Base excision repair

DNA damage during chromothripsis is caused by deoxyinosine formation on accumulated RNA–DNA hybrids in micronuclei that are then recognized by N-methyl-purine DNA glycosylase and cleaved by apurinic/apyrimidinic endonuclease.

Gunn Hildrestrand, Veslemøy Rolseth, and Nicolas Kunath et al. examine mice lacking the NEIL1 and NEIL2 DNA glycosylases involved in base excision repair. Their results suggest that loss of both NEIL1 and NEIL2 dysregulates genes relevant to synaptic function and modulates behavior in mice.

FAM72A differentially controls mutation rates by regulating uracil processing at different stages of the cell cycle, thereby regulating somatic hypermutation and class-switch recombination in B cells.

Kurgina et al. conduct in vitro characterization of the effect of HPF1 on the catalytic output of PARP1 and PARP2 under several experimental conditions. The authors report that the DNAdependent and DNA-independent autoPARylation of PARP1 and PARP2, as well as the heteroPARylation of histones in complex with the nucleosome are stimulated by HPF1 in a certain range of HPF1 and NAD + concentrations.

Ahmadi et al. use a single-molecule tracking method to describe the DNA scanning mode of AlkD, a HEAT-like repeat DNA glycosylase. They show that, contrary to other glycosylases that use a base-flipping mechanism, AlkD scans the DNA without forming a stable interrogation complex.