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

The first genetic compelling evidence for post-meiotic DNA double-strand breaks and its relation to chromatin remodeling in haploid pronuclei is shown.

During meiosis, budding yeast use a checkpoint involving the protein Mec1 to prevent the formation of double-strand breaks in DNA that has not completed replication.

The LIN37-DREAM complex has a critical role in regulating DNA double-strand break end processing and suppressing aberrant homology-directed repair in quiescent cells.

The DNA flanks on either side of an R-loop differ in stability, and CRISPR-Cas12 enzymes form double-strand breaks by targeting the more unstable flank with their single DNase active site.

Genome-wide analysis of sister chromatid exchange using single-cell sequencing reveals that most spontaneous sister chromatid exchange events are not due to the repair of double-strand DNA breaks in wild-type yeast cells.

Irradiation of normal human fibroblasts and mice in conditions mimicking standard external X-ray radiotherapy protocols highlights that noncancerous cells surrounding the planning target volume accumulate DNA single-strand breaks but almost no double-strand breaks, putting them in a pre-cancerous senescent state.

DNA lesions formed by alkylating agents trigger double-strand breaks, in the absence of replication, by the action of MMR and BER at nearby O-alkyl and N-alkyl adducts, respectively.

Genome-wide mapping of heteroduplex DNA (a recombination intermediate) formed during mitotic recombination in yeast demonstrates that the "classical" model of double-strand DNA break repair is inadequate to explain several aspects of mitotic recombination.