Unrestrained 53BP1 activity causes fusions of dysfunctional telomeres and embryonic lethality associated with misrepair of DNA double-strand breaks in BRCA1-deficient mice. However, the physiological role of 53BP1 remains unclear, because it presumably did not evolve to carry out these pathological functions. A new report proposes that 53BP1 activity prevents hyper-resection and thereby promotes error-free DNA repair while suppressing alternative mutagenic pathways.
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Zong, D., Ray Chaudhuri, A. & Nussenzweig, A. More end resection is not merrier. Nat Struct Mol Biol 23, 699–701 (2016). https://doi.org/10.1038/nsmb.3274
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DOI: https://doi.org/10.1038/nsmb.3274
