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<dc:title xml:lang="en">The glutamine-rich N-terminal extension of Drosophila AGO2 mediates antiviral RNA interference in a TRiC/CCT dependent manner</dc:title>
<dcterms:alternative xml:lang="fr">L'extension N-terminale riche en glutamine de la protéine de Drosophile AGO2 joue un rôle critique dans l’ARN interférence antivirale d'une manière dépendante du complexe TRiC / CCT</dcterms:alternative>
<dc:subject xml:lang="fr">Virus</dc:subject>
<dc:subject xml:lang="fr">Drosphile</dc:subject>
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<tef:elementdEntree autoriteExterne="031711480" autoriteSource="Sudoc">Drosophiles</tef:elementdEntree>
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<dcterms:abstract xml:lang="fr">L’analyse par spectrométrie de masse des protéines qu’interagies avec Dicer-2, R2D2 a identifié six sur huit composés du complexe chaperon TRiC / CCT. L’élimination de l'un des six composants du complexe TRiC / CCT identifiés par spectrométrie de masse a conduit à une réplication virale accrue d'au moins un des trois virus testés. L’ensemble des mes résultats suggèrent un rôle nouveau pour le complexe TRiC / CCT dans l'ARNi antiviral. Mes résultats soulèvent la question de savoir pourquoi le GRR d’AGO2 semble être nécessaire dans le contexte d'une réponse antivirale. Mes résultats indiquent que le complexe TRiC / CCT participe à l’étape de dissociation et à la relocalisation dynamique d'AGO2-L pendant l’infection virale.</dcterms:abstract>
<dcterms:abstract xml:lang="en">The mass spectrometry analysis of the complexes associating with Dicer-2, R2D2, and AGO2 identified six out of the eight subunits forming the TRiC/CCT complex. Knockdown of one of the six subunits identified is sufficient to increase the replication of DCV (DrosophilaC Virus). My results identify an interaction between the TRiC/CCT complex and the antiviral RNA interference. This interaction raises the question of how the GRR region of AGO2 is necessary for the antiviral response. My results suggest that the TRiC/CCT complex is involved in the dynamic dissociation and relocalization of AGO2 during viral infection.</dcterms:abstract>
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