Endogenous salicylic acid mediates melatonin-induced chilling-and oxidative-stress tolerance in harvested kiwifruit

Phytohormone melatonin (MT) has shown promise in alleviating chilling injury (CI) in kiwifruit; however, the performance and mechanism remain largely unknown. In this study, the effect of pretreatment of MT at concentration of 0.05 mM on CI in 'Xuxiang' kiwifruit during storage at 1 degrees C for 90 d was investigated, as well as the implication of endogenous salicylic acid (SA) in MT-induced chilling-and oxidative-stress tolerance. MT pre-treatment protected kiwifruit against CI, as figured out by lower CI index, firmness loss and soluble solids accumulation and better pulp appearance than those in control fruit. MT pretreatment stimulated endogenous SA generation by activating the gene expression of phenylalanine ammonia lyase (PAL) and activity of PAL and benzoic acid-2-hydroxylase, therefore up-regulated SA-responsive pathogenesis-related gene 1 expression, and provoked kiwifruit defense response to chilling stress. Moreover, reactive oxygen species in MT-pretreated fruit were neutralized by evaluating endogenous MT, ascorbic acid and glutathione contents and superoxide dismutase, catalase and ascorbate peroxidase activity, thus reducing membrane damage. However, such positive regulations of MT on kiwifruit were counteracted to varying extent by pretreatment of the combination of paclobutrazol PAC, a SA biosynthesis inhibitor, with MT. These findings indicated a mediating role of endogenous SA in chilling-and oxidative-stress tolerance in kiwifruit induced by MT pretreatment that could be operative by evoking defense response to chilling stress and enhancing antioxidative protection.