The GATOR complex regulates TORC1 activity during meiosis.

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.

Enzymes that remove amine groups from cytosine bases in DNA are likely involved in generating the clusters of mutations (kataegis) seen in breast cancer.

Accumulation of mutations in some cancers is correlated with an aberration of DNA repair and access of a DNA deaminase to normal genomic DNA.

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

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.

Transcribed promoters are highly susceptible to mutation by cytidine deaminases, implicating stable exposure of single stranded DNA structures, rather than cofactors, in localising mutation during tumourigenesis and antibody maturation.

Fluorescent derivatives of a bacteriophage protein that binds double-stranded ends can trap and label genome-destabilizing double-strand DNA breaks in bacterial and human cells, and illuminate the origins of spontaneous DNA breakage in both.

MicroRNAs tightly control the cellular level of homologous recombination (HR) factors in the G1 phase, and failure of this control system results in an ectopic increase in HR proteins in G1 cells leading to impaired DNA repair.