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Homologous recombination is the exchange of DNA strands of similar or identical nucleotide sequence. It can be used to direct error-free repair of double-strand DNA breaks and generates sequence variation in gametes during meiosis.
BRCA2 mutations promote tumour formation while also paradoxically causing cell lethality. Here the authors generate conditional BRCA2 loss in a non-transformed human mammary cell line and see increased replication stress due to under-replication of DNA.
The choice between non-homologous end-joining and homologous recombination to repair a DNA double-strand break depends on activation of the end resection machinery. Here the authors show that SUMO E3 ligase CBX4 sumoylates subpopulation of CtIP to regulate recruitment to breaks and resection.
The suppression of homologous recombination in G1 depends on BRCA1–PALB2–BRCA2 complex formation at sites of damage. In mitosis, DNA repair factors prevent the formation of DNA damage by facilitating mitotic replication.