CtIP has emerged as one of the main factors that drives the processing of broken DNA into the homologous recombination pathway. CtIP achieves that by stimulating the activity of two nucleases (MRE11 and DNA2), which resect DNA end creating single-strand DNA overhangs required for the downstream steps in the recombination pathway. Cell lacking CtIP consequently exhibit abrogated DNA end resection and homologous recombination.
A recent study from the Cejka laboratory at IRB, affiliated with USI, shows that a CtIP variant lacking parts of its central domain is even more efficient than the wild type protein. This unexpected result identified that the central domain of CtIP functions as an inhibitor of DNA end resection, and CtIP can regulate the efficacy of DNA end resection both positively and negatively. The study was published in Nucleic Acids Research.
Howard, S. M., I. Ceppi, R. Anand, R. Geiger and P. Cejka
Nucleic Acids Res. 2020