Dissertationen zum Thema „Caenorhabditis elegans – Système nerveux“
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Sauvage, Pascal. „Etude de la locomotion chez C. Elegans et perturbations mécaniques du mouvement“. Paris 7, 2007. http://www.theses.fr/2007PA077110.
Der volle Inhalt der QuelleThis study on the locomotion of C. Elegans aims at a better understanding of its nervous system and at giving birth to news ideas concerning the conception of new biometics models or objects. We first gave a description of the worm, of its physiology, and of its main modes of locomotion, that is to say the swimming - in liquid medium, and the crawling - on gel substract. When swimming, we analyzed how the dissymmetry pf the movement is necessary for the worm to move on when in viscous medium. Thanks to the analysis of the velocity of the local displacements and by supposing that the forces are viscous, we balanced the forces. We thus demonstrated that transversal and longitudinal friction coefficients could be compared to the coefficients obtained theoretically from an oblong ellipsoïd. When crawling, we were able to observe a diminution of the amplitude from the head to the tail. We first studied the worm-substract interaction theorically - lubrification hypothesis, but the friction coefficients predicted were in contradiction with experimental results. This difference, according to our experiments, was due to static friction. We also measured the rigidity of the worm. By confining the worm vertically in liquid medium, we observed a continuous transition from swimming to — crawling. We proved that the movement of the tail, in comparison with the movement of the head, was more and more delayed as the confinement increased. In these conditions, the global movement of the worm got slower. On substract, we were able to constrain the amplitude thanks to a horizontal confinement; we observed that wavelength decreased with amplitude
Millet, Jonathan. „Stratégies d'analyse spatio-temporelle de l‟épissage alternatif chez Caenorhabditis elegans“. Thesis, Bordeaux, 2015. http://www.theses.fr/2015BORD0437/document.
Der volle Inhalt der QuelleAlternative splicing is a regulatory mechanism of gene expression which is increasingly studied in Life Science. Methods exist to study this mechanism but specific tools to follow each alternative splicing event in a spatio-temporal manner are lacking. Yet, the characterization of the regulation and the elements that determines them depends on valide strategies for visualising them in physiological conditions.We have developped a dual-fluorescent reporter-based system in order to follow alternative splicing event regulation in vivo. It has been applied to five different genes in the model organism Caenorhabditis elegans. Among the genes followed, two follow a potentially stochastic scheme, one show no visible sign of alternative splicing. The last display tissue specific splicing patterns but developed a toxic effect in the animal when expressed from a multicopy extrachromosomal array. To remediate this problem, we decided to develop a method that allows for simpler single copy insertion of fluorescent reporter using CRISPR-Cas.Our results indicates that the dual-fluorescent reporter works well. However, this system can be upgraded by getting close to physiological rates of transcription allowed by single-copy insertion in the genome of C.elegans. We also discovered an alternatiove splicing event which follows a spatial, temporal and conditionnal regulation. Moreover, we constructed a set of different reporter to unravel the regulation observed in the gene top-1
Dichio, Vito. „The exploration-exploitation paradigm : a biophysical approach“. Electronic Thesis or Diss., Sorbonne université, 2023. http://www.theses.fr/2023SORUS402.
Der volle Inhalt der QuelleThe study of living systems is notoriously challenging. The often-quoted daunting complexity of biological systems is primarily due to the intricacies of their interactions, their multiple organisation levels and their dynamic nature. In the quest to understand this complexity, parallels drawn with standard physics – in particular, statistical physics -- are both useful and of limited use. On the one hand, they provide a rich set of theoretical and methodological building blocks for constructing theories and designing experiments. On the other hand, life also unfolds according to principles that are unparalleled in the physics of conventional matter. A crucial difference lies in the notion of function: biological systems are shaped by the need to perform specific tasks. A general problem for living systems is to find and promote those configurations that yield improved or optimal functions, we call this the exploration-exploitation (EE) problem. One specific instance of the above is found in evolutionary biology. There, random genetic mutations sustain the exploration of the configuration space, with those leading to higher reproductive success being favoured by natural selection. Inspired by the latter, we develop a novel formalism that encodes a general exploration-exploitation dynamics for biological networks. In particular, our EE dynamics is represented as an exploration of a functional landscape and consists of stochastic configuration changes combined with the state-dependent optimisation of an objective function (F metric). We begin by investigating its main features through the study of simple, analytically tractable functional landscapes. We deploy simulations for more general and complex applications. We then turn to the brain wiring problem, i.e., the development of an individual's nervous system during its early life. We argue that this is another specific instance of the EE problem and therefore can be addressed by using our theoretical framework. In particular, we focus on brain maturation in the nematode C.elegans, the only organism for which a complete network of neurons and neuronal connections has been reconstructed, at multiple developmental time points (seven). We fix the network at birth and use the adult stage to infer (i) a parsimonious maxent (ERG) description of the F metric for the worm brain and (ii) the two parameters of our EE dynamics. According to the topography of its functional landscape, the adult brain is characterised by a tendency to form both triads and high degree nodes. We demonstrate that our EE dynamics in such landscape is capable of tracking down the entire developmental history. In particular, we show that the trajectory we obtain closely reproduces the other experimental time points that we did not use for inference. This is true both in the space of model statistics and for a number of other network properties. Additionally, we discuss a micro-level interpretation of the EE dynamics in terms of the underlying synapse formation process. Our study is a first step towards the system-level understanding of the development of a natural brain and can be extended (i) to encompass more complex functional landscapes, (ii) to different organisms than the C. elegans and (iii) to several different problems than the brain wiring. Indeed, we posit that the exploration-exploitation paradigm is among those life-specific principles that we are just beginning to uncover
Livingstone, David. „Studies on the unc-31 gene of Caenorhabditis elegans“. Thesis, University of Cambridge, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240106.
Der volle Inhalt der QuelleLee, Yuk Wa. „Characterization of Mab21l2 in neural development of vertebrate model /“. View abstract or full-text, 2005. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202005%20LEEY.
Der volle Inhalt der QuelleBirnby, Deborah Ann. „Analysis of daf-11, a transmembrane guanylyl cyclase that mediates chemosensory transduction in C. elegans /“. Thesis, Connect to this title online; UW restricted, 1998. http://hdl.handle.net/1773/10300.
Der volle Inhalt der QuelleStovall, Elizabeth L. „Analysis of mig-10, a gene involved in nervous system development in caenorhabditis elegans“. Link to electronic thesis, 2004. http://www.wpi.edu/Pubs/ETD/Available/etd-0430104-142249/.
Der volle Inhalt der QuelleFicociello, Laura Faraco. „Neuronal migration -- investigating interactions of the cytoplasmic adaptor pProtein MIG-10 in C. elegans“. Worcester, Mass. : Worcester Polytechnic Institute, 2008. http://www.wpi.edu/Pubs/ETD/Available/etd-010908-103637/.
Der volle Inhalt der QuelleBurket, Christopher T. „Two genes, dig-1 and mig-10, involved in nervous system development in C. elegans“. Link to electronic thesis, 2002. http://www.wpi.edu/Pubs/ETD/Available/etd-1115102-141010.
Der volle Inhalt der QuelleLau, Tze Chin. „In vitro and in vivo analyses of the impact of Mab21l2 and its targets on neural patterning and differentiation in vertebrates /“. View abstract or full-text, 2010. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202010%20LAU.
Der volle Inhalt der QuelleDumesnil, Dennis. „Neurological Responses to a Glucose Diet in Caenorhabditis elegans“. Thesis, University of North Texas, 2017. https://digital.library.unt.edu/ark:/67531/metadc1011786/.
Der volle Inhalt der QuelleHoskins, Roger Allen. „Molecular and genetic studies on the unc-30 and unc-31 genes of Caenorhabditis elegans“. Thesis, University of Cambridge, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.334107.
Der volle Inhalt der QuelleKhandekar, Anagha. „Age-related Changes in the Neuronal Architecture of Caenorhabditis Elegans: A Dissertation“. eScholarship@UMMS, 2015. https://escholarship.umassmed.edu/gsbs_diss/798.
Der volle Inhalt der QuelleKhandekar, Anagha. „Age-related Changes in the Neuronal Architecture of Caenorhabditis Elegans: A Dissertation“. eScholarship@UMMS, 2010. http://escholarship.umassmed.edu/gsbs_diss/798.
Der volle Inhalt der QuelleBelicard, Tony. „Base génétique de la sensibilité au virus d'Orsay au sein des populations naturelles de Caenorhabditis elegans“. Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066274/document.
Der volle Inhalt der QuelleCaenorhabditis elegans is a commonly studied animal model in laboratories. The discovery ofthe first natural viral infections of Caenorhabditis brings new models to study animal-virusinteractions.The Orsay virus, specifically infecting C. elegans, and the Santeuil virus, specificallyinfecting C. briggsae, are positive single strand RNA viruses (Hepatites, Chikungunya,Coronavirus etc…) disrupting the structure of intestinal cells of their host. However, weobserved a strong variability in the sensitivity to those viruses at the intraspecific level.To identify the genetic basis of the sensitivity, we performed a genome wide association studyon 97 wild isolates of C. elegans. We were able to identify the center of chromosome IV as aregion containing the locus responsible for this sensitivity. A deletion in the drh-1 gene,coding for a RIG-I-Like protein, confers sensitivity to their carrier. RIG-I is known torecognize viral RNA and to trigger an antiviral response through the production of interferonsin vertebrates. However, C. elegans is not able to produce interferons but it appears thatDRH-1 initiates a viral specific siRNA pathway.Immunity genes are under strong selective pressure. Thus, it is surprising that such animportant protein for the antiviral pathway appears to be disrupted in 23% of the wild isolates.This deletion shows high linkage disequilibrium with a broader region of 3Mb, suggestingthat the deletion propagates with this region. However, this region does not seem to provideany advantage to their owner under laboratory conditions
Soltesz, Zoltan. „Optogenetic investigation of the neural network underlying the oxygen modulation of C. elegans locomotion“. Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708419.
Der volle Inhalt der QuelleClark, Christopher M. „Neural Orchestration of the C. elegans Escape Response: A Dissertation“. eScholarship@UMMS, 2014. https://escholarship.umassmed.edu/gsbs_diss/750.
Der volle Inhalt der QuelleClark, Christopher M. „Neural Orchestration of the C. elegans Escape Response: A Dissertation“. eScholarship@UMMS, 2010. http://escholarship.umassmed.edu/gsbs_diss/750.
Der volle Inhalt der QuelleQuéré, Cécile. „Régulation post-transcriptionnelle du gène unc-54 de Caenorhabditis elegans identifiée in vivo par un système de double rapporteurs fluorescents“. Thesis, Bordeaux, 2014. http://www.theses.fr/2014BORD0347/document.
Der volle Inhalt der QuelleCaenorhabditis elegans development is very tightly regulated, leading to the same number of cells in each individual. Part of this regulation network relies on small single strand RNAs (miRNAs), which can target homologous sequences in the 3’ untranslated regions (3’UTR) of messenger RNAs. We want to investigate the contribution of miRNAs during neurons differentiation. In order to study the miRNA contribution to gene regulation we use double fluorescent reporters that allow us to visualize the posttranscriptional contribution to regulation throughout development. The GFP and the mCherry are expressed under the control of the gene promoter, but followed by either the 3’UTR of interest, or a control 3’UTR. We first chose as a control 3’UTR the unc-54 3’UTR (myosin class II). The gene unc-54 is expressed through all larval stages and in the adult worms. The two colors reporter system showed that unc-54 3’UTR undergoes a regulation in the ADF pair of neurons and partially in the body wall muscle. The characterization of this regulation pointed out a potential role for mir-1820. The GFP was cloned between mir1820 5’ and 3’ sequences and the construction displayed an expression profile overlapping with the regulation pattern observed on unc-54 3’UTR
Ameen, Muhammad T., und Patrick C. Bradshaw. „VITAMIN B2 REDUCES AMYLOID-BETA PROTEOTOXICITY AND IMPROVES HEALTH IN A CAENORHABDITIS ELEGANS ALZHEIMER’S DISEASE MODEL“. Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/asrf/2018/schedule/24.
Der volle Inhalt der QuelleAmeen, Muhammad Tukur. „A Role of Vitamin B2 in Reducing Amyloid-beta Toxicity in a Caenorhabditis elegans Alzheimer’s Disease Model“. Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/etd/3398.
Der volle Inhalt der QuelleFicociello, Laura Faraco. „Neuronal Migration: Investigating Interactions of the Cytoplasmic Adaptor Protein MIG-10 in C. elegans“. Digital WPI, 2008. https://digitalcommons.wpi.edu/etd-theses/41.
Der volle Inhalt der QuelleBelicard, Tony. „Base génétique de la sensibilité au virus d'Orsay au sein des populations naturelles de Caenorhabditis elegans“. Electronic Thesis or Diss., Paris 6, 2014. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2014PA066274.pdf.
Der volle Inhalt der QuelleCaenorhabditis elegans is a commonly studied animal model in laboratories. The discovery ofthe first natural viral infections of Caenorhabditis brings new models to study animal-virusinteractions.The Orsay virus, specifically infecting C. elegans, and the Santeuil virus, specificallyinfecting C. briggsae, are positive single strand RNA viruses (Hepatites, Chikungunya,Coronavirus etc…) disrupting the structure of intestinal cells of their host. However, weobserved a strong variability in the sensitivity to those viruses at the intraspecific level.To identify the genetic basis of the sensitivity, we performed a genome wide association studyon 97 wild isolates of C. elegans. We were able to identify the center of chromosome IV as aregion containing the locus responsible for this sensitivity. A deletion in the drh-1 gene,coding for a RIG-I-Like protein, confers sensitivity to their carrier. RIG-I is known torecognize viral RNA and to trigger an antiviral response through the production of interferonsin vertebrates. However, C. elegans is not able to produce interferons but it appears thatDRH-1 initiates a viral specific siRNA pathway.Immunity genes are under strong selective pressure. Thus, it is surprising that such animportant protein for the antiviral pathway appears to be disrupted in 23% of the wild isolates.This deletion shows high linkage disequilibrium with a broader region of 3Mb, suggestingthat the deletion propagates with this region. However, this region does not seem to provideany advantage to their owner under laboratory conditions
Showemimo, Opeyemi F. „Vitamin B12 Deficiency Does Not Stimulate Amyloid-beta Toxicity in a Ceanorhabditis elegans Model of Alzheimer’s Disease“. Digital Commons @ East Tennessee State University, 2021. https://dc.etsu.edu/etd/3869.
Der volle Inhalt der QuellePetrash, Hilary A. „Maintaining the Balance: Coordinating Excitation and Inhibition in a Simple Motor Circuit: A Dissertation“. eScholarship@UMMS, 2012. https://escholarship.umassmed.edu/gsbs_diss/633.
Der volle Inhalt der QuelleDesbois, Muriel. „Dynamic synaptic changes revealed by a novel trans-synaptic method to visualize connections in vivo in C. elegans“. Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066157/document.
Der volle Inhalt der QuelleThe nervous system is a complex network that senses and processes information and is essential for the survival of both vertebrates and invertebrates as it is involved in behavior responses. Information within the network is transmitted through specialized cell-cell contacts, including synaptic connections. Importantly, the network is not static and is believed to change during development and learning, as well as during pathological or normal age-related decline. Studying the nervous system in vivo requires the use of animal models such as Caenorhabditis elegans. Understanding of behavior and development requires visualization and analysis of synaptic connectivity. However, existing methods are laborious and may not depend on trans-synaptic interactions, or otherwise ‘trap’ the synapses by fixing the connections, thus precluding dynamic studies. In order to study synaptic modifications, we developed a new transgenic approach for in vivo labeling of specific connections in C. elegans, called iBLINC (in vivo Biotin Labeling of INtercellular Contacts). iBLINC involves the biotinylation of an acceptor peptide (AP) by the Escherichia coli biotin ligase BirA. Both are fused to two interacting post- and pre-synaptic proteins, respectively. The biotinylated acceptor peptide fusion is detected by a monomer streptavidin fused to a fluorescent protein that is transgenically expressed and secreted into the extracellular space. The method is directional, bright and dynamic. Moreover it correlates well with electron micrograph reconstruction. Using this new technique to observe synapses, which are part of the thermosensory circuitry of C. elegans, during aging, we could conclude that the connection pattern varies with age and within a population. Changes of the number and size of the synapses were observed during aging. Some segments of the synaptic region seem to be more affected than others by the aging process. Those results were corroborated by using a GABAergic pre-synaptic marker which allowed us to visualize a decline of the vesicle number with aging. In summary, in this thesis I explained a new in vivo trans-synaptic method to visualize synapses in C. elegans. Then I demonstrated that a natural decline in the number of synapses as well as the number of vesicles occurs during aging
Squiban, Barbara. „Criblage par ARN interférence du génome complet de C. elegans pour l' identification de nouveaux gènes impliqués dans l' immunité innée“. Thesis, Aix-Marseille, 2012. http://www.theses.fr/2012AIXM4056.
Der volle Inhalt der QuelleTo investigate innate immune signaling, we study the interaction of C. elegans with the fungus Drechmeria coniospora. One of the responses of the worm to this infection is the up-regulation of a variety of antimicrobial peptide (AMP) genes in the epidermis. Transgenic worms carrying a GFP reporter gene under the control of an AMP promoter fluoresce green after infection by D. coniospora. If a gene required for AMP gene expression is inactivated, the reporter strain will not turn green upon infection. Using this fluorescent read-out, we have been able to screen for signaling molecules required for AMP gene expression using a quantitative semi-automated RNAi approach. We have screened two RNAi libraries that together cover 95% of the ca. 20,000 genes in the C. elegans genome and we obtained 360 high-confidence candidates that reduced the level of induction of green fluorescence after infection, and correspond to 343 genes. A further phenotypic characterization allowed the candidates to be grouped into distinct functional categories and allowed the identification of both a receptor acting upstream the p38 MAPK pathway necessary for the activation of the AMPs, and the implication of stress granules during infection. Altogether, the screen data and its analysis represent the foundation for the establishment of a comprehensive description of the signaling network regulating the innate immune system of the worm and will shed light on the complex interactions between immunity and other physiological processes at the molecular, cellular and organismal level
Sleigh, James Nicholas. „Model systems for exploring new therapeutic interventions and disease mechanisms in spinal muscular atrophies (SMAs)“. Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:378416c5-a586-4a2a-980c-81dfff6803df.
Der volle Inhalt der QuelleBerghoff, Emily Greta. „Circuit transcription factors in Caenorhabditis elegans“. Thesis, 2020. https://doi.org/10.7916/d8-77a8-5z43.
Der volle Inhalt der QuelleBayer, Emily Ann. „Sexually Dimorphic Development of the Caenorhabditis elegans Nervous System“. Thesis, 2020. https://doi.org/10.7916/d8-kcqy-1e23.
Der volle Inhalt der QuelleWeinberg, Peter J. „Mechanisms of sexually dimorphic development in the nervous system of Caenorhabditis elegans“. Thesis, 2017. https://doi.org/10.7916/D8N302MV.
Der volle Inhalt der QuelleBarbier, Louis Wei-Chun. „The Stomatin STO-6 is a Novel Regulator of the Caenorhabditis elegans Motor Circuit“. Thesis, 2012. http://hdl.handle.net/1807/42383.
Der volle Inhalt der QuelleVanDuyn, Natalia M. „Identification and characterization of molecular modulators of methylmercury-induced toxicity and dopamine neuron degeneration in Caenorhabditis elegans“. Thesis, 2014. http://hdl.handle.net/1805/5193.
Der volle Inhalt der QuelleMethylmercury (MeHg) exposure from occupational, environmental and food sources is a significant threat to public health. MeHg poisonings in adults may result in severe psychological and neurological deficits, and in utero exposures can confer significant damage to the developing brain and impair neurobehavioral and intellectual development. Recent epidemiological and vertebrate studies suggest that MeHg exposure may contribute to dopamine (DA) neuron vulnerability and the propensity to develop Parkinson’s disease (PD). I have developed a novel Caenorhabditis elegans (C. elegans) model of MeHg toxicity and have shown that low, chronic exposure confers embryonic defects, developmental delays, reduction in brood size, decreased animal viability and DA neuron degeneration. Toxicant exposure results in an increase in reactive oxygen species (ROS) and the robust induction of several glutathione-S-transferases (GSTs) that are largely dependent on the PD-associated phase II antioxidant transcription factor SKN-1/Nrf2. I have also shown that SKN-1 is expressed in the DA neurons, and a reduction in SKN-1 gene expression increases MeHg-induced animal vulnerability and DA neuron degeneration. Furthermore, I incorporated a novel genome wide reverse genetic screen that identified 92 genes involved in inhibiting MeHg-induced animal death. The putative multidrug resistance protein MRP-7 was identified in the screen. I have shown that this transporter is likely expressed in DA neurons, and reduced gene expression increases cellular Hg accumulation and MeHg-associated DA neurodegeneration. My studies indicate that C. elegans is a useful genetic model to explore the molecular basis of MeHg-associated DA neurodegeneration, and may identify novel therapeutic targets to address this highly relevant health issue.
LeVora, Jennifer K. „THE ROLE OF SMF 1, SMF-2, SMF-3 IN METAL-INDUCED WHOLE ANIMAL VULNERABILITY AND DOPAMINE NEURON DEGENERATION IN CAENORHABDITIS ELEGANS“. Thesis, 2012. http://hdl.handle.net/1805/3177.
Der volle Inhalt der QuelleThe etiology of many neurodegenerative diseases is unknown, but a number of studies indicate that a combination of both genetic and environmental factors contribute to the progression of disease. Exposure to environmental metals, such as Mn2+, Fe2+, Cu2+, and Al3+, has been shown to increase cell death that is characteristic of neurodegenerative disorders such as AD, PD, Wilson’s disease and Menkes disease. These metals are important in numerous biological processes in the brain and their homeostasis is regulated through multiple mechanisms of transport, storage, and secretion. The vertebrate divalent metal transporter-1 (DMT-1) has been implicated in transport and homeostasis of these divalent cations. In these studies I utilize Caenorhabditis elegans (C. elegans) to show that long term exposure to Mn2+ decreases animal viability in a dose-dependent manner, and I demonstrate that C. elegans homologues to DMT-1, SMF-1, SMF-2, and SMF-3, play specific roles in divalent metal ion-induced DA neurodegeneration. I show that SMF-1 contributes to Fe2+-induced DA neuron degeneration, SMF-3 contributes to Al3+-induced DA neuron degeneration, and both SMF-2 and DAT-1 contribute to Cu2+-induced DA neuron cell death. These studies utilize C. elegans as a powerful model to characterize molecules and pathways involved in metal toxicity and metal-induced DA neuron degeneration.