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Graphical scheme summarizing results. In BRCA2-proficient cells, BRCA2 loads RAD51 to protect reversed replication forks, leading to replication restart by homologous recombination and genome stability. In BRCA2-deficient cells, MRE11 and XRCC1 degrade reversed forks, leading to replication restart using microhomology-based mechanisms, the accumulation of signature 3 mutations and poor patient survival.
