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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.
Mutations in homology-directed repair genes like BRCA2 are linked to breast cancer susceptibility. Here the authors generate mice with an inducible DNA break-reporter system and see high levels of homology-directed repair in proliferative mammary tissue and a general reliance on BRCA2 in various tissues.
End-resection of double strand DNA breaks is essential for pathway choice between non-homologous end-joining and homologous recombination. Here the authors show that phosphorylation of WRN helicase by CDK1 is essential for resection at replication-related breaks.
Homologous recombination requires end resection of the DNA at the site of the break, however the Ku dimer can sequester single-ended double-strand breaks. Here the authors show that ATM-dependent phosphorylation of CtIP, along with the actions of Mre11, impair the stable loading of Ku onto DNA.
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.