary element for autoinhibition is the fold the coiled coil of the tail back on itself by means of hinge domains. We used internal deletions, pelleting assays, and thermal stability assays to identify and characterize the flexible hinge domains within the coiled-coil tail of NM-II. These hinges consist of low-stability regions of coiled coil, and can be stiffened by introducing mutations that cause the sequence to mimic a more ideal coiled coil. By defining these essential elements of autoinhibition, this work paves the way for a mechanistic understanding of the complex regulation of NM-II in the cell.
This dissertation contains unpublished co-authored material.<br>2015-07-11
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Sudarsan, Vikram. "Coordinating cell fate signalling during Drosophila development." Thesis, University of Sheffield, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.247190.
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Boukhatmi, Hadi. "Mise en place de l'identité des muscles au cours de la spécification des myoblastes chez la drosophile." Toulouse 3, 2012. http://thesesups.ups-tlse.fr/1777/.
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La formation des muscles squelettiques au cours de l'embryogenèse de la drosophile est un modèle d'étude du contrôle génétique de la différentiation cellulaire. La formation de chaque muscle comprend quatre étapes successives: spécification d'un groupe promusculaire, sélection d'un progéniteur (PC) à partir de ce groupe, division asymétrique de ce progéniteur pour donner des cellules fondatrices de muscles (FC) ; fusion de chaque FC avec des myoblastes compétents (FCM), suivie de la différenciation musculaire. Chaque muscle squelettique est composé d'une fibre. Chaque muscle présente des propriétés spécifiques de taille, forme, position, attachement, et patron d'innervation. Ces propriétés sont groupées sous le terme d'identité musculaire. Cette identité est conférée par l'expression dans chaque PC/FC d'une combinatoire de Facteurs de Transcription identitaires (FTi). Notre laboratoire étudie ce processus, en utilisant comme point d'entrée l'expression et les rôles du FTi Collier (Col) au cours du développement d'un muscle dorso-latéral, le muscle DA3 (Dorsal Acute 3). Au cours de la première partie de ma thèse, j'ai étudié la régulation transcriptionnelle de col durant les phases de spécification des groupes promusculaires et de sélection du PC à l'origine du muscle DA3. Partant de prédictions bioinformatiques j'ai caractérisé le module cis régulateur (CRM) de col actif durant ces phases (CRM précoce). Un CRM " tardif ", actif du stade progéniteur à la complétion de la formation du muscle DA3, avait été préalablement caractérisé dans l'équipe. Afin de déterminer plus précisément les fenêtres temporelles d'activité des deux CRM mésodermiques de col, j'ai mis au point un nouveau gène rapporteur comportant un intron permettant de détecter les transcrits primaires. Ceci m'a permis de montrer que les CRM précoce et tardif reproduisent ensemble l'expression endogène de col. La caractérisation du CRM précoce de col m'a aussi permis de suivre le destin des FCM du groupe promusculaire Col dans les embryons tardifs et de montrer que ces FCM contribuent uniquement à des muscles dorsaux-latéraux. Au cours de la deuxième partie de ma thèse, j'ai caractérisé le rôle, inconnu jusqu'alors, du FT à domaine LIM-Homeodomaine Tailup (Tup)/Islet1 dans la myogenèse. J'ai d'abord montré que Tup est spécifiquement exprimé dans les 4 muscles les plus dorsaux. L'analyse de mutants m'a permis de montrer qu'en absence de Tup, le muscle dorsal DA2 exprime Col et est transformé en muscle dorso-latéral de type DA3. J'ai ensuite montré que le PC du DA2 est à l'origine de la FC DA2 et d'un précurseur musculaire adulte (AMP). Ce PC est sélectionné à partir du groupe promusculaire Col quand les cellules de ce groupe expriment encore le FT à homéodomaine Tinman/NKx2. 5. Tin active tup dans le PC DA2. Tup, en retour, réprime col et cette répression permet de distinguer les identités musculaires DA2 et DA3. En conclusion, mes travaux de thèse m'ont permis de proposer un nouveau modèle permettant de relier le processus de spécification des progéniteurs au contrôle temporel et spatial de l'expression des FTi. Une vision dynamique de ce processus de spécification permet de mieux comprendre le programme identitaire propre à chaque muscle. L'analyse des interactions entre Tin, Tup, et Col au cours de la formation des muscles dorsaux révèle de nouveaux parallèles avec les interactions entre Nkx2. 5, Islet, EBF au cours de la formation des muscles pharyngaux chez les chordés<br>The somatic musculature of the Drosophila embryo is a classical model to study the regulatory processes that generate cellular diversity. Muscle formation is a multistep process: the first step is the specification, within the mesoderm, of a group of competent cells, called promuscular cluster. The second step is the selection of a progenitor cell (PC) from this cluster. Asymmetric division of each PC then generates muscle founder cells (FC). Finally, each FC undergoes a fusion process with fusion competent myoblasts (FCM) to generate a muscle fiber. Each muscle is formed of a single multinucleate fiber. Each Drosophila muscle has a specific identity, as it can be distinguished by its position, shape, orientation, attachment, and innervation pattern. Muscle identity reflects the expression by each PC/FC of a specific combination of identity Transcription Factors (iTF). In the laboratory, we study the control of muscle identity, using as entry point, the expression and requirement of the iTF Collier (Col) during development of a dorso-lateral (DA3) muscle. I started my PhD by characterizing col transcriptional regulation during early steps of DA3 muscle formation. Starting from computational predictions, I identified an early col cis regulatory module (Early CRM) responsible for col activation in a promuscular cluster. A late col CRM, active from the PC stage, had previously been characterized in the laboratory. To determine with more precision the temporal windows of activity of each of these CRM, I designed a novel intron-containing reporter gene in order to detect primary transcripts. This allowed me to show that the late and the early CRMs together reproduce precisely the endogenous col expression pattern. Characterization of the early mesodermal col CRM also allowed to do lineage experiments and determine the fate of FCMs that transiently express Col at the promuscular stage. I found that these myoblasts contribute mostly to dorso-lateral muscles. During the second part of my thesis, I described a new role of the LIM-homeodomain TF Tailup/Islet1 (Tup) in specifying dorsal muscles. I first showed that Tup is specifically expressed in the four dorsal muscles. In tup null mutants, on one hand, the dorsal musculature is severely disorganized and, on the other hand, the dorsal DA2 muscle ectopically expresses Col and is transformed into a dorso-lateral DA3-like muscle. I showed that the DA2 PC is singled out from the Col promuscular cluster when cells of this cluster still express (transitorily) the homeodomain TF Tinman/Nkx2. 5 (Tin). The DA2 PC gives rise to the DA2 FC and a (dorso-lateral) adult muscle precursor (AMP). Tup activation by Tin in the DA2 PC is required to repress col and establish a DA2 instead of DA3 identity. In conclusion, my work allowed to propose a model which connects a temporal sequence of transcriptional regulation of iTFs to the specification of muscle PC identity and final muscle pattern. It provides a novel, dynamic view of how muscle identity is specified. These findings also provide novel parallels with the specification of pharyngeal muscles in vertebrates
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Taffin, de Tilques Mathilde de. "Contrôle transcriptionnel de l'identité musculaire chez la drosophile : modules cis-régulateurs et gènes cibles directs de Collier." Toulouse 3, 2013. http://thesesups.ups-tlse.fr/2232/.
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Les facteurs de transcription (FT) COE (Col-EBF) sont conservés chez les métazoaires et participent au contrôle de divers processus biologiques : hématopoïèse, neurogenèse, myogenèse. Leur dérégulation entraîne de graves dysfonctionnements chez les mammifères (défauts de spécification des lymphocytes B, de sous-types neuronaux. . . ). Cependant les gènes cibles régulés par les FT COE restent majoritairement inconnus. Notre équipe utilise la drosophile comme système modèle pour étudier la spécificité d'action des FT COE selon le contexte cellulaire. Mon travail de thèse est centré sur l'identification de gènes cibles directement régulés par Collier (Col) et la caractérisation des modules cis-régulateurs associés. J'ai identifié un ensemble de gènes cibles de Col par des expériences d'immuno-précipitation de la chromatine (ChIP-SEQ). Cette analyse m'a permis d'identifier le motif ADN sélectivement reconnu par Col in vivo, et de montrer que cette reconnaissance est contextuelle. Plusieurs gènes cibles ont été validés par des expériences d'hybridation in situ et d'analyse fonctionnelle de leurs CRM, parmi lesquels une majorité d'autres FTs. L'ensemble des résultats révèle une complexité inattendue des réseaux de régulation transcriptionnelle contrôlant l'identité musculaire chez la drosophile et confirme que Col est un acteur majeur de différents réseaux dans différents tissus embryonnaires. Au vu de la conservation des FTs COE au cours de l'évolution, les conclusions de cette étude modèle chez la drosophile apportent un éclairage nouveau sur les études en cours sur des modèles mammifères<br>The COE (Collier/Early B cell Factor) family is a metazoan-specific family of transcription factors (TF) that are involved in the control of numerous biological processes, including hematopoiesis, neurogenesis and muscle identity. Mutant analysis of COE TFs across several organisms showed defects in the specification of different cell types, like neuron subtypes or, in mammalians, B lymphocytes and brown adipocytes. However, the COE target genes are mostly unknown. Drosophila (fruit fly) is an excellent model to study the functional diversity of COE TFs. The core of my PhD work was the identification of Collier direct target genes in the DA3 muscle lineage, and the characterization of the corresponding CRM to better understand how COE proteins activate specific target genes in a tissue-dependent manner. I performed chromatin immuno-precipitation on whole embryos followed by systematic sequencing of the immuno-precipitated fragments (ChIPseq). By bio-informatics, I identified Col in vivo binding motif and showed that Col binding in vivo is context-dependent. Several candidate genes were validated by in situ hybridizations and functional analysis of the Col binding CRM. TF are over-represented among these targets. All together, the results reveal an unexpected complexity of gene regulatory networks that control muscle identity in Drosophila and confirm the critical role for Col in several transcription regulatory networks in the embryo. Considering the evolutionary conservation of COE proteins and their in vivo DNA binding properties, these results bring new insight into the complexity of COE function in other organisms, including mammals
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Render, Timothy John. "A study of muscle pattern formation in Drosophila melanogaster." Thesis, University of Cambridge, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240123.
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Harrison, Andrew. "Suppression of indirect flight muscle mutants in Drosophila melanogaster." Thesis, University of York, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297111.
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Collins, Mary Ann. "Mechanisms of nuclear movement during muscle development in Drosophila:." Thesis, Boston College, 2020. http://hdl.handle.net/2345/bc-ir:108690.
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Thesis advisor: Eric S. Folker<br>Skeletal muscle is a syncytial cell type in which the multiple nuclei are evenly spaced along the cell periphery. During muscle development, the myonuclei undergo an elaborate set of movements to achieve this precise positioning throughout the muscle. The importance of proper nuclear positioning is highlighted by the correlation between mispositioned nuclei and muscle disease. However, the mechanisms that govern this energetically expensive process as well as the influence nuclear positioning has on muscle cell function remains to be elucidated. The goal of this thesis is to determine the molecular factors and subsequent mechanisms that regulate nuclear movement and how such pathways are disrupted in various muscle diseases. Since many of the key cellular features are conserved between Drosophila and mammalian muscles, we utilize Drosophila musculature as a model system to study myonuclear positioning during muscle development. In this thesis, we provide the first evidence that nuclei experience attractive and repulsive interactions with one another as they actively migrate. Furthermore, we demonstrate that these nucleus-nucleus interactions are critical for proper nuclear positioning, and that they are distinctly regulated by genes that are associated with two different muscle diseases, Emery-Dreifuss muscular dystrophy and Centronuclear myopathy (Chapter 2). We then elaborate upon the genetic mechanisms through which CNM-linked genes regulate nuclear positioning (Chapter 3). Finally, we show that proper nuclear movement requires both the separation of nuclei from their neighbors as well as the transmission of force, that is generated from the cytoskeleton, to move nuclei within the cell (Chapter 4). Together, the work presented in this thesis provides new perspective and mechanistic insights into the genetic factors and physical forces that regulate nuclear movement during muscle development and how such pathways are disrupted in disease, while emphasizing the importance of studying such dynamic processes within an in vivo system<br>Thesis (PhD) — Boston College, 2020<br>Submitted to: Boston College. Graduate School of Arts and Sciences<br>Discipline: Biology
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Picchio, Lucie. "Mise en place, caractérisation phénotypique et transcriptomique d'un modèle de Drosophilie de la Dystrophie Myotonique de type 1." Thesis, Clermont-Ferrand 1, 2013. http://www.theses.fr/2013CLF1MM15/document.
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La dystrophie myotonique de type 1 (DM1) ou maladie de Steinert est la maladie génétique neuromusculaire la plus commune avec une incidence de 1/8000 à travers le monde. Cette maladie multisystémique touche particulièrement les muscles squelettiques (myotonie, faiblesse et perte musculaires) et le coeur qui présente des symptômes variés comme des troubles de la conduction et des arythmies. La DM1 est causée par une expansion instable de répétitions CTG dans la région 3’ non traduite du gène DMPK. Les individus sains possèdent entre 5 et 37 répétitions CTG tandis que les patients DM1 portent entre 50 et plusieurs milliers de répétitions. Il est bien établi que les expansions de répétitions non codantes forment des foci dans les noyaux musculaires où elles séquestrent le facteur d'épissage MBNL1. Toutefois, l'implication de la stabilisation et l'accumulation de CUGBP1 hyperphosphorylé par la PKC dans la maladie est un sujet controversé dans la communauté DM1. Dernièrement, en plus de la rupture de l'équilibre entre MBNL1/CUGBP1, plusieurs mécanismes ont été mis en cause dans la pathogenèse de la DM1. Parmi eux, l'expression perturbée de facteurs de transcription, la maturation altérée de miARNs, l'activation de kinases... chacune de ces altérations menant au final à une perturbation du transcriptome. Afin d'étudier l'effet de la toxicité des répétitions sur les phénotypes et lestranscriptomes, nous avons généré trois lignées de Drosophile inductibles et site-spécifiques exprimant 240, 600 et 960 répétitions de triplets. Nous avons travaillé en parallèle sur une lignée atténuée pour mbl (orthologue de MBNL1) et deux lignées gain de fonction bru -3 (orthologue de CUGBP1). Exprimées dans les muscles somatiques, les répétitions CTG conduisent à une mobilité réduite, le fractionnement des fibres musculaires, une réduction de leur taille et une altération du processus de fusion des myoblastes de manière dépendante de Mbl et Bru-3. En outre, l'expression des répétitions cause une hypercontraction musculaire dépendante de Mbl et due à un mauvais épissage de dSERCA. L'analyse transcriptionnelle comparative réalisée sur les muscles larvaires des différentes conditions pathologiques montre que l'atténuation de mbl reproduit 70-82% des dérégulations transcriptomiques des larves DM1 alors que le gain de fonction bru-3 représente 32-53% des altérations transcriptomiques des lignées DM1. Ainsi Mbl est un facteur clé des dérégulations observées dans les muscles somatiques des lignées DM1. Au contraire, les analyses physiologiques effectuées sur les coeurs adultes suggèrent que Bru-3 est un facteur clé dans la mise en place des phénotypes cardiaques. En effet, d'une part, l'atténuation de mbl dans le coeur cause une cardiomyopathie dilatée, un symptôme rarement diagnostiqué chez les patients. D'autre part, les lignées gain de fonction bru-3 et DM1 présentent de la fibrillation qui évolue avec l'âge ou la taille des répétitions vers un phénotype qui rappelle l'insuffisance cardiaque chez les patients<br>Myotonic Dystrophy Type 1 (DM1) or Steinert's disease is the most common genetic neuromuscular disorder affecting 1 out of 8000 people worldwide. This multisystemic disease affects particularly the skeletal muscles (myotonia, muscle weakness and wasting) and the heart, which can exhibit various symptoms like conduction disturbances and arrhythmia (auricular fibrillation and flutter). DM1 is caused by an unstable CTG repeat expansion in the 3' non-translated region of the DMPK gene. In healthy individuals, the number of CTG repeats ranges from 5 to 37 whereas DM1 patients carry from 50 to thousands repeats. It is well established that when expanded non-coding repeats aggregate into foci within muscle nuclei and sequester the MBNL1 splicing factor. However, the involvement of the stabilization and accumulation of CUGBP1 following PKC hyper-phosphorylation in the disease is a controversial matter in the DM1 community. Lately, in addition to the disruption of the balance between MBNL1/CUGBP1, several mechanisms were identified as part of the DM1 pathogenesis. Among them, transcription factors perturbations, altered maturation of miRNA, kinases activation… each of them leading eventually to transcriptomic alterations. In order to investigate the effect of toxic repeat expression on phenotypic and transcriptomic alterations, we generated three inducible site-specific Drosophila lines expressing 240, 600 and 960 triplet repeats. We worked in parallel on a mbl (MBNL1 orthologue) knocked-down line and two bru-3 (CUGBP1 orthologue) gain of function lines. When expressed in somatic muscles, CTG repeats lead to altered motility, fiber splitting, reduced fiber size and affected myoblast fusion process in a Mbl and Bru-3 dependent manner. In addition, toxic repeats cause fiber hyper-contraction in a Mbldependentmanner due to dSERCA mis-splicing. Comparative transcriptional profiling performed on larval muscles of different conditions show that mbl attenuation reproduces 70-82% of DM1 transcriptomic deregulations whereas bru-3 gain of function represents 32-53% of transcritomic alterations. Thus Mbl appears as a key factor of transcripts deregulations observed in DM1 muscles. On the contrary, physiologic analyses performed on adult hearts suggest that Bru-3 is a key factor for cardiac phenotypes. Indeed, on one hand, mbl attenuated flies display dilated cardiomyopathy, a symptom barely diagnosed in patients. On the other hand, bru-3 gain of function line and DM1 lines display fibrillation, which evolves withage or repeat size into a phenotype reminiscent of heart insufficiency in patients
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Clayton, Jonathan David. "Suppression of a mutation in the Act88F gene of Drosophila melanogaster." Thesis, University of York, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387180.
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Green, Hannah Jane. "Diverse functions for intern associated proteins in Drosophila adult muscle." Thesis, University of Cambridge, 2017. https://www.repository.cam.ac.uk/handle/1810/264024.
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The ability to adhere to the extracellular matrix (ECM) is critical for numerous cell types and tissues including epithelia and muscle. Cell-ECM adhesion is primarily mediated by integrins which provide a direct link between the ECM and the actin cytoskeleton. Integrin adhesions are frequently associated with a core of 60 different proteins (integrin-associated proteins, IAPs). Integrins are required for muscle attachment and in Drosophila, loss of integrins and several IAPs results in embryonic lethality and muscle detachment. However, the IAPs FAK, RSU1, tensin, vinculin and zyxin are not required for viability or embryonic muscle attachment. Furthermore, FAK, RSU1, tensin and vinculin have been observed to localise to muscle attachment sites in Drosophila, indicating that they have some function in muscle attachment. Unlike FAK, RSU1, tensin and vinculin, it was not previously known whether zyxin is expressed in Drosophila muscles. To test this, I generated a genomic zyxin-GFP construct that should contain most of the endogenous zyxin promotor. The genomic zyxin-GFP construct was not observed at muscle attachment sites, suggesting that it is not normally expressed in muscle. I wished to know whether FAK, RSU1, tensin and vinculin are required for muscle function. Various behavioural assays were employed to test for muscle function in larvae and adult flies. The results suggest that larval muscle function was normal in flies lacking these IAPs, but that adult muscle function might be impaired, although it proved difficult to demonstrate a clear functional defect. I then tested whether the IAPs FAK, RSU1, tensin and vinculin are required for normal morphology of adult muscles, focusing on the adult indirect flight muscles (IFMs). The IFMs are fibrillar muscles which attach to the cuticle via specialised epithelial cells known as tendon cells. At the end of the myofibril, where the myofibril attaches to the tendon cell, is a dense region of actin and IAPs known as the modified terminal Z-band (MTZ). I have found that the MTZ is not a homogenous zone of proteins, but is instead organised into at least three distinct layers. Because of the similarity between the structure of the MTZ with that of a hand, I refer to the layers as ‘fingers’, ‘palm’ and ‘wrist’. I discovered that the IAPs FAK, RSU1, tensin and vinculin are each required for the proper structure of the MTZ in unique ways. The fingers were elongated in IFMs lacking FAK, RSU1, tensin or vinculin, while the palm was disrupted in IFMs lacking RSU1, tensin or vinculin. Finally, I was intrigued by the enrichment of the actin-binding protein filamin/Cheerio in the palm and wished to know if it is required for palm function. Deletion of the C-terminus of filamin/Cheerio resulted in a reduction in palm length. Filamin/Cheerio is a mechanosensitive protein which exists in a closed and open conformation. I found that filamin/Cheerio must be open in order to help form a normal palm. Furthermore, vinculin is required to convert filamin/Cheerio from and closed to an open filamin/Cheerio state so that it can perform its function in the palm.
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Belu, Mirela. "Comparative Analysis of Muscle and Locomotion Patterns in Drosophila Species." Case Western Reserve University School of Graduate Studies / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=case1301331017.
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Miller, Becky M. "Functional analysis of Drosophila melanogaster muscle myosin heavy chain alternative domains /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2004. http://wwwlib.umi.com/cr/ucsd/fullcit?p3138951.
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Chang, Whei-meih. "Identification of transcriptional regulatory elements in muscle promoter of Ca⁺⁺-activated potassium channel, slowpoke, in Drosophila /." Digital version accessible at:, 1998. http://wwwlib.umi.com/cr/utexas/main.
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Ricketson, Derek Lee. "Drosophila non-muscle myosin II bipolar filament formation : importance of charged residues and specific domains for self-assembly /." Connect to title online (Scholars' Bank) Connect to title online (ProQuest), 2009. http://hdl.handle.net/1794/10285.
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Gunthorpe, D. "Muscle differentiation in Drosophila : analysis of the roles of DMEF2 and Dmeso47C." Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.599783.
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In this dissertation, two approaches are taken to gain a greater understanding of muscle differentiation in <I>Drosophila.</I> The first is to analyse the role of a gene, <I>Dmef2</I>, which is already known, from work in both vertebrates and <I>Drosophila,</I> to be essential for this process. Two specific aspects of the role of <I>Dmef2</I> in muscle differentiation are analysed: the function of different levels of the protein and the role of the different isoforms. It is shown that different properties within a cell require distinct threshold levels of DMEF2, as do different cells within a muscle-type and different muscle-types. Furthermore, there is a DMEF2 activity range that is compatible with the proper differentiation of different muscle-types. In addition, each DMEF2 isoform is found to function similarly, both when ectopically expressed in the ectoderm and, strikingly, in the rescue of each aspect of the <I>Dmef2</I> mutant phenotype assayed. The second approach taken is to characterise and analyse the function of a novel gene, <I>Dmeso47C</I>, whose expression pattern in the somatic and visceral musculature is suggestive of a role in the differentiation of these muscle types. The full length coding sequence of <I>Dmeso47C</I> is obtained and shown to encode a putative nuclear protein. Both loss-of-function and gain-of-function experiments indicate that <I>Dmeso47C</I> does indeed play a role in muscle differentiation. Further, analysis of its expression pattern in different genetic backgrounds allows <I>Dmeso47C</I> to be placed in the genetic framework of visceral and somatic muscle differentiation.
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Wong, Ming-Ching. "Regulation of twist activity during mesoderm and somatic muscle development in drosophila /." Access full-text from WCMC, 2008. http://proquest.umi.com/pqdweb?did=1642921011&sid=7&Fmt=2&clientId=8424&RQT=309&VName=PQD.
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Laurichesse, Quentin. "Caractérisation génétique des précurseurs de tendons appendiculaires au cours des étapes précoces de la métamorphose chez Drosophila melanogaster : rôle du Krüppel-like factor Dar1 dans le développement des précurseurs de tendons appendiculaires." Thesis, Université Clermont Auvergne (2017-2020), 2019. http://www.theses.fr/2019CLFAC072.
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La mise en place de l’architecture musculo-squelettique émerge d’un développement coordonné inter-tissulaire entre muscles et tissus conjonctifs, dont l’agencement requiert une communication permanente lors des stades embryonnaires. En dépit de l’absence de squelette interne, la patte de la drosophile possède à l’instar des vertébrés des longs tendons internes, auxquels sont rattachés les muscles. Ces sites d’attachements partagent avec mammifères, à la fois l’aspect fonctionnel des tendons à savoir rattacher les muscles et permettre la locomotion, mais également des aspects moléculaires, avec l’identification d’orthologues requis pour leur développement et homéostasie. Chez la drosophile, les tendons appendiculaires sont les seuls sites d’attachement à proposer une telle architecture. Sur la base de ces observations et connaissances, nous avons pris le parti d’étudier plus précisément quels pouvaient être les gènes responsables du développement de ces tendons. Mes travaux de thèse ont consisté à la mise en place d’une méthode cellule-spécifique adaptée à des populations rares que sont les précurseurs de tendons appendiculaires, dans le but d’étudier leur transcriptome. Les données de RNA-seq obtenues ont permis de mettre en exergue environ 900 gènes, dont 68 facteurs de transcription enrichis au sein des précurseurs de tendons. Suite à crible ARN interférent, j’ai identifié le gène dar1 qui est spécifiquement exprimé au sein des tendons de la patte au moment de la métamorphose. La perte de ce gène entraîne une perte des longs tendons appendiculaires et induit une désorganisation drastique de l’architecture musculaire. De manière intéressante, Dar1 est un représentant de la famille des Krüppel-like factor, dont les orthologues KLF4 et 5 sont retrouvés au sein de données transcriptomiques de certains tendons chez les vertébrés, sans que leurs rôles n’aient encore pu être élucidés. A travers cette étude, Dar1 est aujourd’hui proposé comme marqueur spécifique des tendons appendiculaires, et tend à mettre en lumière des relations potentiellement intéressantes entre les tendons de drosophile et les multiples tissus conjonctifs des vertébrés<br>Musculoskeletal development is a coordinated process that requires the integration of multiple cues and the interaction between muscles and connective tissues (CT). Despite the lack of internal skeleton, the drosophila leg, like the vertebrate limb, shows long internal tendons, which are connected with muscle fibres. These muscle attachment sites share similar function with their mammalian counterpart; they transmit the strength generated by the muscles to allow locomotion. They also share well-known molecular orthologs that are required for their development and homeostasis. Thus, the study of this long internal tendons within the drosophila leg is of great interest to understand the development of this sort of structure. Based on these observations and knowledge, we decided to investigate the genes that are responsible for the development of such particular tendons. We focused on leg tendon precursors, which in fly, develop into tube-like CT structures. We developed a cell-specific approach to isolate tendon precursors and perform RNAseq analysis. This experiment led us to identify approximately 900 transcripts enriched in tendon precursors, in which 68 of them encode for transcription factors (TF). Amongst them, the Krüppel-like factor Dar1 is specifically expressed in tendon leg precursors during the early stages of metamorphosis. Tissue sections of fly legs with attenuated dar1 expression revealed aberrant leg muscle organization with a loss of internal appendicular tendons. These results suggest that Dar1 plays a key role in tendon development. Interestingly, Dar1 orthologs KLF- 4 and 5 are also expressed in mouse tendon precursors and studies conducted on chicken explants suggest that it could impact CT development. This work allowed Dar1 to be identified as a specific marker of long tendon of the leg that could also be required for the development of connective tissues in the vertebrate limb
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Schönbauer, Cornelia [Verfasser], and Matthias [Akademischer Betreuer] Mann. "Genetic analysis of Drosophila adult muscle type specification / Cornelia Schönbauer. Betreuer: Matthias Mann." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2013. http://d-nb.info/1052778852/34.
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Katzemich, Anja R. "Expression and function of the large modular muscle protein Obscurin in Drosophila melanogaster." Thesis, University of York, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.533525.
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Weitkunat, Manuela Verfasser], and Ulrike [Akademischer Betreuer] [Gaul. "Mechanistic dissection of adult muscle formation in Drosophila / Manuela Weitkunat. Betreuer: Ulrike Gaul." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2014. http://d-nb.info/1066206600/34.
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Jagla, Teresa. "Etude de la fonction des genes a homeoboite, ladybird, dans la myogenese chez drosophila melanogaster (doctorat)." Clermont-Ferrand 1, 2000. http://www.theses.fr/2000CLF1MM09.
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Perkins, Alexander David. "A systematic analysis of the role of the cytoskeleton in Drosophila melanogaster muscle maintenance." Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/44235.
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Animal muscles must maintain their function while bearing substantial mechanical loads and undergoing numerous contraction/extension cycles. How muscles withstand persistent mechanical strain is presently not well understood. The basic unit of muscle is the sarcomere, which is primarily composed of cytoskeletal proteins. I hypothesized that cytoskeletal proteins undergo renewal via protein turnover and that this is required to maintain muscle function. Using the adult flight muscles of the fruit fly, Drosophila melanogaster, I confirmed that the sarcomeric cytoskeleton undergoes turnover throughout the life of the organism. To uncover which cytoskeletal components are specifically required to maintain adult muscle function I performed an RNAi-meditated knockdown screen in adult D. melanogaster targeting the entire fly “cytoskeletome”, the set of known cytoskeletal and cytoskeletal-associated proteins. Systematic gene knockdown was restricted to adult flies and muscle function was analyzed with behavioural assays. This approach identified 47 genes required for maintaining muscle function, 40 of which had no previously known role in this process. Detailed analysis of the role of candidate genes in adult muscles using confocal and electron microscopy showed that while muscle architecture was largely maintained after gene knockdown, maintenance of sarcomere length was disrupted. Specifically, I found that the ongoing synthesis and turnover of the key structural sarcomere component Projectin (bent) was required to maintain M-line integrity. Together, these results provide direct in vivo evidence of muscle protein turnover and identify possible roles for this process by uncovering specific functional defects associated with reduced expression of a subset of cytoskeletal proteins in the adult animal.
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Manieu, Seguel Catalina Paz. "The role of muscle-tendon cell interaction during epithelial notum morphogenesis of Drosophila melanogaster." Tesis, Universidad de Chile, 2018. http://repositorio.uchile.cl/handle/2250/168536.
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Grado de Doctora en Ciencias biomédicas<br>Tissue-tissue interaction is essential to drive morphogenesis and contributing to the final shape of tissues and organs. The interaction between muscles and tendons during the establishment of the muscle-skeletal system is a great model to study this problem.
During Drosophila melanogaster metamorphosis a group of cells of the dorsal thorax (notum) epithelium, specialized as tendon cells, attach to the developing Indirect Flight Muscles (IFMs). Likewise, epithelial cells anchor to the cuticle exoskeleton through apical projections. Both interactions enable the adaptation of notum epithelium to mechanical strain generated by muscle contraction, by modulating its mechanoresponse. However, scarce evidence exists about how muscle-tendon interaction contributes to the final shape of the notum. Thus, we hypothesized that the interaction between IFMs and tendon cells plays a role in notum epithelium morphogenesis. Geometric morphometric analysis of adult thorax shape shows that interfering with muscle development results in dorsal thorax deformation, however, the absence of muscles does not affect,collective-epithelial movement of the epithelium towards anterior during notum morphogenesis, suggesting that early cellular mechanisms such as cell division, rearrangements and cell delamination are not altered. Conversely, force distribution along epithelium plane changes in muscle depletion condition during notum morphogenesis, displaying anisotropic tendency in tendon-cell and midline domains. Further, impairing muscle-contraction does not affect adult thorax shape compared with wild-type conditions, indicating that muscle function as a structural support for thorax epithelium. On the other hand, the ability of notum epithelium to adapt to the mechanical strain during IFMs contraction becomes crucial to maintain the shape and integrity of the tissue. Notum epithelium lacking Chascon, a scaffold/adaptor protein involved in cytoskeleton organization upstream of Jbug/Filamin, displays epithelium deformations and impaired collective-epithelial movement during morphogenesis. Interestingly, IFMs ablation rescues backward epithelial movement associated with chascon knockdown condition, resembling wild-type phenotype, although it affects tissue-movement velocity and the ability of tendon cells to guide collective cell movement. Since notum epithelium anchors apically to the cuticle we tested whether Chascon is required for this interaction. We found that chascon knockdown in tendon cells results in epithelial detachment from the cuticle during muscles shortening stage, supporting the role of Chascon in cell adhesion and collective epithelial-cell movement. Additionally, we observed an increased anisotropy at tendon cell domains in absence of Chascon after muscle shortening, indicating the great unbalance in mechanical homeostasis after muscle pulling under this condition.
Since muscle-tendon interaction is required for tendon cell differentiation in embryos we tested whether muscle was required for the expression of chascon and dumpy, a membrane protein responsible for exoskeleton-epithelium attachment, which along with Chascon is enriched in tendon cell domains during terminal differentiation. We found no significant differences in mRNA levels of chascon and dumpy, between animals lacking muscles versus wild type during muscle shortening, suggesting a muscle-independent alternative regulation of chascon and dumpy expression.
Our results support the notion that Chascon is required for tension-adaptation response of notum epithelium during muscle-contraction, ensuring collective-epithelial cell movement through regulation of tendon-cell attachment to the cuticle. We suggest that Chascon, along with a multi-protein complex, regulate the mechano-response of tendon-cells during muscle contraction, by enabling collective-epithelial cell movement under mechanical load due to muscle development. Finally, these analyses will contribute to a better understanding of the role of tissue-tissue interaction in tissue morphogenesis and differentiation.
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Jacques, Cécile. "Etude du rôle et du mécanisme d'action des facteurs de transcription glial cell deficient/glial cells missing au cours du développement." Université Louis Pasteur (Strasbourg) (1971-2008), 2007. https://publication-theses.unistra.fr/public/theses_doctorat/2007/JACQUES_Cecile_2007.pdf.
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Les facteurs de transcription Gcm et Gcm2 sont connus pour leur rôle de déterminants gliaux et plasmatocytaires chez l’embryon de drosophile. Lors de ma thèse, j’ai mis en évidence que les gènes gcm-gcm2 sont requis pour la différenciation terminale d’une sous-population de cellules tendon. Par la suite, nous avons montré que l’orthologue c-GCM1 chez le poulet est requis lors de l’embryogenèse pour la différenciation des précurseurs neuraux de la moelle épinière en neurones. De façon surprenante, nous avons également mis en évidence que les gènes de type gcm sont exprimés et requis dans des lignages neuronaux du cerveau de la drosophile aux stades post-embryonnaires. Toutes ces études nous ont permis de montrer que le rôle spécifique des facteurs de transcription Gcm dépend du contexte cellulaire où ils sont exprimés. Un crible double-hybride m’a permis l’identification du cofacteur dpias et son étude m’a permis de montrer une implication de Gcm au cours l’hématopoïèse larvaire<br>Gcm-Gcm2 transcription factors are known for their role in glial and plasmatocytes differentiation in Drosophila embryo. During my PhD, I have shown that gcm-gcm2 genes are required for terminal differentiation of a subpopulation of tendon cells. Thereafter, we showed that the chicken c-GCM1 orthologue is required during embryogenesis for the differentiation of spinal cord neural precursors into neurons. We have also shown that gcm genes are expressed and required in post-embryonic neural brain lineages of Drosophila. All these studies show that the specific role of Gcm transcription factors depends on the cellular context in which they are expressed. A two hybrid screen enabled me to identify the cofactor dpias and its study has allowed me to show the implication of Gcm in larval hematopoiesis
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Rodriguez, Deyra Marie. "Isolation and characterization of stretchin-myosin light chain kinase mutants in drosophila melanogaster." The Ohio State University, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=osu1079994503.
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Suslak, Thomas James. "There and back again : a stretch receptor's tale." Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/10474.
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Mechanotransduction is fundamental to many sensory processes, including balance, hearing and motor co-ordination. However, for such an essential feature, the mechanism(s) that underlie it are poorly understood. The mechanotransducing stretch receptors that relay information on the tonicity and length of skeletal muscles have been well-defined, particularly at the gross anatomical level, in a wide variety of species, encompassing both vertebrates and invertebrates. To date, there exists a wealth of data describing them, anatomically, as well as good electrophysiological data from stretch receptors of some larger organisms. However, comparatively few studies have succeeded in identifying putative mechanotransducing molecules in such systems. Nonetheless, this class of sensory mechanotransducers perhaps offer the best means of identifying molecules that permit the stretch-sensitivity of such endings, revealing new information about the underlying mechanisms of stretch receptors, and mechanoreceptors more generally. However, a different approach is clearly needed; a theoretical approach, utilising mathematical modelling, offers a powerful means of pooling the current wealth of knowledge on the reported electrophysiological behaviour of muscle stretch receptors. This study, therefore, develops an extended theoretical model of a stretch receptor system in order to reproduce, in silico, the reported behaviour of both vertebrate and invertebrate stretch receptors, within the same modelling environment, thus enabling the first quantitative framework for comparing these data, and moreover, making predictions of the likely roles of specific molecular entities within a stretch receptor system. Subsequently, this study utilises a model in vivo system to test these theoretical predictions. The genetic toolbox of D. melanogaster offers a wide range of tools that are extremely suitable for identifying mechanotransducing molecules in stretch receptors. However, very little is currently known about such endings in this organism. This study, therefore, firstly characterises a putative stretch receptor organ in larval Drosophila, the dbd neuron, via a novel experimental approach. It is shown that this neuron exhibits known properties of stretch receptors, as previously observed in other, similar organs. Furthermore, these observations bear out the predictions of the mathematical model. Having defined the dbd neuron as a muscle stretch receptor, pharmacological and genetic assays in this system, combined with predictions from the mathematical model, identify a key role for the recently-discovered DmPiezo protein as an amiloride-sensitive, mechanically-gated sodium channel (MNaC) in dbd neurons, with TRPA1 also acting in this system in a supporting role. These data confirm the essential role of an MNaC in mechanosensory systems, but also supply important evidence that, whilst the electrophysiological mechanisms in stretch receptors are remarkably similar across taxa, different species likely employ various molecular mechanisms to achieve this.
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Zhou, Lili. "The role of Lasp in the «Drosophila» male stem cell niche and in muscle development." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=95064.
Full textAbstract:
Drosophila Lasp is the only member of the nebulin family in Drosophila. Lasp has an amino-terminal LIM domain, two actin-binding nebulin repeats and a carboxyl-terminal SH3 domain and exhibits very high homology to human Lasp. To assess Lasp function in vivo, we generated a null mutant in Drosophila Lasp, named Lasp1. Lasp1 mutants are homozygous viable, but male sterile. Lasp localizes to cyst cells, early germ cells, hub cells and actin cones. In Lasp1 mutants, the stem cell niche is no longer anchored to the apical tip of the testis, and actin cone migration is perturbed resulting in improper spermatid individualization. Lasp colocalizes with βPS integrin and genetically interact with βPS integrin resulting in complete hub cell mislocalization, which indicates that Lasp modulates integrin adhesion in this context. Lasp1 mutant larvae and flies also have impaired crawling, climbing and flying ability. Lasp localizes to Z lines of third instar larval body wall muscles. In Lasp1 mutant indirect flight muscle, thin filament and sarcomere length is reduced while sarcomere ultrastructure is not significantly affected. The same applies to larval body wall muscles, where we observe a misregulation of sarcomere length in both absence and overexpression of Lasp. This phenotype is very similar to nebulin mutant knock-out mice indicating that Lasp plays a role in regulating thin filament lengths, but with only two nebulin repeats.<br>Chez la drosophile, Lasp est la seule protéine représentante de la famille des Nébuline. Lasp contient un domaine LIM, deux répétitions de type Nébuline et un domaine SH3, et présente une forte homologie avec la famille Lasp des mammifères. Afin identifier le rôle de Lasp, nous avons généré une mutation nulle, nommée Lasp1. Les mutants Lasp1 sont homozygotes viables, mais les mâles stériles. Lasp se localise dans cellules kyste, dans les cellules germinales, les cellules hub et au niveau des cônes d'actine. Chez les mutants Lasp1, les cellules souches ne sont plus ancré à l'extrémité apicale du testicule, et la migration des cônes d'actine est perturbée, conduisant à une individualisation irrégulière des spermatides. Lasp est colocalisée avec l'intégrine βPS et interagit génétiquement avec l'intégrine βPS, amenant une délocalization des cellules hub, indiquant que Lasp module adhésion intégrine dans ce contexte. Les larves mutantes pour Lasp se déplacent avec difficulté et les adultes ont avec une capacité d'escalade et de vols réduite. Lasp se localise aux lignes Z dans les muscles des larves du troisième stade. Chez les adultes Lasp1, les muscles des ailes présentent une longueur réduite des filaments minces ainsi que des sarcomères, alors que l'ultrastructure du sarcomère ne semble pas être significativement affectée. Les muscles larvaires présentent le phenotype. De plus, on observe un dérèglement de la longueur du sarcomère en surexprimant Lasp dans un contexte sauvage. Ce phénotype est très similaire à celui des souris mutantes pour la nébuline, indiquant que Lasp joue un rôle dans la régulation de la longueur du filament mince, mais avec seulement deux répétitions nébuline.