WorldCat Identities

Perron, Muriel

Overview
Works: 22 works in 25 publications in 2 languages and 30 library holdings
Roles: Thesis advisor, Opponent, Other, Author, Contributor
Publication Timeline
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Most widely held works by Muriel Perron
NEUROGENESE CHEZ XENOPUS LAEVIS : ETUDE DE XEL-1, UN HOMOLOGUE DU GENE ELAV DE DROSOPHILE by Muriel Perron( Book )

2 editions published in 1996 in French and held by 3 WorldCat member libraries worldwide

LES PROTEINES DE LA FAMILLE ELAV/HU SONT SPECIFIQUES DU SYSTEME NERVEUX ET POSSEDENT TROIS MOTIFS RRM (RNA RECOGNITION MOTIF) CAPABLES DE FIXER LE RNA. DEUX GENES DE CETTE FAMILLE ONT ETE CLONES CHEZ LA DROSOPHILE, ELAV ET RBP9. ELAV EST ESSENTIEL AU DEVELOPPEMENT ET A LA MAINTENANCE DU SYSTEME NERVEUX. ON CONNAIT TROIS MEMBRES DE CETTE FAMILLE CHEZ L'HOMME, HUD, HUC ET HEL-N1, DECOUVERTS COMME AUTO-ANTIGENES DANS UNE MALADIE AUTO-IMMUNE NEURO-DEGENERATIVE. AFIN D'ETUDIER LA FONCTION DES PROTEINES DE LA FAMILLE ELAV/HU AU COURS DU DEVELOPPEMENT CHEZ LES VERTEBRES, J'AI ISOLE UN GENE DE CETTE FAMILLE CHEZ LE XENOPE. J'AI APPELE CE NOUVEAU GENE XEL-1 POUR XENOPUS ELAV LIKE 1. XEL-1 EST EXPRIME A PARTIR DU STADE JEUNE BOURGEON CAUDAL DANS LES SYSTEMES NERVEUX CENTRAL ET PERIPHERIQUE. AU NIVEAU DU SYSTEME NERVEUX CENTRAL, XEL-1 EST EXPRIME EN PERIPHERIE DU TUBE NEURAL OU SONT SITUES LES NEURONES POST-MITOTIQUES, ET NON DANS LES CELLULES EN DIVISION DE LA ZONE GERMINATIVE. AFIN DE MIEUX COMPRENDRE LA FONCTION DE XEL-1, J'AI ETUDIE SA DISTRIBUTION SUBCELLULAIRE A L'AIDE D'UNE TECHNIQUE PERMETTANT D'IDENTIFIER DE MANIERE SPECIFIQUE, GRACE A L'UTILISATION D'UN EPITOPE MYC, UN SEUL MEMBRE DE LA FAMILLE ELAV/HU. CES EXPERIENCES MONTRENT QU'UNE PROTEINE XEL-1 EXOGENE EST PRINCIPALEMENT CYTOPLASMIQUE A UN STADE OU XEL-1 ENDOGENE EST EXPRIME. CES RESULTATS SUGGERENT QUE LES PARTENAIRES ET LES CIBLES (PROTEIQUES ET/OU RNA) DE XEL-1 SERAIENT CYTOPLASMIQUES. AINSI XEL-1 POURRAIT ETRE IMPLIQUEE DANS LA STABILITE CYTOPLASMIQUE ET/OU DANS LA REGULATION DE LA TRADUCTION DE MESSAGERS DU SYSTEME NERVEUX. L'ETUDE DE LA FONCTION DE LA PROTEINE XEL-1 AU COURS DU DEVELOPPEMENT DU SYSTEME NERVEUX A ETE REALISEE PAR INJECTION DE RNA XEL-1 DANS DES EMBRYONS DE XENOPE, AFIN DE PERTURBER L'EXPRESSION NORMALE DE LA PROTEINE. LA SUREXPRESSION DE XEL-1 PROVOQUE DES MALFORMATIONS A PARTIR DU STADE BOURGEON CAUDAL, CE QUI ENTRAINE NOTAMMENT UNE ABSENCE D'IL DU COTE DE L'EMBRYON QUI A SUBI L'INJECTION. AU NIVEAU DU TUBE NEURAL, LA ZONE PROLIFERATIVE EST CLAIREMENT AFFECTEE, EVOQUANT UN ARRET PRECOCE DES DIVISIONS CELLULAIRES. CES RESULTATS SUGGERENT QUE XEL-1 POURRAIT BLOQUER LES DIVISIONS CELLULAIRES. D'AUTRE PART, L'EXPRESSION ECTOPIQUE DE XEL-1 DANS L'ECTODERME PROVOQUE DES EXCROISSANCES. CERTAINES CELLULES DE CES EXCROISSANCES EXPRIMENT LE MARQUEUR DE GLANDE ADHESIVE XAG1. L'EXPRESSION NORMALE DE CE GENE EST ACTIVEE PAR LES CELLULES DU NEURECTODERME ANTERIEUR, CE QUI SUGGERE QUE L'EXPRESSION ECTOPIQUE DE XEL-1 INDUIT UNE DIFFERENCIATION NEURALE QUI ENTRAINERAIT L'EXPRESSION DU GENE XAG1 DANS LES CELLULES ADJACENTES. L'ENSEMBLE DE CES RESULTATS SUGGERE QU'AU COURS DU DEVELOPPEMENT NORMAL DU SYSTEME NERVEUX DU XENOPE, LE GENE XEL-1 SERAIT UN FACTEUR DE LA DIFFERENCIATION NEURALE ET AGIRAIT AU NIVEAU CYTOPLASMIQUE
Etude de facteurs transcriptionnels et post-transcriptionnels impliqués dans la spécification des cellules rétiniennes chez Xenopus laevis by Sébastien Boy( Book )

2 editions published in 2004 in French and held by 2 WorldCat member libraries worldwide

Retina is an interesting model to study vertebrate neurogenesis because it is simply organised in three layers and contains only few cell types. Numerous transcription factors are involved in retinogenesis. Among them, bHLH factors play important roles. bHLH activators promote neural differentiation, neurons formation and specification. bHLH repressors tend to limit neuroblasts differentiation and promote gliogenesis.During my thesis, I aimed to isolate post-transcriptionnal factors involved in retinogenesis since genetic regulators so far known to be involved in this process are all transcription factors. I have focused my studies on one of them, a new putative RNA binding protein called XSEB4R. Using overexpression and loss of function experiments, I have shown that Xseb4R is involved in retinogenesis and has a function related to bHLH activators function. I have also shown that some of these factors are upstream Xseb4R. During my thesis, I have also been interested in another novel gene, Xhes2 (Hairy Enhancer of Split). I highlighted that, in addition to promote gliogenesis, as other genes of this family, it also controls neuronal specificity. I have also participated to the determination of the function of the Hedgehog cascade in the development of retinal pigmented epithelium, which is adjacent to neural retina
Diversité neuronale au sein de la rétine : Etude de régulateurs transcriptionnels et post-transcriptionnels by Jean-Philippe Dullin( Book )

in French and held by 2 WorldCat member libraries worldwide

Retinal Degeneration and Regeneration--Lessons From Fishes and Amphibians by Divya Ail( )

1 edition published in 2017 in English and held by 2 WorldCat member libraries worldwide

Etude du rôle de la cascade Hedgehog dans la prolifération des cellules souches rétiniennes chez Xenopus laevis by Marcos Alberto Amato( Book )

2 editions published in 2005 in French and held by 2 WorldCat member libraries worldwide

Au cours de ma thèse, je me suis j'ai analysé le rôle de la cascade Hedgehog (Hh) dans la prolifération des cellules souches et des précurseurs, en utilisant comme modèle la rétine de xénope. Ce modèle constitue un observatoire privilégié pour l'étude du système nerveux grâce à son accessibilité et sa relativement simple organisation ainsi qu'à la présence d'un nombre limité de types cellulaires, ainsi que par la présence, pendant toute la vie de l'animal, d'une population de cellules souches e de neuroblastes en différentiation. Nous avons démontré que les gènes appartenant à la voie Hh, Gli2, Gli3 et Smoothened s'expriment de façon spécifique dans les cellules souches de la rétine de xénope. En outre, les résultats obtenus ont démontré que (1) les cellules souches rétiniennes ont besoin de l'activité de la voie Hh pour se maintenir dans un état prolifératif. (2) La surexpression de la cascade provoque, au contraire, une hyperprolifération des cellules souches et des précurseurs ainsi (3) qu'une forte augmentation des cellules de Müller, les seules cellules gliales de la rétine.Par ailleurs, je me suis intéressé aussi à un autre aspect, peu connu, du développement du système nerveux: la régulation post-transcriptionnelle. Les protéines liant l'ARN représentent les effecteurs de la régulation post-trascriptionnelle. À ce propos, nous avons analysé en détail l'expression de six protéines liant l'ARN appartenant à différentes familles. Nous avons publié un article descriptif récapitulant les expressions de cinq de ces protéines dans la rétine. De plus, j'ai participé à la réalisation d'une étude du rôle de la protéine Xseb4R dans la différentiation rétinienne
Prdm13 forms a feedback loop with Ptf1a and is required for glycinergic amacrine cell genesis in the Xenopus Retina by Nathalie Bessodes( )

1 edition published in 2017 in English and held by 2 WorldCat member libraries worldwide

Exploring nervous system transcriptomes during embryogenesis and metamorphosis in Xenopus tropicalis using EST analysis by Ana C Fierro( )

1 edition published in 2007 in English and held by 2 WorldCat member libraries worldwide

CARACTERISATION DU RESEAU DE SIGNALISATION IMPLIQUE DANS LA MAINTENANCE ET LA PROLIFERATION DES CELLULES SOUCHES DE LA RETINE DU XENOPE by Pauline Cabochette( )

1 edition published in 2014 in French and held by 1 WorldCat member library worldwide

Contrairement aux mammifères adultes, la rétine des amphibiens possède la particularité de croître durant toute la vie de l'animal grâce à l'activité continue d'une population de cellules souches localisée au sein d'une niche bien délimitée, la zone marginale ciliaire (ZMC). Ce modèle offre ainsi la possibilité d'étudier in vivo les mécanismes moléculaires à l'origine du maintien et de la prolifération des cellules souches neurales à des stades post-embryonnaires. Dans ce but, l'identification et la caractérisation des différentes voies de signalisation présentes au sein de la niche biologique des cellules souches rétiniennes est une première étape indispensable. Mon projet de thèse a été divisé en deux objectifs principaux: l'étude des interactions entre les voies Wnt et Hedgehog au sein de la ZMC chez le xénope et la réalisation de l'étude fonctionnelle de Yap, l'effecteur principal de la voie de signalisation Hippo dans ce modèle. Par des approches génétiques et pharmacologiques, la première partie de ce projet a permis de mettre en évidence un antagonisme inattendu entre les signaux Wnt et Hedgehog au sein de la ZMC qui régule l'activité proliférative des cellules souches et des progéniteurs rétiniens. Ce travail nous a conduit à proposer un modèle dans lequel ces deux voies réguleraient la balance prolifération/différenciation dans la rétine post-embryonnaire. Dans un deuxième temps, les expériences de gain et de perte de fonction du gène Yap ont montré que ce dernier joue un rôle essentiel dans la régulation du programme temporel de la phase de réplication de l'ADN des cellules souches rétiniennes. En effet, l'inhibition de Yap entraîne une importante réduction de la durée de la phase S du cycle cellulaire associée à une instabilité génomique. Une surexpression de c-Myc et de la voie p53-p21 semble impliquée dans ce phénotype. Nos travaux nous ont également permis d'identifier un nouveau partenaire de YAP, le facteur de transcription PKNOX1. L'ensemble de ces données nous a ainsi conduit à proposer un modèle selon lequel le complexe YAP/PKNOX1 pourrait être nécessaire au bon déroulement de la phase de réplication des cellules souches, indispensable à la maintenance de l'intégrité du génome de ces cellules et de leur descendance
Unravelling photoreceptor planar polarity and pathology using expansion microscopy by Anna Verschueren( )

1 edition published in 2019 in English and held by 1 WorldCat member library worldwide

L'effet Stiles-Crawford (SCE) est un effet psychophysique, caractérisé par la différence d'intensité perçue entre un faisceau passant par le centre de la pupille (perçu comme plus lumineux) et un faisceau passant par sa périphérie. Son mécanisme physiologique est attribué à un alignement des photorécepteurs vers l'ouverture pupillaire par phototropisme. Nous avons concentré nos recherches sur un complexe protéique pouvant expliquer cet effet : l'interactome des protéines Usher. La fonction de cet interactome dans les photorécepteurs est inconnue. Nous proposons ici qu'à l'instar de son rôle dans les cellules ciliées d'audition, il pourrait jouer un rôle mécanique dans les cônes. Nous avons utilisé la microscopie à expansion comme technique de super-résolution pour étudier la distribution 3D détaillée des protéines du syndrome de Usher et du cytosquelette dans les photorécepteurs de primates. Nous avons montré que ce réseau protéique peut expliquer le maintien de l'alignement des compartiments d'un cône malgré les contraintes mécaniques voire un alignement actif par déformation du réseau d'actine. Nous avons de plus découvert que les cônes suivent une polarité planaire dans la rétine centrée autour de la fovéa. Cette orientation spécifique pourrait contribuer au phototropisme associé au SCE. Pour permettre l'observation future de cet alignement à l'échelle de la rétine entière, nous avons utilisé la microscopie à expansion pour améliorer la résolution de la microscopie en feuille de lumière. Ce couplage de techniques nous a permis de développer un nouvel outil inestimable pour l'observation immunohistochimique normale et pathologique de la rétine entière
Etude de la signalisation Hippo/YAP dans les cellules gliales de Müller en conditions physiologiques et pathologiques de dégénérescence rétinienne chez la souris by Annaïg Hamon( )

1 edition published in 2017 in French and held by 1 WorldCat member library worldwide

Retinal dystrophies are one of the main causes of blindness. Among the different therapeutic strategies currently studied, our team is interested in the regenerative potential of endogenous retinal cells. A cellular source of interest are Müller cells, which are the main type of glial cells in the retina. These cells are able to reactivate in case of retinal degeneration and adopt various characteristics of stem cells. They enter a state called reactive gliosis. While in some species such as the fish, they allow the complete regeneration of the retina, they have very limited and ineffective regenerative capacities in mammals. Increasing our knowledge of the complex molecular response of Müller cells to retinal degeneration is thus essential for the development of promising new therapeutic strategies. In this context, the aim of my thesis project was to study the role of the co-transcription factor YAP in Müller cells reactivation. This protein is the main effector of the Hippo signaling pathway which is a crucial player in the field of stem cell biology and regeneration.As a first step, we performed a transcriptomic analysis, which revealed that the Hippo/YAP pathway is one of the main signaling deregulated in a mouse model of photoreceptor degeneration. In particular, we found that YAP is specifically expressed in Müller cells and strongly upregulated upon retinal degeneration, when these cells are reactivated. We thus uncovered for the first time a link between the Hippo/YAP pathway and reactive gliosis in the retina. Consequently, the second part of my thesis project was to undertake a functional study of YAP in Müller cells. For this purpose, we generated, by crossing, a mouse model allowing for Yap conditional knockout specifically in these cells. This model allowed us to show that Yap deletion leads to deregulation of several Müller cell specific genes. A phenotypic analysis revealed that these molecular deregulations lead to premature aging of Müller cells and visual defects in old mice. These results suggest that YAP is required for normal function of Müller glial cells. We then studied the impact of Yap deletion in Müller cells under degenerative conditions. A transcriptomic analysis revealed that various aspects of the molecular response of reactive Müller cells are affected in the absence of Yap. Among the deregulated biological processes, we focussed in particular in the regulation of cell proliferation. We found that YAP is required to trigger cell cycle gene upregulation that occurs in Müller glial cells following photoreceptor cell death. Furthermore, our results suggest that some components of the EGFR signaling pathway, which is known for its central role in the reactivation of Müller cells in pathological conditions, are regulated by YAP in Müller cells.Taken together, these results highlight the importance of YAP (i) in Müller cell function under physiological conditions to maintain retinal homeostasis, and (ii) in the regulation of Müller cell reactivation process under degenerative conditions. Moreover, these data allow us to propose a model in which YAP would be involved in the control of Müller glia cell cycle re-entry through its interaction with the EGFR signaling pathway. Therefore, this work has contributed to increase our knowledge of the signaling network involved in the reactivation of Müller cells in the mammalian retina
Finding novel Neural Crest regulators : Pfkfb4, a key glycolysis partner, controls Neural Crest early patterning in Xenopus laevis by Caterina Pegoraro( )

1 edition published in 2012 in English and held by 1 WorldCat member library worldwide

Neural Crest (NC) is a transient population of multipotent cells that arises at the border between neural and non-neural ectoderm, in a region named the neural border (NB). As the neural border elevates to form the neural tube, NC cells undergo an Epithelial-To-Mesenchymal Transition (EMT), migrate extensively into the whole body to reach their final destinations and differentiate. They give rise to multiple derivatives: neurons and glia, head cartilage, bones and connective tissue, pigment cells, sympatho-adrenal cells. All these processes are regulated by the concerted actions of several genes that form a complex Gene Regulatory Network (GRN), in which many interactions have been elucidated, but even more relationships still need to be understood. Misregulation of genes normally involved in NC formation causes birth defects called neurocristopathies. Moreover, the EMT that NC cells undergo before migration also takes place when cancer cells become metastatic: the molecular events and many of the genes involved in EMT and migration are shared between NC development and cancer. The links with metastasis, neurocristopathies and the fact that still little is known about the earliest steps of NC formation, highlight the importance and the interest in understanding the Gene Regulatory Network (GRN) leading to NC formation and EMT.In the laboratory, we are interested in the early steps of NC induction and specification. In order to identify genes preferentially involved in early NC development compared to genes involved in neural and non-neural ectoderm formation, a transcriptome screen on different microdissected embryonic tissues has been performed. The validation of the results of the screen revealed several interesting genes with a potential function in NC formation. We focused particularly on two of them, due to their original function compared to the majority of the genes involved in NC development: serca1 and pfkfb4, a calcium homeostasis regulator and a glycolysis regulator respectively. We analysed the expression patterns of serca and pfkfb family genes during Xenopus laevis development. Then, due to its specific expression in NC, we studied more in details the role of pfkfb4 in NC formation. This analysis revealed that pfkfb4 is necessary for neural and neural crest specification. However, despite its known role in glycolysis, pfkfb4 morphant phenotype in Xenopus laevis embryos is not due to an alteration of the glycolytic pathway.In conclusion, our results reveal a novel extra-glycolytic role for Pfkfb4 during Xenopus laevis embryonic development
Profil de méthylation de l'ADN des cellules souches d'épiblaste issues d'embryons après fécondation ou clonage et comparaison avec les cellules souches embryonnaires chez la souris by Anne-Clémence Veillard( )

1 edition published in 2013 in French and held by 1 WorldCat member library worldwide

Pluripotent stem cells are of great therapeutic interest because of their capability to give rise to all the cells composing an organism. We can derive two types of these stem cells from the mouse embryo: embryonic stem cells (ESCs) from the blastocyst and epiblast stem cells (EpiSCs) from the egg cylinder stage. These two cell types share their pluripotent properties but are distinct on several features, like their culture conditions and gene expression. We showed that reprogramming using cloning by nuclear transfer allows the obtention of EpiSCs with a methylome and a transcriptome similar to those of EpiSCs derived from embryo after fertilisation. We also characterised the DNA methylation pattern of EpiSCs and showed their tendency to present a hypermethylation at their promoters compared to ESCs and epiblast. We also observed that the absence of DNA methylation blocks the conversion of ESCs into EpiSCs. As a conclusion, it seems that EpiSCs are strongly dependant of DNA methylation to regulate gene expression, which distinguishes them from ESCs
Degeneration and Regeneration in the Vertebrate Retina by Gabriele Colozza( Book )

1 edition published in 2011 in English and held by 1 WorldCat member library worldwide

Degeneration and Regeneration in the Vertebrate Retina
Rôle des répresseurs transcriptionnels Hes1/4 dans la maintenance des cellules souches rétiniennes chez Xenopus laevis by Warif Abdelhamid El yakoubi( )

1 edition published in 2012 in French and held by 1 WorldCat member library worldwide

The retina of fish and amphibian contains genuine neural stem cells located at the most peripheral edge of the ciliary marginal zone (CMZ). However, their cell-of-origin as well as the mechanisms that sustain their maintenance during development are presently unknown. We identified Hes1 and Hes4 (previously named XHairy1 and XHairy2, respectively), genes encoding bHLHO transcriptional repressors, as stem cell specific markers of the CMZ that are positively regulated by the canonical Wnt pathway and differentially regulated by Hedgehog signalling. We found that during retinogenesis, Hes1/4 labels a small territory, located first at the pigmented epithelium (RPE)/neural retina (NR) border and latter in the retinal margin, that likely gives rise to adult retinal stem cells. Our gain of function experiments show that Hes1/4 cell autonomously prevent retinal precursor cells from commitment towards retinal fates and maintain them in a proliferative state. Besides, our data highlight for the first time that Hes1/4 may also constitute crucial regulators of cell cycle kinetics. Hes1/4 gain of function indeed significantly slow down cell division, mainly through the lengthening of G1 phase. As a whole, we propose that Hes1/4 maintain particular stemness features in a cellular cohort dedicated to constitute the adult retinal stem cell pool, by keeping it in an undifferentiated and slowly proliferative state along embryonic retinogenesis
The Transcription Factor Barhl2 Inhibits Wnt Canonical Signaling during Xenopus Embryogenesis by Elena Sena( )

1 edition published in 2018 in English and held by 1 WorldCat member library worldwide

Etude des mécanismes de maintenance et de spécification des cellules souches et progénitrices de la rétine du xénope by Nicolas Mazurier( )

1 edition published in 2012 in French and held by 1 WorldCat member library worldwide

My thesis research work aimed to better understand the molecular mechanisms underlying proliferation and specification of retinal progenitors in Xenopus through three main projects. As the mechanisms governing specification of retinal progenitors towards the different neuronal subtypes are still poorly understood, I focused my work on the role of Ascl1, a bHLH transcription factor, in cell-subtype determination during retinogenesis. Using in vivo gain- and loss-of-function experiments, I have investigated Ascl1's epistatic relationships with other bHLH factors and identified its transcriptional targets. My results indicate that Ascl1 (i) is implicated in the genesis of retinal GABAergic neurons (ii) is epistatic to glutamatergic factors such as Neurog2, NeuroD1 and Atoh7 (iii) that its basic DNA-biding domain is sufficient for its GABAergic-inducing activity (iv) and that this activity involves a direct regulation of the Ptf1a transcription factor. The correct order of neural cell types and subtypes formation is tightly coordinated with the timing of cell-cycle exit of retinal progenitors. Ongoing work in the laboratory, to which I have contributed, was therefore investigating the role of signaling pathways controlling retinal precursor proliferation in this process. Using in vivo genetic and pharmacological tools, we have shown that an antagonistic cross-regulation between Wnt and Hedgehog signaling governs stem cell and progenitor proliferation in post-embryonic retina. Preliminary data shows that Wnt and Hedgehog have opposite effects on both cell cycle exit and kinetics and may therefore regulate the proliferation/differentiation balance in the post-embryonic retina. Lastly, in order to broaden our knowledge on the transcriptional and signaling networks which govern proliferation and cell fate determination in the retina, I have participated in a large scale screen by in situ hybridization aiming to identify new molecular markers of different retinal cell population. Many genes that are exclusively expressed in retinal stem cells or progenitors are promising candidates for future functional studies
L'étude des mécanismes moléculaires de l'épissage alternatif du gène NXNL1 et celle de l'origine de la signalisation métabolique de RdCVF by Najate Ait-Ali( )

1 edition published in 2018 in French and held by 1 WorldCat member library worldwide

The nucleoredoxin-like 1 gene (NXNL1), which is composed by two exons and one intron, encodes for RdCVF made from an unspliced mRNA and RdCVF-long (RdCVFL), an active thioredoxin, when the intron is excised. RdCVFL is an enzyme that protects photoreceptors against oxidative stress. RdCVF is only expressed and secreted by the rods and interacts with its receptor basigin 1 (BSG1), expressed by cones and stimulates glucose entry. So in retinitis pigmentosa, characterized by progressive rods degeneration, RdCVF is no longer expressed and cones die. RdCVF corresponds to a truncated thioredoxin-like protein with no thiol-oxidoreductase activity. According to the knowledge of retina evolution, the cones are rods ancestors and NXNL1 originally encode for the RdCVFL, and today, mammalian cones only expresses this protein. In hydra that appeared 600 million years ago, ancestral NXNL gene was found, RdCVFL protects it against free radicals attack and RdCVF already existed. But hydra basigin doesn't interact with RdCVF, so it lacks one of the metabolic signaling actors of RdCVF in hydra. 400 million years ago, In lamprey only rods produce RdCVF. Lamprey BSG1 binds RdCVF; actors signaling were present in oldest vertebrate that present functional rods. This original alternative splicing system has played a role during evolution by adding a new function of NXNL1 gene leading to a benefit in vision. I identified a sequence in 3' RNA of exon n°1 of NXNL1 gene that binds the nucleolin protein involved in splicing and expressed by the rods but not by the cones. This protein must regulate the NXNL1 alternative splicing
Role of the Glycogen Synthase Kinase 3 for the Retinal Development and Homeostasis by François Paquet-Durand( )

1 edition published in 2018 in English and held by 1 WorldCat member library worldwide

Étude du lignage des cellules progénitrices rétiniennes chez le poulet : origine des classes et types neuronaux by Franck Maurinot( )

1 edition published in 2019 in French and held by 1 WorldCat member library worldwide

Les mécanismes régulant la génération des différents types neuronaux du système nerveux pendant le développement des vertébrés sont encore mal connus. Au cours de cette thèse, la composition et l'organisation des clones de neurones générés par des cellules progénitrices rétiniennes (RPC) individuelles ont été étudiées chez le poulet avec la stratégie Brainbow. Celle-ci permet de marquer de façon permanente les RPC avec des combinaisons de couleurs distinctes pour suivre leur lignage. Des approches ont été développées pour : 1) déclencher le marquage Brainbow à différents stades de développement ou dans des RPC spécifiques ; 2) caractériser en 3D l'organisation cellulaire des clones rétiniens et identifier les types cellulaires générés. Une dispersion tangentielle inédite des RPC a été mise en évidence dans le neuroépithélium rétinien avant la phase de neurogenèse, conduisant à l'intercalation uniforme des clones. La composition des clones a été analysée pour comprendre si les RPC précoces pourraient être biaisées à générer certains types neuronaux et contribuer par leur intercalation à leur répartition régulière dans la rétine. Ce travail a permis l'étude des potentialités d'une population de progéniteurs neuraux et l'exploration des liens entre développement précoce et organisation d'un tissu par de nouvelles approches applicables à des problématiques variées
Caractérisation du rôle clé de Mab21l2 dans le développement de la rétine et du rhombencéphale chez le poisson-zèbre by Anaïs Vitrac( )

1 edition published in 2020 in French and held by 1 WorldCat member library worldwide

Mutations in the MAB21L2 gene have been associated with major eye developmental malformations including coloboma and microphtalmia, occasionally coupled with skeletal dysplasia and intellectual disability. Mab21l2, one of three members of Mab21 gene family, indeed plays a key role in cell fate and differentiation during embryonic development while its lack leads to severe defects in the formation of the vertebrate visual system. However, Mab21l2 function remains poorly understood, and although it is highly expressed in the hindbrain, the impact of its depletion on this developing structure had yet to be investigated. My PhD project thereby aimed at : (i) refining the characterisation of the phenotype associated with the lack of Mab21l2 both in the visual system and in the hindbrain during development of the zebrafish via a dual approach of partial (i.e., antisense RNA technology) or total (establishment of a mutant line using the CRISPR/Cas9 strategy) loss of function; and (ii) identifying Mab21l2 target genes by a comparative transcriptomic analysis. My results have so far shown that partial or total loss of Mab21l2 leads to similar defects such as abnormal architecture of the retina, defects in axon outgrowth and navigation of the retinal ganglion cells, and a severe disorganisation of the hindbrain metameric structure. Moreover, using the tools I have developed in the lab, I observed that the lack of Mab21l2 resulted in changes in gene expression, which pointed at a regulating role for Mab21l2 in the cell cycle as well as in major molecular pathways such as Wnt and FGF signalling
 
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Associated Subjects
Degeneration and Regeneration in the Vertebrate Retina
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Alternative Names
Muriel Perron wetenschapper

Languages
French (15)

English (8)