Effect of nitric oxide treatment on chilling injury, antioxidant enzymes and expression of the CmCBF1 and CmCBF3 genes in cold-stored Hami melon (Cucumis melo L.) fruit

•NO treatment can alleviate and delay CI of cold-stored Hami melon fruit.•Two novel CBF genes from Hami melon fruit were isolated and identified.•NO enhanced the activities of antioxidant enzymes.•CI was ameliorated by NO via CmCBF1 and CmCBF3 up-regulation. Short-term exposure to a low concentration of nitric oxide (NO) treatment can prevent or alleviate chilling injury (CI), and extend the postharvest life of various fresh fruits and vegetables. However no research on this topic has been reported for Hami melon fruit. In this study, Hami melon fruit were pre-treated with 60μL/L NO for 3h at 25°C, and then stored at 1±0.5°C with a relative humidity (RH) of 75–80% for 49d. The results showed that NO treatment effectively decreased the CI index and CI incidence, reduced the increases in membrane permeability and malondialdehyde (MDA) content, inhibited superoxide anion (O2−) production rates, reduced H2O2 content, and sustained higher activity of superoxide dismutase (SOD), peroxidase (POD), catalase (CAT) and ascorbate peroxidase (APX) in the rind of Hami melon fruit during storage at 1±0.5°C. C-repeat/dehydration responsive element (CRT/DRE)-binding factors (CBFs) are the best-characterized transcription factors controlling cold-responsive gene expression and cold acclimation. To investigate the molecular regulation of cold resistance by NO treatment in Hami melon fruit, a 639-bp CmCBF1 gene and a 615-bp CmCBF3 gene were identified, and the effect NO on the expression of CmCBF1 and CmCBF3 was measured by RT-qPCR. The results showed that the expression of CmCBF1 and CmCBF3 were induced, the expression of the CmCBF1 and CmCBF3 in NO treated fruit was significantly higher than in control fruit during storage at 1±0.5°C. These results indicate that NO treatment can alleviate and delay CI in cold-stored Hami melon fruit via enhancing the activities of antioxidant enzymes and up-regulating the expression of CmCBF1 and CmCBF3.