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21 September 2017: One event

  • Biochemistry, Biophysics and Structural Biology department

    Thursday 21 September 15:30-16:30 - Pr Shunichi Takeda - Department of Radiation Genetics, Graduate School of Medicine, Kyoto University, Kyoto, Japan

    The role Mre11-Rad50-Nbs1 complex in double-strand-break repair – Myth and Facts

    Résumé : Homologous recombination initiates double-strand break (DSB) repair by digesting 5’-termini at DSBs, the biochemical reaction called DSB resection, during which DSBs are processed by nucleases to generate 3’ single-strand DNA. Rad51 recombinase polymerizes along resected DNA, and resulting Rad51-DNA complex undergoes homology search. Although DSB resection by the Mre11 nuclease plays a critical role in HR in Saccharomyces cerevisiae, it remains elusive whether DSB resection by Mre11 significantly contributes to HR-dependent DSB repair in mammalian cells. Depletion of Mre11 decreases the efficiency of DSB resection only by a few times in mammalian cells. We show that although Mre11 is required for efficient HR-dependent repair of ionizing-radiation-induced DSBs, Mre11 is largely dispensable for DSB resection in both chicken DT40 and human TK6 B cell lines. Moreover, 2- to 3-fold decrease in DSB resection has virtually no impact on the efficiency of HR. Thus, although a large number of literatures have reported the vital role of Mre11-mediated DSB resection in HR, the role may not explain the very severe defect in HR in Mre11-deficient cells including their lethality. We here show experimental evidences for the additional roles of Mre11 in (i) elimination of chemical adducts from DSB ends for subsequent DSB repair, and (ii) maintaining homologous recombination intermediates for their proper resolution.
    Contact : Jean-Baptiste Charbonnier

    Lieu : Salle de Conférences - Bâtiment 144, Campus de Saclay

    En savoir plus : Biochemistry, Biophysics and Structural Biology department