Abstract
Oxidative stress is an imbalance between free radical formation and anti‐oxidant defense. Reactive Oxygen Species (ROS) have been implicated in several pathological disorders. Here, we reveal a novel function of the nucleotide excision repair protein DDB2 in ROS accumulation. DDB2 deficient cells fail to accumulate ROS following DNA damage. The lack of ROS accumulation in DDB2 deficiency results from high‐level expression of the anti‐oxidant genes, in vitro and in vivo. In the absence of DDB2, the antioxidant genes MnSOD and Catalase are expressed at high levels leading to an inhibition of ROS accumulation. DDB2 represses the expression of these anti‐oxidant genes by recruiting Cul4a and Suv39h and by increasing Histone‐H3K9 tri‐methylation. Moreover, expression of DDB2 also is induced by ROS. Together, our results show that upon oxidative stress, DDB2 functions in a positive feedback loop by repressing the ROS scavenger genes, such as MnSOD and Catalase, to cause a persistent accumulation of ROS in the cell.
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