Molecular analyses and unbiased CRISPR screens reveal that extensive end resection occurs in quiescent cells after inducing DNA double strand breaks, in a manner dependent on DNA-PK.

A single-cell assay reveals that the genetic rewiring that underlies PARP inhibitor resistance drives altered DNA double-strand break end resection pathway choice.

Hundreds of proteins are involved in the DNA damage response but only three sensors for DSB were known but now SIRT6 is identified as a fourth DSB sensor.

Kinesin Kif2C is recruited to DNA damage sites, modulates the mobility and dynamics of DNA damage foci, and promotes DNA double strand break repair.

The involvement of SETD2 in an important DNA repair pathway could explain the high frequency of SETD2 mutations in several cancers and may provide an alternative mechanism to evade the p53-mediated checkpoint.

The conversion of the ends of a double-strand break from double-stranded to single-stranded DNA, which is necessary to initiate homologous recombination, is responsible for loss of transcription and RNA polymerase occupancy around the double-strand break in Saccharomyces cerevisiae.

A comprehensive catalogue of somatic mutations accumulating in MMR-deficient tumors highlights their relevance in the context of human genetic evolution, for the diagnosis of microsatellite instability and the provision of targeted treatment options.

A sharp transition in the fate of DNA ends with telomere sequences is identified, which suggests a boundary between DNA double-strand breaks and telomeres.

The exogenous DNA DSBs improve meiotic chromosome pairing in mouse inter-subspecific hybrids, thus providing an evidence for a DSB-dependent mechanism of the PRDM9-controlled synapsis failure and infertility.

A structural investigation reveals details of the mechanism by which the nuclease RecJ processes DNA ends to repair double strand breaks.