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Études sur la régulation de la résection de l'ADN des cassures double brin (DSB) induites par les ions
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ISBN10: 620898419X
ISBN13: 9786208984199
Publisher: Editions Notre Savoir
Published: Jun 20 2025
Pages: 120
Weight: 0.38
Height: 0.28 Width: 6.00 Depth: 9.00
Language: French
ISBN13: 9786208984199
Publisher: Editions Notre Savoir
Published: Jun 20 2025
Pages: 120
Weight: 0.38
Height: 0.28 Width: 6.00 Depth: 9.00
Language: French
Les cassures double brin complexes de l'ADN (DSB) constituent les dommages les plus graves subis par l'ADN, car elles représentent un défi considérable pour la cellule, qui doit non seulement les réparer fidèlement, mais aussi les réparer tout court. Deux voies de réparation principales sont connues pour réparer les DSB: la jonction classique des extrémités non homologues (c-NHEJ) et la recombinaison homologue (HR). La c-NHEJ est disponible dans toutes les phases du cycle cellulaire, tandis que la voie HR ne fonctionne qu'en S/G2 lorsque la chromatide soeur est disponible comme matrice. En outre, une autre voie de réparation est disponible pour les cellules: la jonction alternative non homologue (alt-NHEJ), qui peut opérer sur les extrémités réséquées des cassures de l'ADN. La résection de l'ADN est une étape importante dans la décision de la cellule quant à la voie de réparation des DSB à choisir. La résection de l'ADN a lieu non seulement dans les cellules S/G2, mais aussi dans les cellules G1 à la suite de dommages complexes à l'ADN induits par un rayonnement ionisant lourd. L'objectif de ce travail est d'élucider le mécanisme de régulation de la résection dans les cellules G1 après irradiation par des ions lourds. Il se concentre spécifiquement sur le rôle des facteurs de régulation de la résection RIF1 et BRCA1. Les cellules en état de quiescence, les cellules G0, constituent un modèle utile pour étudier le mécanisme de limitation de la résection.
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