Senataxin and DNA-PKcs Redundantly Promote Non-Homologous End Joining Repair of DNA Double Strand Breaks During V(D)J Recombination.

According to a preprint abstract from biorxiv.org, non-homologous end joining (NHEJ) is necessary for repairing DNA double strand breaks (DSBs) during lymphocyte antigen receptor gene assembly. The senataxin helicase, along with the RECQL5 helicase and the HLTF translocase, plays a redundant role in NHEJ. Loss of senataxin leads to a defect in repairing DSBs when DNA-PKcs is inactivated. The study suggests that ATM and DNA-PKcs regulate the functions of senataxin and RECQL5/HLTF, respectively, to provide redundant support for NHEJ. This research has not yet undergone peer review. [Extracted from the article]