In addition to causing DNA damage, R-loops cause genomic instability by interfering with DNA repair.

Experiments on E. coli show that multiple mechanisms contribute to extreme resistance to ionizing radiation in bacteria, with mutations to three genes for DNA repair having a prominent role in one evolved population.

Biochemical studies revealed novel property of human tumor suppressor PALB2, which significantly contribute into DNA repair in cells and can be targeted for the development of novel anticancer treatment.

The repair of spontaneous DNA damage can introduce mutators that lead to further genetic changes, which could underlie evolutionary change, disease and aging.

Polyglutamine expansion in mutant huntingtin disrupts a novel transcription-coupled DNA repair complex, providing an undescribed mechanism of neuronal toxicity and degeneration in Huntington's disease.

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.

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

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.