Structural and biochemical analysis of human CtIP provides new insights into DNA break recognition, binding and bridging during homologous recombination.

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.

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

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.

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 disordered C-terminal tail allows XRCC4-like factor (XLF) to find and bind the XRCC4-Lig4 complex, enabling DNA end synapsis and subsequent ligation during non-homologous end joining.

The role of the bacterial protein RadA in homologous recombination – a DNA repair pathway vital to all cells – is defined.

Linking the DNA repair template to the Cas9 ribonucleoprotein complex enhances homology-directed repair of the induced DNA double strand break.

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.

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