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<dc:title xml:lang="fr">Etude du complexe de réparation par excision de nucléotides</dc:title>
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<dc:subject xml:lang="fr">Réparation de l'ADN</dc:subject>
<dc:subject xml:lang="fr">Facteur de transcription</dc:subject>
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<dc:subject xml:lang="fr">Trichothiodystrophies</dc:subject>
<dc:subject xml:lang="en">NER</dc:subject>
<dc:subject xml:lang="en">TFIIH</dc:subject>
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<dcterms:abstract xml:lang="fr">Mon travail de thèse s’est axé sur deux projets, le premier a porté sur l’étude fonctionnelle de la sous unité TTDA de TFIIH, un facteur général de transcription impliqué dans la réparation NER, afin d’identifier de nouveaux partenaires de la sous unité TTDA nous avons réalisé un crible double hybride et ainsi sélectionné ZBTB38, une protéine impliqué dans la répression de gènes portant des methylations CpG, nous avons confirmé son interaction avec TTDA, et son implication dans la réparation NER. La deuxième partie a porté sur l’étude du recrutement des facteurs NER sur la chromatine en absence de lésions de l’ADN. En utilisant le système rapporteur LacO/LacR nous avons observé que l’immobilisation de l’un des facteurs NER sur la chromatine non endommagée permet l’assemblage du PInC de façon séquentielle et ordonnée. Nous avons aussi révélé que TTDA, connue pour être impliquée dans la trichothiodystrophie, joue un rôle clé dans la complétion du PInC.</dcterms:abstract>
<dcterms:abstract xml:lang="en">During my thesis I worked on two projects, the first one was focused on the functional study of TTDA subunit of TFIIH, which is a general transcription factor involved in NER, we made a double hybrid screening to identify new interactants of TTDA subunit, and we could select ZBTB38, which is known to be implicated in methyl dependant gene repression; we confirmed its interaction with TTDA and its involvement in NER. The second project was entiteled Molecular Insights into the formation of the nucleotide excision repair complex revealed on undamaged chromatin. we analyzed the formation of the PInC independently of DNA damage by using the LacO-LacR system. We observed a sequential and ordered self-assembly of the PInC operating upon immobilization of individual NER factors on undamaged chromatin and mimicking that functioning on a bona fide NER substrate. We also revealed that the recruitment of TTDA, involved in Trichothiodystrophy disorder, was key in the completion of the PInC.</dcterms:abstract>
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