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Chilling stress can cause cellular DNA damage, affecting the faithful transmission of genetic information. Cold acclimation enhances chilling tolerance, but it is not clear that the process of cold adaption involves DNA damage responses, as cold acclimation does not form real chilling stress. Here we showed with cucumber fruit that pre-storage cold acclimation (PsCA) reduces chilling injury and upregulates DNA damage inducible protein1 ( CsDDI1 ), suggesting that the chilling tolerance induced by cold acclimation involves  CsDDI1  transcription. Application of nitric oxide (NO), abscisic acid (ABA) or H 2 O 2  biosynthesis inhibitor before PsCA treatment downregulates  CsDDI1  and aggravates chilling injury, while H 2 O 2  generation inhibition plus exogenous NO or ABA application before PsCA treatment restores chilling tolerance, but does not restore  CsDDI1  expression, suggesting H 2 O 2  plays a crucial role in triggering cold adaption.  CsDDI1  overexpression  Arabidopsis  lines show faster growth, stronger chilling tolerance, lower reactive oxygen species levels, enhanced catalase and superoxide dismutase activities and higher expression of nine other  Arabidopsis  defense genes under chilling stress, suggesting  CsDDI1  strengthens defenses against chilling stress by enhancing antioxidant defense system. Taken together,  CsDDI1  positively regulates chilling tolerance induced by cold acclimation in cucumber. In addition, H 2 O 2  is involved in initiation of cold acclimation. While  CsDDI1  upregulation requires H 2 O 2  as a key signaling molecule, the upregulation of  CsDDI1  activates an antioxidant system to reduce biotoxic accumulation of H 2 O 2  and helps in DNA repair.

DNA Damage Inducible Protein 1 is Involved in Cold Adaption of Harvested Cucumber Fruit