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Nowak, Victor. "Caractérisation de l'expression de facteurs potentiellement impliqués dans la spécification en épiblaste dans l'embryon de souris préimplantatoire". Electronic Thesis or Diss., Université Clermont Auvergne (2021-...), 2023. http://theses.bu.uca.fr/nondiff/2023UCFA0033_NOWAK.pdf.
Pełny tekst źródłaAfter fertilization the mouse embryo performs two rounds of differentiation before implantation. The first allows the formation of outer cells which, that give the Trophectoderm (TE) and the inner cells which give the Inner Cell Mass (ICM). The second step takes place within the ICM by producing the Epiblast (Epi) and the Primitive Endoderm (PrE) cells positioning in a “salt and pepper” pattern in the ICM. Recent studies show that NANOG is necessary for Epi specification, but not sufficient, suggesting that other factors may be involved in the initiation of this differentiation.My goal was to identify other factors that could be involved, as NANOG, in the initiation of Epi specification. I focused on the Fgf4 gene, which is a known Epi marker and a target gene of NANOG, to identify in-silico several potentially implicated factors: TEAD4, SOX2, SOX21 and OCT4. Analysis of their expressions highlighted the heterogeneity of those factors at different stages and between, and also an inverted correlation between SOX2 and SOX21 expressions during the development. Those results and data from literature made me hypothesize that TEAD4 and SOX21 would be repressors while NANOG and SOX2 would be activators of FGF4 expression and Epi specification. There would be then a competition between those factors. But nowadays, my work on the analysis of SOX21 overexpression in the embryo didn't allow me to validate this hypothesis. In parallel, I started to develop embryonic stem cells allowing an overexpression of SOX21 or TEAD4. Thanks to these cells, we will be able to study the DNA binding mechanisms of those factors and the impact on the target genes, and also the putative competition between them
Koné, Maïmouna. "Nucléologenèse et régulation de l'expression de l'hétérochromatine péricentromérique dans l'embryon précoce de souris". Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLA030.
Pełny tekst źródłaIn mice, the preimplantation period is characterized by several events, the most important is the activation of the embryonic genome (EGA) taking place between the late 1-cell (minor phase) and late 2-cell (major phase) stages. Among the genes expressed are the ribosomal DNAs required for the formation of the ribosomes and the pericentromeric heterochromatin (sense and antisense RNA) important for the formation of heterochromatin clusters. It is known that the ribosomal RNAs are synthesized in the nucleolus. In the embryo after fertilization, the nucleolus is replaced by nucleolus precursor bodies (NPBs). These NPBs then evolve during embryonic development to form nucleoli but the mechanisms involved in the formation of nucleoli remain mostly unknown. Moreover, there are very few data on the organization of ribosomal genes based on their transcriptional status (active or inactive) in embryos. I therefore focused during my PhD thesis on the nucleologenesis process and on the organization of ribosomal genes in the mouse preimplantation embryo. Furthermore, it is well known that the two parental pronuclei (paternal and maternal) progress asynchronously after fertilization, the pericentromeric heterochromatin organizing faster around NPBs in the maternal pronucleus. In the second part of my thesis, I therefore focused on the role NPBs may have in the organization of pericentromeric hetero-chromatin during development and on the contribution of each gamete
Guyot, Romain. "Organogenèse testiculaire chez la souris, implications des protéases et des antiprotéases : conséquences de l'expositions in utéro à des perturbateurs endocriniens". Lyon 1, 2004. http://www.theses.fr/2004LYO11002.
Pełny tekst źródłaAoidi, Rifdat. "Étude du rôle de la voie ERK/MAPK dans le développement embryonnaire chez la souris". Doctoral thesis, Université Laval, 2017. http://hdl.handle.net/20.500.11794/27476.
Pełny tekst źródłaLes mammifères possèdent deux MAP kinases kinases (MEK1 et MEK2), impliquées dans l’activation de la voie ERK/MAPK essentielle pour la différenciation, la prolifération et la survie cellulaire. Le premier objectif de cette thèse était de déterminer si les fonctions des kinases MEK1 et MEK2 sont redondantes durant le développement embryonnaire. Les souris Mek1-/- meurent à mi-gestation d’une malformation du placenta. Les souris Mek2-/- ne présentent aucun phénotype majeur, suggérant que ces deux protéines ont des rôles différents. Cependant, la plupart des mutants Mek1+/-Mek2+/- meurent pendant la gestation d’un sous-développement du placenta, indiquant que Mek1 et Mek2 ont chacun un rôle dans le développement des tissus extraembryonnaires. À ce jour aucune évidence claire ne permet de statuer sur la redondance fonctionnelle de MEK1 et MEK2. Afin de vérifier la spécificité fonctionnelle de Mek1 et Mek2, nous avons généré au laboratoire un allèle « knockin », exprimant l’ADNc de Mek2 sous contrôle du locus Mek1 (Mek12). L’analyse de ces souris a révélé la redondance fonctionnelle entre MEK1 et MEK2. L’analyse de combinaisons alléliques de Mek a démontré qu’une expression minimale de protéines MEK est cruciale pour le développement embryonnaire et la survie. Le second objectif de cette thèse était de caractériser les mutants Mp1. Les protéines d’échafaudage permettent de moduler l’activité de la voie ERK/MAPK et facilitent la transmission rapide du signal. Parmi les protéines d’échafaudage connues, seule MP1 (Mek Partner 1) a été identifiée comme étant un partenaire spécifique de MEK1 et ERK1. Cette spécificité suggère que MP1 pourrait contribuer à la différence d’activation de MEK1 et MEK2 en spécifiant le signal qui passe par Mek1. Afin d’étudier le rôle de Mp1 au cours du développement chez la souris, nous avons généré des souris Mp1-/-. L’analyse de ces mutants indique que le gène Mp1 est essentiel pour la survie et que sa fonction est nécessaire suite à la post-implantation. La dérégulation de la voie ERK/MAPK dans le développement chez l’homme a aussi des conséquences phénotypiques. Au cours des dernières années, une classe de syndromes a été caractérisée : Les « Rasophaties ». Ces syndromes partagent des caractéristiques communes qui sont, une mutation dans des gènes de la voie ERK/MAPK, une dysmorphologie cranio-faciale, des malformations cardiaques et cutanées ainsi qu’un retard mental. Parmi les mutations de la voie ERK/MAPK qui ont été identifiées, une mutation ponctuelle dans le gène Mek1 (Mek1Y130C) cause le syndrome Cardio-Facio-Cutané (CFC). Le dernier objectif de cette thèse était de générer un modèle animal pour le CFC portant la mutation Mek1Y130C. Les souris portant l’allèle Mek1Y130C présentent les phénotypes associés au CFC (i.e sténose pulmonaire, dysmorphologie cranio-faciale et défauts neurologiques).
Mammals possess two MAP kinase kinase (MEK1 and MEK2), involved in ERK/MAPK pathway. This pathway is essential for proliferation, differentiation and cell survival. The first objective of my thesis was to determinate if MEK1 and MEK2 kinases are redundant during embryonic development. Mek1-/- mice die at embryonic day E10.5 due to placental defects, whereas Mek2-/- mice survive with a normal lifespan suggesting that MEK1 possesses functions not shared by MEK2. However, most Mek1+/-Mek2+/- embryos also die from placental defects, indicating that both Mek genes contribute to placental development. To date, no clear evidence on MEK1 and MEK2 redundancy has been provided. To assess the functional specificity of the Mek1 and Mek2 genes, we produced a Mek1-knockin allele in which the Mek2 coding sequences were placed under the control of Mek1 regulatory sequences. Analyzing these mice allowed us to demonstrate that MEK1 and MEK2 can substitute for each other and that a minimal amount of MEK is critical for placenta development and embryo survival. The second objective of my thesis was to characterize Mp1 mutants. Scaffold proteins modulate MAPK pathway by providing spatial and temporal specificity. Among known ERK/MAPK scaffold proteins, only MP1 (Mek Partner 1) is specific to MEK1 and ERK1, raising the question of the specificity of MP1 in the regulation of ERK/MAPK pathway via MEK1. In order to investigate Mp1 function in vivo, we generated Mp1 knock-out mice. Analyzing these mice enable us to suggest that Mp1 is required for embryonic development and is essential during post-implantation. Deregulation of Ras/MAPK pathway also causes developmental phenotypes in human. During the last decade, a new class of syndromes, which share common phenotypes such as mutations in Ras/MAPK pathway, cranio-facial dysmorphology, cardiac and cutaneous malformations and neurological delay has been described and named Rasophaties. Among the DNA mutations found in rasopathies, the Mek1 mutation, Mek1Y130C, causes cardio-facio-cutaneous syndrome (CFC). The last objective of my thesis was to generate a mouse model of CFC, with the Mek1Y130C mutation. I found that mice carrying the Mek1Y130C mutation partially recapitulate CFC syndrome (i.e pulmonary stenosis, crani-facial dysmophia and neurological defects).
Truchet, Sandrine. "Voies de signalisation de l'interféron-gamma dans les ovocytes et les embryons pré-implantatoires de souris". Paris, Muséum national d'histoire naturelle, 2003. http://www.theses.fr/2003MNHN0003.
Pełny tekst źródłaInterferon-gamma (IFNg) is a cytokine which is best known for its role in the immune system and exerts pleitropic biological activities such as antiviral, antitumoral and antiproliferative effects. Upon binding of IFNg on its specific cellular receptor (IFNGR), intracellular signal transduction relies on two protein families, namely the Janus Kinases (JAKs) which are associated to each receptor's subunits, and the transcription factor STAT1 (Signal Transducer and Activator of Transcription 1). Interaction between IFNg and its receptor triggers a cascade of phosphorylations which leads to the phosphorylation of cytoplasmic STAT1, its dimerization and nuclear translocation. Once in the nucleus, activated STAT1 binds to specific DNA elements named GAS (Gamma Activated Sequence/Site) located in the promoters of IFNg inducible genes and activates their transcription. Nevertheless, some publications suggest that the IFNg/IFNGR complexe may play a role in intracellular trafficking of STAT1 and even in its nuclear translocation which could be mediated by the nuclear localization sequence (NLS) of IFNg. Indeed, no NLS has been identified in STAT proteins. The aim of this study was to use mouse ovocytes and preimplantation embryos as models to explore the signal transduction induced by IFNg in these cells and the mechanisms underlying the intracellular trafficking of its receptor eventually leading the nuclear localization of IFNg and/or its receptor. It was first shown, both by indirect immunofluorescence and RT-PCR, that the two subunits (IFNGR1 and IFNGR2) of the IFNg receptor are naturally expressed in mouse ovocytes and preimplantation embryos. However, despite the apparent binding of IFNg to its receptor, no massive nuclear accumulation of STAT1 is observed in mouse ovocytes and preimplantation embryos upon IFNg stimulation, whatever the doses or the stimulation times tested. Conversely, STAT1 as well as other members of this transcription factors family appear to be permanently phosphorylated and reside in the nuclear compartment, associated with interchromatin granules clusters (IGCs) or "speckles". On the other hand, anti-IFNGR1 antibody recognizes systematically an epitope associated with the nucleolar compartment, in mouse ovocytes and preimplantation embryos, as well as in several somatic cell lines. This epitope was purified from nucleoli preparations and immunoprecipitated from total nuclear extracts. In both cases, a single peptide with an apparent molecular weight of about 31 kDa was detected by Western blot analysis. This epitope is now being identified by mass spectrometry
Escuin, Sarah. "Fonctions de la kinase NIK dans la migration neuronale radiale au cours du développement du cortex cérébral chez la souris". Université Louis Pasteur (Strasbourg) (1971-2008), 2007. http://www.theses.fr/2007STR13141.
Pełny tekst źródłaMenard, Claudine. "Ontogénèse des canaux calciques de type L. Influence de l'acide rétinoi͏̈que". Montpellier 2, 1999. http://www.theses.fr/1999MON20098.
Pełny tekst źródłaMiladinović, Olivera. "Molecular profiling of the embryonic hematopoietic stem cell niche". Electronic Thesis or Diss., Sorbonne université, 2023. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2023SORUS025.pdf.
Pełny tekst źródłaHematopoietic stem cells (HSCs) constitute a rare population of cells at the foundation of the adult hematopoietic system. During mouse ontogeny, the first adult-type HSCs are autonomously generated in the Aorta-Gonad-Mesonephros (AGM) region at mid-gestation. More precisely, HSCs emerge from aortic endothelial cells through an endothelial to hematopoietic transition. The AGM hematopoietic microenvironment is composed of diverse cell types including mesenchymal stromal cells, sympathetic nerve cells, macrophages and vascular smooth muscle cells. Although the subaortic mesenchyme is known to play a key role in AGM hematopoiesis, its molecular identity still remains elusive. To address this critical issue, we designed a laser capture strategy to isolate in the mouse embryo the dorsal and ventral aortic tissues at three developmental stages. By combining bulk and single cell transcriptomics and lineage tracing, I contributed to reveal the existence of a unique mesenchymal cell population expressing both neuronal and mesenchymal genes in the subaortic tissue at embryonic day 11.5. Using loss-of-function experiments and genetic tools in the zebrafish model that I implemented in the team, I showed that Decorin, encoding an extracellular matrix protein, is necessary for HSC development in vivo. Taken together, my PhD project provides new insights on the molecular identity of the AGM hematopoietic microenvironment and leads to the identification of potential novel HSC regulators in the embryo
Boeri, Juliette. "Propriétés d’excitabilité des cellules de Renshaw au cours du développement embryonnaire de la moelle épinière, chez la souris". Thesis, Sorbonne université, 2018. http://www.theses.fr/2018SORUS381.
Pełny tekst źródłaAs many developing neuronal networks, embryonic spinal cord spontaneously generates recurrent synchronized neural activity, which is involved in multiple aspects of motor circuit maturation. During an initial embryonic period (E12.5 to E14.5 in mice), this activity is mainly under the control of acetylcholine, GABA and glycine release. In motoneurons, this activity is characterized by giant depolarizing potentials (GDPs), mainly evoked by a release of GABA, the latter being regulated by the activation of cholinergic receptors, suggesting a recurrent loop between motoneurons and GABAergic interneurons. The mechanisms of this neurotransmitters release and the identification of the first functional GABAergic interneurons interacting with motoneurons are unknown. On this basis, we show that at E12.5, Renshaw cells (RCs) express GABA and also generate GDPs that can evoke multiple action potentials or "plateau potentials". Distinct firing patterns of RCs, in response of injected current, were observed and classified as single-spiking, repetitive-firing or sodium plateau potentials. Between E12.5 and E14.5, while motoneurons intrinsic excitability classically increases, RCs intrinsic excitability surprisingly transitory regresses. We show that the ratios of persistent sodium and potassium voltage-dependent conductances play a major role in determining firing patterns and account for the regression of RCs intrinsic excitability
Jachowicz, Joanna Weronika. "Molecular mechanisms underlying heterochromatin formation in the mouse embryo". Thesis, Strasbourg, 2015. http://www.theses.fr/2015STRAJ094/document.
Pełny tekst źródłaTo study the formation of heterochromatin in mouse preimplantation embryo, I focused on two different genetic regions – pericentric repeats and L1 transposable elements - in order to investigate the mechanisms that lead to their repression and the distinct role that these regions can play during the process of development and cell division. My experiments show that the specific spatial organization of pericentric domains is essential for their repression and for their correct organization. Moreover, my findings suggest that defects in organization of heterochromatin lead to improper cell division and proliferation. The second part of my thesis shows that the tight regulation of L1 transposable elements is required for the preimplantation development of mouse embryos. Additionally, it is the first attempt to elucidate the biology of L1 elements in the early mouse embryo through the use of targeted transcription modifiers
Geiselmann, Anna Maria. "The PI3K/AKT pathway regulates cell fate identities during early mouse development". Electronic Thesis or Diss., Sorbonne université, 2022. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2022SORUS138.pdf.
Pełny tekst źródłaThe early mouse embryo is a unique paradigm for regulative development which requires a fine-tuned balance between plasticity and commitment. In just a few days, the fertilized egg forms a multicellular embryo which is able to attach to and develop intricate connections with the mother's uterine tissue. Initially equivalent, early embryonic cells become restricted in their developmental potential and commit to a specific cell identity while keeping short windows of responsiveness to react to external cues or developmental perturbations. Shortly before implantation, the inner cell mass (ICM) of early blastocysts differentiates into the epiblast (Epi), that will give rise to the fetus, and the primitive endoderm (PrE), at the origin of extraembryonic tissues. Previous studies have established a regulatory network, involving the transcription factors (TFs) NANOG and GATA6 and the FGF/ERK signaling, which controls many aspects of this differentiation process. However, several questions remain about the underlying mechanisms controlling the generation of the first embryonic lineages. The objective of this thesis was to study the role of PI3K/AKT signaling during blastocyst development when first Epi, then PrE cells arise from the uncommitted pool of ICM cells. My work demonstrates that PI3K/AKT is constitutively active during preimplantation development and that variations of signaling activities occur during mid to late blastocyst stages. By modulating pathway activity, I could demonstrate that PI3K/AKT activity is a premise for Epi formation as the Epi-specific TFs NANOG and SOX2 are dramatically reduced and endodermal SOX17 is activated in the absence of PI3K/AKT. I further provide evidence that the regulation of TF patterning in the ICM is, at least in part, mediated by the PI3K/AKT downstream target GSK3. Single cell RNA sequencing (scRNAseq) revealed that PI3K/AKT inhibition induced marginal alterations in the inner cell transcriptome, indicating that PI3K/AKT regulates TFs levels through post-transcriptional mechanisms. Surprisingly, I observed upregulation of SOX17 when PI3K/AKT is inhibited in Gata6 mutant embryos which suggests that initiation of PrE fate requires the release of PI3K/AKT inhibition. In conclusion, this PhD project illustrates that PI3K/AKT, a pathway often associated with controlling survival, proliferation and metabolism, acts also as a mediator of cell fate during a specific and limited period of early mouse development. We propose that PI3K/AKT guards the pluripotency of forming Epi progenitors by maintaining the expression of key Epi markers while simultaneously preventing differentiation towards PrE fate. Thus, my work gives novel and important insights into the regulation of the Epi master TF NANOG in early embryos and identifies signals other than FGF/ERK signaling that participate in lineage decisions independently of the latter
Auclair, Ghislain. "Identification de cibles et régulateurs de la méthylation de l'ADN chez la souris". Thesis, Strasbourg, 2015. http://www.theses.fr/2015STRAJ061.
Pełny tekst źródłaDNA methylation is an epigenetic modification which is established during embryonic development on the mammalian genome. In my thesis, I determined the kinetics of DNA methylation acquisition on the mouse genome during early embryogenesis, and determined the specific and redundant roles of the DNA methyltransferases DNMT3a and DNMT3b in this process. I also studied the roles of two factors involved in setting up DNA methylation in embryos. First, I determined that the G9a enzyme plays an essential role for the in vivo repression and DNA methylation of specific genomic sites, including in particular the CpG island promoters of germline genes. Second, the study of the E2F6 factor allowed me to show that this protein is also involved in recruiting DNA methylation at a set of germline gene promoters than are distinct from those regulated by G9a
Glaser, Juliane. "Functional characterization of the imprinted Liz/Zdbf2 locus in mice : from the early embryo to adult physiology". Electronic Thesis or Diss., Sorbonne université, 2018. http://www.theses.fr/2018SORUS243.
Pełny tekst źródłaGenomic imprinting refers to the epigenetic mechanism by which approximately 120 genes are expressed in a parent-of-origin manner. This parental asymmetry in gene expression is mediated through differential profiles of DNA methylation established in the oocyte and the sperm and maintained after fertilization in the developing individual. In mammals, imprinted genes are essential for normal embryo development as well as behavioral and physiological functions after birth. Clarifying the regulation and the function of those genes is thus fundamental in the field of developmental biology and health. During my PhD, I functionally characterized the imprinted Zdbf2 locus in mice. Zdbf2 is a paternally expressed gene, conserved from mouse to human, whose biological function was unknown. I revealed that Zdbf2 activation in the post-natal brain requires an indelible epigenetic signal that is established during the first days of embryogenesis. Additionally, I provided in vivo evidence that early programming of Zdbf2 is essential for proper growth after birth. By generating multiple CRISPR-mediated genetic mutants with varied doses of Zdbf2 in the hypothalamo-pituitary axis, I finally demonstrated that Zdbf2 is a growth-promoting gene, with a dose-sensitive effect and acting independently of its parental origin. Altogether, my work shed light onto the crucial function of a mammalian imprinted gene, from its regulation in the early embryo to its role in adult physiology
Martin, Julie. "Impact du microenvironnement des cancers du sein sur le protéome membranaire endothélial (MiMEndo)". Electronic Thesis or Diss., Reims, 2023. http://www.theses.fr/2023REIMS046.
Pełny tekst źródłaThe multifunctional endocytosis receptor LRP1 plays a crucial role in regulating cancer cell aggressiveness, fibroblast behavior and angiogenesis. In breast cancer microenvironment, cancer-associated fibroblasts (CAF) play a key role in formation and remodeling of the extracellular matrix and tumor niche. The role of LRP1, highly expressed in CAF, remains poorly described in terms of its influence on endothelial cell behavior.To study the impact of stromal LRP1 expression on angiogenesis, we used different cell models: murine embryonic fibroblasts (MEF-1), MEF-1 invalidated for LRP1 (PEA-13) and CAF2 cells derived from breast cancer, invalidated or not for LRP1 by RNA interference. We used conditioned media and fibroblast-derived matrices to simulate the angiogenic effects of fibroblasts and CAF on endothelial cells.Our results show that LRP1 invalidation in embryonic fibroblasts and mammary CAF results in distinct effects on critical endothelial cell parameters. LRP1 expression in MEF-1 does not affect endothelial functions, while its presence in CAF diminishes angiogenic capacities and directs matrix remodeling processes in a manner unfavorable to endothelial migration. Through a comprehensive proteomic analysis of endothelial surface signaling platforms regulated by CAF-derived signals, we observed differential expression of secreted matrix compounds, surface receptors and membrane-associated proteins as a function of LRP1 expression in secretory cells. Analysis of CAF2-conditioned media revealed LRP1-dependent angiocrine signals, although no differences were detected in glycosaminoglycan composition. In conclusion, LRP1 expression in MEFs has no impact on endothelial functions, whereas in CAFs the receptor reduces angiogenic capacities. The identification of LRP1-modulated targets on the surface of endothelial cells will enable us to decipher the angiogenic pathways controlled by LRP1 in the fibroblastic compartment
Porchet, Nicolas. "Role of signaling pathays in cell-fate specification in the early mouse embryo". Thesis, Université de Paris (2019-....), 2019. http://www.theses.fr/2019UNIP7096.
Pełny tekst źródłaDuring the early mouse embryogenesis, cell-fate specification events result in the formation of the pre-implantation blastocyst. Those events are mainly regulated by the action of signaling cascades activated upon fixation of the signaling molecules at the cell membrane. The activity of these signaling pathways allow the transcriptional regulation of a specific pool of genes responsible for cell-fate decisions and the formation of tissues. Here, I am interested in the roles of both ACTIVIN/NODAL and βCATENIN signaling pathways in the specification of cell identities during the maturation of the mouse blastocyst
Ravens, Sarina. "A genome-wide characterization of Mof or Tip60 containing complexes in mouse embryonic stem cells". Thesis, Strasbourg, 2014. http://www.theses.fr/2014STRAJ097.
Pełny tekst źródłaHistone acetylation is involved in transcriptional activation of genes and is carried out by histone acetyltransferases (HATs), which are part of molecular protein complexes. This study focuses on the genome-wide role of Mof-containing MSL and NSL complexes and the Tip60-p400 complex in mouse embryonic stem cells (mESCs). I have analysed these complexes by ChIP-seq, shRNA knockdown and biochemical approaches. The genome-wide binding studies show that NSL, MSL and Tip60-p400 have a global overlap at promoters, but also bind to specific gene sets. There distinct binding profiles propose distinct roles in transcriptional regulation. MSL is the main H4K16 acetylase in mESCs.NSL binds mainly to housekeeping genes, whereas MSL and Tip60 are also present at developmental genes. Importantly, these developmental genes are directly regulated by MSL during cellular differentiation
Barruet, Emilie. "Rôle de la voie de transduction P38MAPK dans la différenciation des cellules souches embryonnaires de souris". Thesis, Aix-Marseille 2, 2010. http://www.theses.fr/2010AIX20697.
Pełny tekst źródłaEmbryonic stem (ES) cells give rise, in vivo, to all of the three germ layers and, invitro, to differentiate into a broad variety of cell lineages which opens up largeperspectives in regenerative medicine. We previously found that the p38MAPKpathway controls the commitment of ES cells toward either cardiomyogenesis (p38on) or neurogenesis (p38 off ). In this study, we show that p38a knock-out ES cellsdo not differentiate into cardiac, endothelial, smooth muscle, and skeletal musclelineages. Reexpression of p38MAPK in these cells partially rescues theirmesodermal differentiation defects and corrects the high level of spontaneousneurogenesis of knock-out cells. Wild-type ES cells were treated with a p38MAPKspecificinhibitor during the differentiation process. These experiments allowed us toidentify 2 early independent successive p38MAPK functions in the formation ofmesodermal lineages. Further, the first one correlates with the regulation of theexpression of Brachyury, an essential mesodermal-specific transcription factor, byp38MAPK. Moreover, we also showed that p38MAPK is required for the late stageskeletal muscle differentiation. In conclusion, by genetic and biochemicalapproaches, we demonstrate that p38MAPK activity is essential for the commitmentof ES cell into cardiac, endothelial, smooth muscle, and skeletal muscle mesodermallineages
Izvolskaia, Marina. "Rôle potentiel des catécholamines dans la différenciation et la migration des neurones à GnRH chez les foetus de rat et de mouton". Tours, 2004. http://www.theses.fr/2004TOUR4011.
Pełny tekst źródłaGnRH neurons control endocrine processes of reproduction in adult mammals. Most of the GnRH neurons migrate from the olfactory epithelium towards the forebrain during prenatal development. We studied the influence of catecholamines on the migration and differentiation of GnRH neurons in rat and sheep foetuses. We showed that the catecholaminergic influence is most important at the level of penetration of GnRH neurons to the forebrain where the catecholaminergic fibres are opposed to the GnRH neurons. These neurons expressed α2A-adrenergic receptors during migration. Finally, using the model of catecholamine depletion in rat foetuses, we have shown that these molecules stimulate GnRH neurons migration from the nasal part of the head to the forebrain, and control the secretion of GnRH by GnRH neurons. This work confirms the hypothesis that neurotransmitters controlling the regulation of GnRH neurons in the adult are also involved in their development in foetus
Klein, Schneegans Anne-Sophie. "Autoimmunité héréditaire chez la souris : Etiopathologie et traitements". Strasbourg 1, 1988. http://www.theses.fr/1988STR15082.
Pełny tekst źródłaNadeau, Valérie. "Implication de MEK1 et MEK2 dans la morphogenèse du placenta de souris". Doctoral thesis, Université Laval, 2015. http://hdl.handle.net/20.500.11794/25734.
Pełny tekst źródłaThe mammalian genome contains two ERK/MAP kinase kinase genes, Mek1 and Mek2, which encode dual-specificity kinases responsible for ERK/MAP kinase activation. In the mouse, the loss of Mek1 function causes embryonic lethality, whereas Mek2 mutants survive with a normal lifespan, suggesting that Mek1 rescues the lack of Mek2 function. The first objective of my thesis was to clarify potential functions of Mek2 during mouse embryogenesis. To do, I have analyzed the loss of Mek2 function in the presence of Mek1 haploinsufficiency. Most Mek1+/-Mek2+/- embryos die during gestation from placenta defects affecting extra-embryonic tissues. Thus, even though Mek1 plays a predominant role, these results enlightened the function of Mek2 in placenta development. The histological characterization of Mek1+/-Mek2+/- placentas revealed a diminution of the vascularization and an aberrant formation of multinucleated trophoblast giant (MTG) cells. Genetic experiments on the SynT-II cellular lineage in vivo demonstrated that MTG cells derive from the aberrant SynT-II differentiation and that their formation results from a cell-autonomous effect. The second objective of my thesis was to determine in which cell types the ERK/MAPK activation is essential for placenta development. Genetic analyses combined with histological studies revealed that MTG formation resulted from the ectopic fusion between both layers of SynT, which normally participate in an independent way in the blood-placental barrier. The blood-placental barrier is constituted of a double layer of SynT and by the cells derived from the allantois, the endothelial cells and their perycites. The deletion of both Mek1 alleles in allantois-derived tissues in a Mek1+/-Mek2+/- placenta environment increases the penetrance and the expressivity of the MTG phenotype. These results demonstrate the role of the ERK/MAPK pathway in defined embryonic and extraembryonic cell populations for correct placenta formation. Using mouse genetics, we also demonstrated that the normal development of syncytiotrophoblasts type I into a thin layer of multinucleated cells depends on the presence of the syncytiotrophoblasts type II. Finally, the combined mutations of Mek1 and Mek2 genes alter the expression of several genes involved in cell fate specification, cell fusion and cell polarity that likely explain the underdeveloped placenta and the MTG phenotype seen in Mek1Mek2 mutants.
Lescroart, Fabienne. "Recruitment of progenitor cells at the poles of the mouse heart : clonal analyses reveal common origins with a subset of skeletal muscles". Paris 6, 2011. http://www.theses.fr/2011PA066339.
Pełny tekst źródłaDubois, Marilyn, i Marilyn Dubois. "Stimulation cérébrale profonde : développement d'un prototype pour étude chez le petit animal". Master's thesis, Université Laval, 2018. http://hdl.handle.net/20.500.11794/30960.
Pełny tekst źródłaLa stimulation cérébrale profonde (SCP) est une procédure chirurgicale utilisée dans le traitement de divers contextes pathologiques. Ce système, composé d’électrodes implantées dans une région cible du cerveau et d’un neurostimulateur reliés par un fil, permet de délivrer un courant électrique dans une région voulue du cerveau. À ce jour, les mécanismes d’action de la SCP et les effets cellulaires qu’elle engendre demeurent mal connus. Cette problématique découle du fait qu’il existe peu de prototypes de micro-stimulation dans le domaine de la recherche, sans compter que ceux-ci ne répondent pas bien aux critères de cette recherche. Mes travaux de maîtrise visaient donc à développer un système de microstimulation pouvant être utilisé chez la souris et de développer et valider toutes les techniques nécessaires à l’implantation de ce système chez la souris. Au terme de ces travaux, nous avons développé un système de micro-stimulation : 1) utilisable chez la souris 2) pour des protocoles de stimulation chronique de longue durée (jusqu’à 1 mois), 3) possédant des paramètres électriques, semblables à ceux utilisés chez l’humain en clinique, 4) pouvant être ajustés à différents contextes pathologiques. Nous avons aussi développé toutes les techniques nécessaires à son implantation chez la souris. Cet outil novateur permettra d’approfondir notre connaissance des mécanismes d’action et des mécanismes cellulaires sous-jacents aux effets de la SCP et pourra mener, à long terme, à l’identification de nouvelles cibles thérapeutiques.
Deep brain stimulation (DBS) is a surgical procedure used in the treatment of various pathologies. This system, composed of electrodes implanted in a target area in the brain and of a neurostimulator connected by a wire, allows the delivery of an electrical current in a specific area in the brain. To this day, mechanisms of action and cellular effects resulting from DBS remain poorly understood because of a lack of micro-stimulation tools available in the domain and by the fact that these tools do not properly address requirements of this research. To address this challenge, the objectives of my master’s research were to develop a micro-stimulation system usable in mice and to develop and validate required techniques to make this system work in small-sized rodents. Through this study, we have developed a micro-stimulation system that is : 1) usable in mice, 2) able to sustain a long term chronic stimulation (up to 1 month), 3) similar to those used in human in terms of electrical parameters and 4) offering the possibility of adjusting those parameters to various pathological contexts. We also developed the required techniques for its use in mice. This novel tool will allow to deepen our knowledge on the mechanisms of action and cellular mechanisms underlying DBS effects and possibly lead to the identification of new therapeutic targets.
Deep brain stimulation (DBS) is a surgical procedure used in the treatment of various pathologies. This system, composed of electrodes implanted in a target area in the brain and of a neurostimulator connected by a wire, allows the delivery of an electrical current in a specific area in the brain. To this day, mechanisms of action and cellular effects resulting from DBS remain poorly understood because of a lack of micro-stimulation tools available in the domain and by the fact that these tools do not properly address requirements of this research. To address this challenge, the objectives of my master’s research were to develop a micro-stimulation system usable in mice and to develop and validate required techniques to make this system work in small-sized rodents. Through this study, we have developed a micro-stimulation system that is : 1) usable in mice, 2) able to sustain a long term chronic stimulation (up to 1 month), 3) similar to those used in human in terms of electrical parameters and 4) offering the possibility of adjusting those parameters to various pathological contexts. We also developed the required techniques for its use in mice. This novel tool will allow to deepen our knowledge on the mechanisms of action and cellular mechanisms underlying DBS effects and possibly lead to the identification of new therapeutic targets.
Autret, Laurence. "Rôle de l'activité dépendante du calcium au cours du développement et de la maturation des neurones ganglionnaires vestibulaires de souris". Montpellier 2, 2005. http://www.theses.fr/2005MON20126.
Pełny tekst źródłaPothion, Stéphanie. "Déficits comportementaux liés au stress chronique léger imprévisible chez différentes lignées de souris adultes et âgées". Tours, 2004. http://www.theses.fr/2004TOUR4021.
Pełny tekst źródłaEnvironmental factors influence the development of major depression. The unpredictable chronic mild stress (UCMS) model consists to expose mice to differents stressors that mimic stressful events of life. In our study, UCMS induced physical and behavioural alterations in mice : weight loss, sucrose consumption reduction, memory deficit, similar to the symptomatology of human depression. The alterations were different according to the age of animals and according to the strain of mice, suggesting a difference of sensitivity to stress according to the age and the genetic influence in depression. The efficacity of an antidepressant in the restauration of the normal behaviour has also been shown in mice exposed to UCMS. Therefore, the UCMS model allowed the investigation of stress effects on depressive state, cognitive deficits and aging
Richard, Jacques. "La culture d'embryons de rat en tératologie expérimentale". Montpellier 1, 1991. http://www.theses.fr/1991MON13501.
Pełny tekst źródłaLaurent, Audrey. "ZFPIP : identification et caractérisation d’un nouveau gène du développement chez les vertébrés, études chez la souris et le xénope". Rennes, Agrocampus Ouest, 2008. http://www.theses.fr/2008NSARI048.
Pełny tekst źródłaChagraoui, Abdeslam. "Analyse d'effets biochimiques et comportementaux d'agonistes dopaminergiques indirects (Dexamphetamine, GBR 12783, Amineptine) chez la souris". Rouen, 1991. http://www.theses.fr/1991ROUEA003.
Pełny tekst źródłaDebat, Vincent. "Approche théorique et morphométrique du contrôle de la variabilité phénotypique : application à des modèles actuels et fossiles". Montpellier 2, 2000. http://www.theses.fr/2000MON20218.
Pełny tekst źródłaAlescio-Lautier, Béatrice. "Arginine 8-Vasopressine : effet sur les processus mnésiques et sites d'action centraux". Aix-Marseille 1, 1988. http://www.theses.fr/1988AIX11163.
Pełny tekst źródłaPoosti, Roya. "Biochimie et pharmacologie du récepteur CCK-A de rat et de souris : importance de la structure primaire du récepteur". Montpellier 2, 2000. http://www.theses.fr/2000MON20097.
Pełny tekst źródłaTanguay, Gilbert. "L'insuffisance circulatoire et certains de ses effets comportementaux chez la souris de laboratoire". Thèse, Université du Québec à Trois-Rivières, 1990. http://depot-e.uqtr.ca/5642/1/000583343.pdf.
Pełny tekst źródłaNic, Dhonnchadha Brid Aine. "Implication des récepteurs 4-HT2 dans trois modèle animaux d'anxiété chez la souris". Nantes, 2003. http://www.theses.fr/2003NANT23VS.
Pełny tekst źródłaThis thesis explored the role of the 5-HT2 receptor subtypes (5-HT2A, 5-HT2B and 5-HT2C) in the four plate test (FPT), the elevated plus maze (EPM) and the light/dark paradigm (L/D) in mice. Selective acute administration of the 5-HT2A and 5-HT2B receptor agonists (DOI and BW 723C86, respectively) induced potent and consistent anxiolytic-like effects in the FPT. Antidepressants (ADs) are widely employed to treat anxiety disorders. The anxiolytic-like profile of acute paroxetine administration, a selective serotonin reuptake inhibitor (SSRI) in the FPT involves the 5-HT2A receptor subtypes, whereas both the 5-HT2A and 5-HT2B receptors are involved in the effects of venlafaxine, a serotonin and noradrenaline reuptake inhibitor (SNRI). DOI possessed a potent anxiolytic-like profile in the EPM, while BW 723C86 and RO 60-0175 had weaker effects, that were not reproduced, indicating that this model is subject to greater uncontrollable influences. Both selective agonists and antagonists lacked effects in the L/D paradigm. These results indicates that the 5-HT2A and 5-HT2B receptors are involved in the fear induced by the FPT and possibly in that of the EPM, while all three receptor subtypes seem to not participate in the aversive nature of the L/D paradigm. The administration of an anxiolytic dose of DOI in the FPT and EPM reduced serotoninergic activity in the hippocampus and hypothalamus, implicating these structures in the anxiolytic-like effects subsequent to 5-HT2A receptor stimulation
Strassel, Catherine. "Etude du rôle de la GPIbβ dans la thrombopoïèse et les fonctions plaquettaires". Université Louis Pasteur (Strasbourg) (1971-2008), 2004. http://www.theses.fr/2004STR13197.
Pełny tekst źródłaThe glycoprotein (GP) Ib-V-IX complex is a specialized multisubunit receptor abundantly expressed at the surface of platelets and whose physiological role is to ensure normal haemostasis. This property is best illustrated by the existence of a severe bleeding tendency in patients with the rare Bernard-Soulier syndrome resulting from a genetic defect of the GPIb-V-IX complex. Increased bleeding is mainly due to the lack of platelet adhesion to VWF mediated by the complex, resulting in defective platelet plug formation at sites of vessel wall injury. These patients additionally have platelets with enlarged size and decreased numbers in the circulation. The purpose of this work was to evaluate the role, in vivo and in vitro, of the GPIb-V-IX complex, and more particularly the role of GPIb within this complex, in platelet function and in platelet production. For this study, two genetically modified mouse models were engineered. A Bernard-Soulier-like knock-out strain was generated by inactivating the GPIbβ gene (GPIbβ KO) and a knock-in strain was created by interrupting the sequence coding for the GPIbβ intracellular domain (GPIbβC). The GPIbβKO mice exhibited the Bernard-Soulier phenotype, which is thrombocytopenia, giant platelets and a severely prolonged bleeding time. The further perspectives of this work will be to evaluate the function of GPIbβ in haemostatic function and in artertial thrombosis. Another aspect of this work was to evaluate, in vitro, the function of the GPIbβ subunit by transfecting mutated GPIb-IX complex into CHO cells. Three mutations from patients were reproduced and analysed. This study underlined the key role of the GPIbβ in the biosynthesis process and precised the structural domains essential for the complex expression. Overall, these results have provided direct evidence for the involvement of the GPIbβ in platelet function and the transgenic mice will proved useful to directly evaluate the role of this subunit in in vivo thrombosis
Landry-Truchon, Kim. "Étude du rôle tissu-spécifique des gènes Hoxa5 et Yy1 dans le développement du système respiratoire de la souris". Master's thesis, Université Laval, 2015. http://hdl.handle.net/20.500.11794/26542.
Pełny tekst źródłaHox genes encode transcription factors governing complex developmental processes including the anteroposterior patterning of the embryo axis, the specification of the axial and appendicular skeletons as well as the formation of the nervous system and several organs. In the respiratory system, the role of Hoxa5 is critical since the loss of Hoxa5 function causes death at birth of a high proportion of mutant pups due to respiratory distress. HOXA5 protein expression in the mesenchyme of the respiratory tract and in the phrenic motor neurons of the central nervous system led us to address the specific contribution of Hoxa5 in each component to lung development. Using a conditional gene targeting approach, we demonstrated that the genetic ablation of Hoxa5 function in the mesenchyme established the importance of Hoxa5 in trachea development, lung epithelial cell differentiation and lung growth. In parallel, the specific deletion of Hoxa5 in motor neurons resulted in abnormal innervation of the diaphragm, altered diaphragm musculature and lung hypoplasia which are responsible for the neonatal lethality observed in null mutants. Thus, this confirms that a defective diaphragm mainly contributes to impair survival at birth. Hoxa5 expression is under the control of many regulatory elements, one of which is responsible for Hoxa5 expression in the respiratory and digestive tracts. Yin Yang 1 (YY1) is a multifunctional zinc-finger-containing transcription factor that plays crucial roles in numerous biological processes by selectively activating or repressing transcription, depending upon promoter contextual differences and specific protein interactions. We have shown that YY1 regulates Hoxa5 expression in the lung by binding to the lung-specific regulating sequence. However, the mesenchymal loss of Yy1 function causes a lung phenotype similar to the one observed in Hoxa5-/- mutants including neonatal mortality. We then studied how the epithelial-specific inactivation of Yy1 impacts on lung development. The Yy1 epithelial mutation resulted in neonatal death due to respiratory failure. It impaired tracheal cartilage formation, altered cell differentiation, abrogated lung branching and caused airway dilation similar to that seen in human congenital cystic lung diseases, such as the pleuropulmonary blastoma (PPB). Together, our data demonstrate the crucial requirement for YY1 in lung morphogenesis and identify Yy1 mutant mice as a potential model for studying the genetic basis of PPB.
Di, Malta Laure. "Clonage et caractérisation pharmacologique du récepteur de la cholécystokinine de type 1 de souris". Montpellier 1, 2000. http://www.theses.fr/2000MON13520.
Pełny tekst źródłaPopa, Daniela. "Sommeil, sérotonine et dépression : étude de leurs interactions fonctionnelles". Paris 5, 2005. http://www.theses.fr/2005PA05P614.
Pełny tekst źródłaBesse, Laurianne. "Etude de la fonction du gène Ftm/Rpgrip1l dans la régionalisation et la morphogenèse du télencéphale chez la souris". Paris 6, 2011. http://www.theses.fr/2011PA066069.
Pełny tekst źródłaChassagnon, Serge. "Imagerie de perfusion des crises épileptiques temporo-limbiques : zones épileptogènes et non épileptogènes". Université Louis Pasteur (Strasbourg) (1971-2008), 2006. https://publication-theses.unistra.fr/restreint/theses_doctorat/2006/CHASSAGNON_Serge_2006.pdf.
Pełny tekst źródłaTo assess the contribution of the ictal SPECT to the definition of the epileptogenic zone (EZ) prior to surgery in focal drug-resistant epilepsies, we investigated the effect of the variability of clinical and technical parameters upon patterns of perfusion, that could account for ictal cerebral blood flow (CBF) changes beyond the EZ. We studied CBF patterns in a rat model of amygdala-kindled seizures to assess the influence of the timing of injection of the tracer and the extent of seizure spread, with respect to a control group (interictal CBF measurements in kindled rats), during secondary generalized (SGS, n=26 fully-kindled rats) and focal seizures (FS, n=19 partially kindled rats), in 29 regions of interest, with the quantitative [14C]-iodoantipyrine autoradiographic method. During SGS, the correct lateralization and localization of the focus within limbic structures was only possible at early ictal and post-ictal times, in between we observed widespread rCBF increases. The switch from hyper to hypoperfusion was observed at the time of late ictal injection. The accurate localization of the EZ was obtained for the study of the more FS (stage 0). At stage 1 of the kindling, there was already widespread spreading of hyperperfusion. In humans, we studied 26 pairs of ictal and interictal SPECTs from patients with mesial temporal lobe epilepsy, classified in 3 groups according to the progression of ictal semiology. Using visual analysis of subtracted SPECTs (SISCOM) and group comparisons with a control group (using SPM), we observed more widespread combined hyper and hypoperfusion with the increasing complexity and duration of seizures at the time of the ictal SPECT. In the first group with motionless seizures, SISCOM analysis allowed correct localization of the focus in 4/8 patients, whereas SPM analysis failed to detect significant changes, due to individual variation, spatial normalization and small magnitude of CBF changes. In seizures with impairement of consciousness and automatisms (group 2) and dystonic posturing (group 3), SISCOM and SPM analysis showed antero-mesial temporal hyperperfusion (overlapping the EZ), extending to the insula, basal ganglia, and thalamus in the third group. Ictal hypoperfusion involved pre-frontal and parietal regions, the anterior and posterior cingulate gyri, with a greater extent in the 3rd group. In both human and animals studies, we observed a positive correlation between the spatial extent of composite patterns of hyper/hypoperfusion and the severity of seizures, as well as the recruitment of remote sub-cortical structures. We suggest that ictal purposeless human motor automatisms in MTLE results from the hypoactivity of the above mentioned set of hypoperfused areas, whose role in perceptual decision making and motor planning is transiently disrupted under the effect of hyperactive temporo-limbic structures
Ribes, Vanessa. "Importance du contrôle enzymatique des niveaux d'acide rétinoïque au cours du développement murin". Strasbourg 1, 2006. http://www.theses.fr/2006STR13041.
Pełny tekst źródłaThe initial steps of vertebrate development are tightly controlled by the combined action of extrinsic factors, such as retinoic acid (RA) and the proteins Shh and Fgfs. Their integration at the level progenitors leads to the establishment of a spatial identity and to their differentiation. My PhD work dealt with the relevance of the regulated RA levels by two sets of enzymes, the RA-synthesizing enzyme Raldh2 and the cytochrome oxidoreductase Por, whose function is required for the activity of the RA degrading enzymes, the Cyp26s. Using two mouse mutants for these enzymes, we show that appropriate levels of RA are required for the specification of limb bud cells along the antero-posterior and the proximo-distal axis, for the maintenance of several progenitor domains within the forebrain, as well as for the correct patterning of the epiblast, that will give rise to the neuroectoderm and the mesoderm. Morphogenesis of tissues was also severely affected in our mutants, probably as a consequence of cell cycle and/or cell movement defects. Our data also indicate that RA signalling interferes with Shh and Fgf signalling at different levels depending on the cell type examined. These findings support the idea that the competence to a cell to respond to Shh signalling relies on RA activity
Le, Pape Gilles. "Etude expérimentale des facteurs génétiques et épigénétiques de la variabilité interindividuelle du comportement chez la souris domestique mus musculus". Tours, 1985. http://www.theses.fr/1985TOUR4001.
Pełny tekst źródłaSlezak, Michal. "New transgenic mouse models for astrocyte-specific, inducible somatic mutagenesis". Université Louis Pasteur (Strasbourg) (1971-2008), 2007. https://publication-theses.unistra.fr/public/theses_doctorat/2007/SLEZAK_Michal_2007.pdf.
Pełny tekst źródłaAstrocytes, being the most numerous cell population in the central nervous system play a role in synaptogenesis, synaptic transmission, homeostatic processes and development. Unfortunately, most of the data concerning astrocytes comes from in vitro studies. Therefore in my project I have generated new transgenic mouse lines enabling inducible gene manipulation specifically in astrocytes. In these lines tamoxifen-inducible Cre-ERT2 recombinase is expressed under the control of astrocyte-specific promoters: ApoE, Aqp4, Cx30 and Glast). Whereas in lines Tg(ApoE-Cre ERT2) and Tg(Aqp4-Cre ERT2) the level of Cre-mediated recombination is low in the brain, the strong Cre activity was detected in Tg(Cx30-Cre-ERT2) and Tg(GLAST-Cre ERT2) lines. Since the recombination was shown to be astrocyte-specific, the latter two lines shall serve for better understanding the role of astrocytes in vivo
Cocquempot, Olivier. "Invalidation du gène Gasp1 et étude de sa fonction chez la souris". Limoges, 2010. https://aurore.unilim.fr/theses/nxfile/default/7cd780e3-7411-4300-b87e-0c87aa0632e4/blobholder:0/2010LIMO4002.pdf.
Pełny tekst źródłaGenetic mechanisms of myogenesis concern many research projects. Among recent progresses, the identification of the role of myostatin has opened a new way to create new therapeutics for several myopathies. Variants of Gdf8, gene coding for myostatin, were discovered. Myostatin amount are controlled by several mechanisms. Thus Gasp1 is able to link with the myostatin or the myostatin propeptide. It has been shown that Gasp1 controls the proteolytic cleavage necessary to obtain the active form of myostatin. During my thesis, I knock-out the Gasp1 gene in the mouse, and to get better inside into the molecular mechanisms controlling myostatin rates in muscles. Moreover, Gasp1 expression has been studied during embryogenesis and myogenesis
Faideau, Béatrice. "Tolérance à la proinsuline chez la souris". Paris 5, 2005. http://www.theses.fr/2005PA05P626.
Pełny tekst źródłaDeciphering the mechanisms involved in immune tolerance in a normal individual is essential to understand how it can be broken and to propose new therapeutic approaches in type 1 diabetes. Proinsulin is a major autoantigen. The aim of our study is to define how CD4+ T cell tolerance to proinsulin-2 is established and maintain in a non diabetes-prone strain of mice. Proinsulin-2 deficient mice are intolerant to proinsulin-2 in contrast to wt mice. We evidenced the unique functional role of proinsulin-2 expression by radioresistant thymic cells in tolerance induction. Coexpression of proinsulin-2 and an intolerant T cell repertoire did not induce diabetes in normal mice. Although proinsulin-2 expressing islets were able to initiate a non destructive T and B cell immune response b islet cells seem mostly ignored by autoreactive T lymphocytes. Induction of central T cell tolerance and peripheral ignorance are two successive barriers involved in immune tolerance to proinsulin-2
Le, Floc'h Johann. "Imagerie ultrasonore quantitative haute fréquence : application au suivi de la formation du système cardiaque au stade embryonnaire chez la souris". Lyon, INSA, 2003. http://theses.insa-lyon.fr/publication/2003ISAL0031/these.pdf.
Pełny tekst źródłaThe mouse is most notably used to understand the contents of the human genome. Ultrasound is an imaging modality that allows a non-invasive and in vivo study of its development over time. At the same time, however, the mouse imposes constraints linked to spatial and temporal resolution. The development of the cardiovascular system and the backscattering from blood at the very high frequency in the mouse embryo were studied in vivo by using ultrasound frequencies higher than those used in the case of humans. Between 7 and 15 MHz, the evolution of hemodynamic parameters, such as cardiac frequency, was measured. A 3D quantification using a 3D deformable model, was also performed through the segmentation of a volume of ultrasound images. At 40 MHz, changes in blood echogenicity were observed within the embryonic mouse heart between Eds 13. 5 and 17. 5. A 13 dB decrease was measured between Eds 13. 5 and 17. 5, a decrease most likely due to the morphological changes in RBCs
Labussière, Hélène. "Absorption de l'acide oléique : étude en culture organotypique d'intestin de souris adulte". Dijon, 1985. http://www.theses.fr/1985DIJOS027.
Pełny tekst źródłaRielland, Maïté. "Caractérisation des modifications cellulaires et moléculaires responsables des anomalies de développement du trophoblaste chez les embryons de souris issus de transfert nucléaire". Paris 11, 2009. http://www.theses.fr/2009PA112060.
Pełny tekst źródłaReprogramming of a nuclear activity through nuclear transfer (NT) into enucleated oocytes gives rises to living animals although the developmental rate is very low. In the mouse the foetal development of clones is always accompanied by placental hypertrophy. The aim of our study is to understand the primary causes of cellular and molecular abnormalities at the origin of these trophoblast development problems. For this we have taken advantage of the possibility to derive trophoblast stem cells (TS) in vitro. We have derived and characterised TS cell lines from fertilised (TS) and cloned (ntTS) embryos. We have shown that ntTS cells are derived more efficiently and more rapidly than control TS cells. Our results show that ntTS cells are less dependent upon the embryonic factors essential for their self-renewal, FGF4 and Activin A highlighted in particular by the maintenance of self-renewal when the supply of these growth factors is reduced. Nevertheless, FGF4 and Activin pathways seem not to be directly altered in ntTS lines. We are facing a new phenomenon where ntTS cells display some properties close to cancerous cells while still being under control of their environment. Moreover our transcriptomic analyses show that the expression abnormalities observed in ntTS lines are well correlated with the early phenotypes of modified growth in ntTS cells, but could also give some clues about the implantation failures and the later placental defects exhibited by cloned foetuses. To conclude, the model of ntTS cells is particularly pertinent for studying the making-up of the placenta after cloning
Gourbal, Benjamin. "Relations interspécifiques dans le modèle souris BALB/c/Taenia crassiceps. Le "comment" avant le "pourquoi" de la manipulation". Montpellier 2, 2002. http://www.theses.fr/2002MON20078.
Pełny tekst źródłaCrozet, Fabien. "Isolement de gènes spécifiquement exprimés dans l'oreille interne de la souris". Montpellier 1, 1996. http://www.theses.fr/1996MON1T020.
Pełny tekst źródłaGraber, Céline. "Caractérisation fonctionnelle de la protéine de l’hétérochromatine HP1γ chez la souris". Strasbourg, 2011. http://www.theses.fr/2011STRA6171.
Pełny tekst źródłaHP1 proteins are one of the main heterochromatin components. The molecular functions of these proteins have been well characterized but physiological roles of HP1γ are still unknown. In order to elucidate the in vivo functions of HP1γ, I have worked on the consequences of the inactivation of Cbx3 gene, coding for HP1γ, in a murine model. Although some observations remain to be fully established, the results of my work suggest that HP1γ exerts important functions in several physiological processes. We have shown the implication of this protein in several mechanisms of immune response : namely, HP1γ is essential for Th cells migration to spleen and for B cells development during final maturation stages. Furthermore, HP1γ plays a role in class switch recombination by promoting IgG1-expressing cells production. HP1γ is also required for spermatogenesis initiation and for mature spermatozoa release in seminiferous tubes lumen, and this protein seems to be involved in sub-nuclear organization of Sertoli cells. My results suggest that HP1γ, but not HP1α, allows the association of HP1β and TIF1β to heterochromatin, and that this recruitment allows to establish and/or maintain a specific sub-nuclear organization with functional implications. All in all, my results bring new evidences that HP1 family proteins have non-redundant functions in murine physiology
Guillon, Hélène. "Etude du point chaud de recombinaison méiotique Psmb9 chez la souris". Montpellier 2, 2003. http://www.theses.fr/2003MON20093.
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