Playing the end game: DNA double-strand break repair pathway choice.

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RIF1 Is Essential for 53BP1-Dependent Nonhomologous End Joining and Suppression of DNA Double-Strand Break Resection (2013, background): “We recently showed that while 53BP1 forms foci at DSBs in G1 and S cell-cycle phases, it is excluded from the core of foci in an S phase and BRCA1-dependent manner (Chapman et al., 2012a).”
Highly Efficient Targeted Mutagenesis of Drosophila with the CRISPR/Cas9 System (2013, background): “Cell Reports 4, 220–228, July 11, 2013 ª2013 The Authors 225 (legend on next page) 226 Cell Reports 4, 220–228, July 11, 2013 ª2013 The Authors The double-strand breaks generated are predominantly repaired by NHEJ but can also be repaired by homologous recombination (HR) (Chapman et al., 2012).”
Homologous recombination and human health: the roles of BRCA1, BRCA2 and associated proteins (2015, background): “Special cases are the programmed DSBs, which are channeled into defined repair pathways, for example, HR for SPO11-generated DSBs during meiosis (see Lam and Keeney 2015) and NHEJ for RAG-induced DSBs in the immune system (Chapman et al. 2012b).”
ATM, ATR, and DNA-PK: The Trinity at the Heart of the DNA Damage Response. (2017, background): “This process, termed DNA-end resection, is a key determinant of DSB repair pathway choice (Chapman et al., 2012), and is stimulated by ATM (Adams et al.”