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.

Biochemical analysis in Xenopus egg extracts reveals that the MutSα mismatch sensor retains the DNA-bound replication clamp to maintain a post-replicative temporal window permissive to strand-specific repair of mismatches.

When mismatch repair is compromised heterozygous loss of Pol ε proofreading is sufficient to drive a subset of the observed clinical characteristics of Pol ε tumors.

Non-coding mutations in microsatellite-instable (MSI) colorectal tumors are prevalent and activate cancer-specific enhancers, thereby disrupting gene expression control.

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

Eukaryotic pathogens, like Cryptococcus deuterogattii, can use elevated mutation rates to more rapidly adapt to stresses, such as drug challenges, but at the cost of lower fitness in less stressful environments.

The mechanical stability of a nucleosome is enhanced upon the introduction of a single base pair mismatch that makes DNA more bendable, with implications on mismatch repair in vivo.

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

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.

Meiotic cells employ a specific pathway to limit the amount of gene conversion occuring at recombination sites.