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Unraveling the impact of IL1RAPL1 mutations on synapse formation : towards potential therapies for intellectual disability

Author: Mariana RamosPierre BilluartPatricia GasparBarbara BardoniCyrille VaillendAll authors
Publisher: 2015.
Dissertation: Thèse de doctorat : Neurosciences : Sorbonne Paris Cité : 2015.
Edition/Format:   Computer file : Document : Thesis/dissertation : English
Summary:
L'intégrité des synapses neuronales est primordiale pour le développement et le maintien des capacités cognitives. Des mutations dans des gènes codant pour des protéines synaptiques ont été trouvées chez des patients atteints de déficience intellectuelle (DI), qui est une maladie neurodéveloppementale ayant des conséquences sur les fonctions intellectuelles et adaptatives. Ce travail de thèse porte sur
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Genre/Form: Thèses et écrits académiques
Material Type: Document, Thesis/dissertation, Internet resource
Document Type: Internet Resource, Computer File
All Authors / Contributors: Mariana Ramos; Pierre Billuart; Patricia Gaspar; Barbara Bardoni; Cyrille Vaillend; Université Sorbonne Paris Cité.; École doctorale Bio Sorbonne Paris Cité (Paris).; Université Paris Descartes (1970-2019).
OCLC Number: 957262541
Notes: Titre provenant de l'écran-titre.
Description: 1 online resource
Responsibility: Mariana Ramos ; sous la direction de Pierre Billuart.

Abstract:

L'intégrité des synapses neuronales est primordiale pour le développement et le maintien des capacités cognitives. Des mutations dans des gènes codant pour des protéines synaptiques ont été trouvées chez des patients atteints de déficience intellectuelle (DI), qui est une maladie neurodéveloppementale ayant des conséquences sur les fonctions intellectuelles et adaptatives. Ce travail de thèse porte sur l'étude de l'un de ces gènes, IL1RAPL1, dont les mutations sont responsables d'une forme non-syndromique de DI liée au chromosome X, et sur le rôle de la protéine IL1RAPL1 dans la formation et le fonctionnement des synapses. IL1RAPL1 est une protéine trans-membranaire qui est localisée dans les synapses excitatrices où elle interagit avec les protéines post-synaptiques PSD-95, RhoGAP2 et Mcf2l. De plus, IL1RAPL1 interagit en trans- avec une protéine phosphatase présynaptique, PTPd, via son domaine extracellulaire. Nous avons étudié les conséquences fonctionnelles de deux nouvelles mutations qui affectent le domaine extracellulaire d'IL1RAPL1 chez des patients présentant une DI. Ces mutations conduisent soit à une diminution de l'expression de la protéine, soit à une réduction de l'interaction avec PTPd affectant ainsi la capacité d'IL1RAPL1 à induire la formation de synapses excitatrices. En absence d'IL1RAPL1, le nombre ou la fonction des synapses excitatrices est diminué, ce qui mène à un déséquilibre entre les transmissions synaptiques excitatrice et inhibitrice dans des régions spécifiques du cerveau. Dans le cas particulier de l'amygdale latérale, nous avons montré que ce déséquilibre conduit à des défauts de mémoire associative chez la souris déficiente en Il1rapl1. L'ensemble des résultats qui font partie de ce travail montre que l'interaction IL1RAPL1/PTPd est essentielle pour la formation des synapses et suggère que les déficits cognitifs des patients avec une mutation dans il1rapl1 proviennent du déséquilibre de la balance excitation/ inhibition. Ces observations ouvrent des perspectives thérapeutiques visant à rétablir cette balance dans les réseaux neuronaux affectés.

Preserving the integrity of neuronal synapses is important for the development and maintenance of cognitive capacities. Mutations on a growing number of genes coding for synaptic proteins are associated with intellectual disability (ID), a neurodevelopmental disease characterized by deficits in adaptive and intellectual functions. The present work is dedicated to the study of one of those genes, IL1RAPL1, and the role of its encoding protein in synapse formation and function. IL1RAPL1 is a trans-membrane protein that is localized at excitatory synapses, where it interacts with the postsynaptic proteins PSD-95, RhoGAP2 and Mcf2l. Moreover, the extracellular domain of IL1RAPL1 interacts trans-synaptically with the presynaptic phosphatase PTPd. We studied the functional consequences of two novel mutations identified in ID patients affecting this IL1RAPL1 domain. Those mutations lead either to a decrease of the protein expression or of its interaction with PTPd, affecting in both cases the IL1RAPL1-mediated excitatory synapse formation. In the absence of IL1RAPL1, the number or function of excitatory synapses is perturbed, leading to an imbalance of excitatory and inhibitory synaptic transmissions in specific brain circuits. In particular, we showed that this imbalance in the lateral amygdala results in associative memory deficits in mice lacking Il1rapl1. Altogether, the results included in this work show that IL1RAPL1/PTPd interaction is essential for synapse formation and suggest that the cognitive deficits in ID patients with mutations on IL1RAPL1 result from the imbalance of the excitatory and inhibitory transmission. These observations open therapeutic perspectives aiming to reestablish this balance in the affected neuronal circuits.

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<http:\/\/www.worldcat.org\/oclc\/957262541<\/a>> # Unraveling the impact of IL1RAPL1 mutations on synapse formation : towards potential therapies for intellectual disability<\/span>\n\u00A0\u00A0\u00A0\u00A0a \nbgn:Thesis<\/a>, schema:MediaObject<\/a>, bgn:ComputerFile<\/a>, schema:CreativeWork<\/a> ;\u00A0\u00A0\u00A0\nbgn:inSupportOf<\/a> \"Th\u00E8se de doctorat : Neurosciences : Sorbonne Paris Cit\u00E9 : 2015.<\/span>\" ;\u00A0\u00A0\u00A0\nlibrary:oclcnum<\/a> \"957262541<\/span>\" ;\u00A0\u00A0\u00A0\nlibrary:placeOfPublication<\/a> <http:\/\/id.loc.gov\/vocabulary\/countries\/fr<\/a>> ;\u00A0\u00A0\u00A0\nschema:about<\/a> <http:\/\/experiment.worldcat.org\/entity\/work\/data\/3809883527#Thing\/synapses<\/a>> ; # Synapses<\/span>\n\u00A0\u00A0\u00A0\nschema:about<\/a> <http:\/\/dewey.info\/class\/612.8\/<\/a>> ;\u00A0\u00A0\u00A0\nschema:about<\/a> <http:\/\/experiment.worldcat.org\/entity\/work\/data\/3809883527#Thing\/il1rapl1<\/a>> ; # IL1RAPL1<\/span>\n\u00A0\u00A0\u00A0\nschema:about<\/a> <http:\/\/experiment.worldcat.org\/entity\/work\/data\/3809883527#Thing\/balance_excitation_inhibition<\/a>> ; # Balance excitation\/inhibition<\/span>\n\u00A0\u00A0\u00A0\nschema:about<\/a> <http:\/\/experiment.worldcat.org\/entity\/work\/data\/3809883527#Topic\/reseaux_neuronaux_physiologie<\/a>> ; # R\u00E9seaux neuronaux (physiologie)<\/span>\n\u00A0\u00A0\u00A0\nschema:about<\/a> <http:\/\/experiment.worldcat.org\/entity\/work\/data\/3809883527#Topic\/deficience_intellectuelle<\/a>> ; # D\u00E9ficience intellectuelle<\/span>\n\u00A0\u00A0\u00A0\nschema:about<\/a> <http:\/\/experiment.worldcat.org\/entity\/work\/data\/3809883527#Topic\/neurosciences_cognitives<\/a>> ; # Neurosciences cognitives<\/span>\n\u00A0\u00A0\u00A0\nschema:author<\/a> <http:\/\/experiment.worldcat.org\/entity\/work\/data\/3809883527#Person\/ramos_mariana_1985<\/a>> ; # Mariana Ramos<\/span>\n\u00A0\u00A0\u00A0\nschema:contributor<\/a> <http:\/\/experiment.worldcat.org\/entity\/work\/data\/3809883527#Person\/vaillend_cyrille<\/a>> ; # Cyrille Vaillend<\/span>\n\u00A0\u00A0\u00A0\nschema:contributor<\/a> <http:\/\/experiment.worldcat.org\/entity\/work\/data\/3809883527#Organization\/universite_sorbonne_paris_cite<\/a>> ; # Universit\u00E9 Sorbonne Paris Cit\u00E9.<\/span>\n\u00A0\u00A0\u00A0\nschema:contributor<\/a> <http:\/\/experiment.worldcat.org\/entity\/work\/data\/3809883527#Person\/billuart_pierre<\/a>> ; # Pierre Billuart<\/span>\n\u00A0\u00A0\u00A0\nschema:contributor<\/a> <http:\/\/experiment.worldcat.org\/entity\/work\/data\/3809883527#Organization\/universite_paris_descartes_1970_2019<\/a>> ; # Universit\u00E9 Paris Descartes (1970-2019).<\/span>\n\u00A0\u00A0\u00A0\nschema:contributor<\/a> <http:\/\/experiment.worldcat.org\/entity\/work\/data\/3809883527#Person\/gaspar_patricia<\/a>> ; # Patricia Gaspar<\/span>\n\u00A0\u00A0\u00A0\nschema:contributor<\/a> <http:\/\/experiment.worldcat.org\/entity\/work\/data\/3809883527#Person\/bardoni_barbara<\/a>> ; # Barbara Bardoni<\/span>\n\u00A0\u00A0\u00A0\nschema:contributor<\/a> <http:\/\/experiment.worldcat.org\/entity\/work\/data\/3809883527#Organization\/ecole_doctorale_bio_sorbonne_paris_cite_paris<\/a>> ; # \u00C9cole doctorale Bio Sorbonne Paris Cit\u00E9 (Paris).<\/span>\n\u00A0\u00A0\u00A0\nschema:datePublished<\/a> \"2015<\/span>\" ;\u00A0\u00A0\u00A0\nschema:description<\/a> \"Preserving the integrity of neuronal synapses is important for the development and maintenance of cognitive capacities. Mutations on a growing number of genes coding for synaptic proteins are associated with intellectual disability (ID), a neurodevelopmental disease characterized by deficits in adaptive and intellectual functions. The present work is dedicated to the study of one of those genes, IL1RAPL1, and the role of its encoding protein in synapse formation and function. IL1RAPL1 is a trans-membrane protein that is localized at excitatory synapses, where it interacts with the postsynaptic proteins PSD-95, RhoGAP2 and Mcf2l. Moreover, the extracellular domain of IL1RAPL1 interacts trans-synaptically with the presynaptic phosphatase PTPd. We studied the functional consequences of two novel mutations identified in ID patients affecting this IL1RAPL1 domain. Those mutations lead either to a decrease of the protein expression or of its interaction with PTPd, affecting in both cases the IL1RAPL1-mediated excitatory synapse formation. In the absence of IL1RAPL1, the number or function of excitatory synapses is perturbed, leading to an imbalance of excitatory and inhibitory synaptic transmissions in specific brain circuits. In particular, we showed that this imbalance in the lateral amygdala results in associative memory deficits in mice lacking Il1rapl1. Altogether, the results included in this work show that IL1RAPL1\/PTPd interaction is essential for synapse formation and suggest that the cognitive deficits in ID patients with mutations on IL1RAPL1 result from the imbalance of the excitatory and inhibitory transmission. These observations open therapeutic perspectives aiming to reestablish this balance in the affected neuronal circuits.<\/span>\" ;\u00A0\u00A0\u00A0\nschema:description<\/a> \"L\'int\u00E9grit\u00E9 des synapses neuronales est primordiale pour le d\u00E9veloppement et le maintien des capacit\u00E9s cognitives. Des mutations dans des g\u00E8nes codant pour des prot\u00E9ines synaptiques ont \u00E9t\u00E9 trouv\u00E9es chez des patients atteints de d\u00E9ficience intellectuelle (DI), qui est une maladie neurod\u00E9veloppementale ayant des cons\u00E9quences sur les fonctions intellectuelles et adaptatives. Ce travail de th\u00E8se porte sur l\'\u00E9tude de l\'un de ces g\u00E8nes, IL1RAPL1, dont les mutations sont responsables d\'une forme non-syndromique de DI li\u00E9e au chromosome X, et sur le r\u00F4le de la prot\u00E9ine IL1RAPL1 dans la formation et le fonctionnement des synapses. IL1RAPL1 est une prot\u00E9ine trans-membranaire qui est localis\u00E9e dans les synapses excitatrices o\u00F9 elle interagit avec les prot\u00E9ines post-synaptiques PSD-95, RhoGAP2 et Mcf2l. De plus, IL1RAPL1 interagit en trans- avec une prot\u00E9ine phosphatase pr\u00E9synaptique, PTPd, via son domaine extracellulaire. Nous avons \u00E9tudi\u00E9 les cons\u00E9quences fonctionnelles de deux nouvelles mutations qui affectent le domaine extracellulaire d\'IL1RAPL1 chez des patients pr\u00E9sentant une DI. Ces mutations conduisent soit \u00E0 une diminution de l\'expression de la prot\u00E9ine, soit \u00E0 une r\u00E9duction de l\'interaction avec PTPd affectant ainsi la capacit\u00E9 d\'IL1RAPL1 \u00E0 induire la formation de synapses excitatrices. En absence d\'IL1RAPL1, le nombre ou la fonction des synapses excitatrices est diminu\u00E9, ce qui m\u00E8ne \u00E0 un d\u00E9s\u00E9quilibre entre les transmissions synaptiques excitatrice et inhibitrice dans des r\u00E9gions sp\u00E9cifiques du cerveau. Dans le cas particulier de l\'amygdale lat\u00E9rale, nous avons montr\u00E9 que ce d\u00E9s\u00E9quilibre conduit \u00E0 des d\u00E9fauts de m\u00E9moire associative chez la souris d\u00E9ficiente en Il1rapl1. L\'ensemble des r\u00E9sultats qui font partie de ce travail montre que l\'interaction IL1RAPL1\/PTPd est essentielle pour la formation des synapses et sugg\u00E8re que les d\u00E9ficits cognitifs des patients avec une mutation dans il1rapl1 proviennent du d\u00E9s\u00E9quilibre de la balance excitation\/ inhibition. Ces observations ouvrent des perspectives th\u00E9rapeutiques visant \u00E0 r\u00E9tablir cette balance dans les r\u00E9seaux neuronaux affect\u00E9s.<\/span>\" ;\u00A0\u00A0\u00A0\nschema:exampleOfWork<\/a> <http:\/\/worldcat.org\/entity\/work\/id\/3809883527<\/a>> ;\u00A0\u00A0\u00A0\nschema:genre<\/a> \"Th\u00E8ses et \u00E9crits acad\u00E9miques<\/span>\" ;\u00A0\u00A0\u00A0\nschema:inLanguage<\/a> \"en<\/span>\" ;\u00A0\u00A0\u00A0\nschema:name<\/a> \"Unraveling the impact of IL1RAPL1 mutations on synapse formation : towards potential therapies for intellectual disability<\/span>\" ;\u00A0\u00A0\u00A0\nschema:productID<\/a> \"957262541<\/span>\" ;\u00A0\u00A0\u00A0\nschema:url<\/a> <http:\/\/www.theses.fr\/2015USPCB058\/abes<\/a>> ;\u00A0\u00A0\u00A0\nschema:url<\/a> <https:\/\/tel.archives-ouvertes.fr\/tel-01356238<\/a>> ;\u00A0\u00A0\u00A0\nschema:url<\/a> <http:\/\/www.theses.fr\/2015USPCB058\/document<\/a>> ;\u00A0\u00A0\u00A0\nschema:url<\/a> <http:\/\/app.parisdescartes.fr\/cgi-bin\/WebObjects\/TheseWeb.woa\/wa\/show?t=1195&f=4887<\/a>> ;\u00A0\u00A0\u00A0\nwdrs:describedby<\/a> <http:\/\/www.worldcat.org\/title\/-\/oclc\/957262541<\/a>> ;\u00A0\u00A0\u00A0\u00A0.\n\n\n<\/div>\n\n

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