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.

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

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.

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.

Uracil/adenine base pairs in HIV-1 DNA are attacked by the uracil base excision repair machinery in macrophages, which leads to HIV restriction and viral genome diversification by transcription-associated mutagenesis.

SPOP mutations underlie a novel, genomically unstable subclass of prostate cancer by altering DNA repair.

Visualization of the sliding clamp in DNA mismatch repair shows how a transient complex is activated.