Short-term calorie restriction enhances DNA repair by non-homologous end joining in mice

Abstract Calorie restriction (CR) improves health, reduces cancer incidence and extends lifespan in multiple organisms including mice. CR was shown to enhance base excision repair and nucleotide excision repair pathways of DNA repair, however, whether CR improves repair of DNA double-strand breaks has not been examined in in vivo system. Here we utilize non-homologous end joining (NHEJ) reporter mice to show that short-term CR strongly enhances DNA repair by NHEJ, which is associated with elevated levels of DNA-PK and SIRT6

MOESM5 of DNA double-strand break repair is impaired in presenescent Syrian hamster fibroblasts

Additional file 5: Table S1. Colocalization of gH2AX with 53BP1, DNA-PK, pATM and p-ATM/ATR substrates in Syrian hamster fibroblasts at two time points after BL treatment

MOESM2 of DNA double-strand break repair is impaired in presenescent Syrian hamster fibroblasts

Additional file 2: Figure S2. Proliferation is arrested in Syrian hamster fibroblasts at the 5th passage. EdU was incorporated for 30 min in untreated Syrian hamster cells at the 1st (p 1) and the 5th (p 5) passages. Proliferating cells at the 1st passage are Ki-67-positive, S-phase cells incorporate EdU, G0 cells are Ki-67- and EdU-negative. All cells at the 5th passage are Ki-67- and EdU-negative. DNA in cell nuclei is counterstained with DAPI. Bar is 10 Âľm