MDC1 promotes nuclear localization of Beclin-1 and supports its role in ATM pathway in response to oxidative stress

and doxorubicin treated HeLa cells. Furthermore, we observed that in Hela cells depleted of MDC1, the translocation of Beclin-1 to the nucleus was abrogated, which adversely affected both the DDR and autophagy response in these cells. Additionally, we have analyzed the effect of CHK2 kinase activity on this interaction, and the presence of phospho-CHK2 probably supports the nuclear activity of Beclin-1 through its phosphorylation, but is dispensable for the nuclear translocation of Beclin-1. In conclusion, our findings contribute to the understanding of the crosstalk between DDR and autophagy for cell survival under genotoxic stress, with potential implications on the efficacy of drug treatment.