Abscisic acid alleviates chilling injury in cold-stored peach fruit by regulating ethylene and hydrogen peroxide metabolism.

Peach (Prunus persica (L.) Batsch) is susceptible to chilling injury under improper low-temperature storage (2°C-5°C). Previous research has shown that abscisic acid (ABA) alleviates chilling injury in fruits and vegetables, but the potential mechanism is still unclear. To explore its effectiveness and potential mechanism in alleviating chilling injury during cold storage, exogenous ABA was applied to peach fruit by immersion in 100 µmol L-1 solutions for 10 min. In our experiment, ABA alleviated chilling injury by reducing hydrogen peroxide (H2O2) content and ethylene production. In addition, ABA inhibited the expression of the ethylene synthesis-related genes PpACO1 and PpEIN2. At the same time, ABA activated the antioxidant enzymatic pathway and the ascorbate-glutathione (AsA-GSH) cycle, the transcript abundance encoding genes related to antioxidant enzyme activities also changed correspondingly. The results suggested that ABA alleviated chilling injury by scavenging excessive H2O2 by promoting antioxidant enzymes and the AsA-GSH pathway.

Nitric oxide alleviates chilling injury by regulating the metabolism of lipid and cell wall in cold-storage peach fruit.

Peach fruit are prone to development of chilling injury during cold storage at around 0-7 °C. Nitric oxide (NO) has been proven to alleviate chilling injury, but the mechanism was still unclear. In this study, peach fruit were immersed in a NO donor (sodium nitroprusside, SNP) solution for 10 min, then stored at 0 °C. The SNP alleviated chilling injury, including decreasing the internal browning index, malondialdehyde content, electrolyte leakage, and lipoxygenase activity, and maintaining firmness. Furthermore, SNP maintenance of fruit firmness was associated with reduction of xyloglucan endotransglycosylase/hydrolase family member gene expression and decrease of cell wall hydrolase activity, especially the activities of polygalacturonase, xyloglucan endoglycosyl transferase, cellulase, and ß-galactosidase. Meanwhile, SNP regulated the lipid metabolism by up-regulating the expression of genes encoding glycerol-3-phosphate acyltransferase, ketoacy-ACP synthase, phosphatidylinositol bisphosphate and long-chain acyl-CoA. Thus, the results of this study indicate that SNP alleviates chilling injury of post-harvest peach fruit by regulating cell wall and lipid metabolism.

Postharvest nitric oxide treatment induced the alternative oxidase pathway to enhance antioxidant capacity and chilling tolerance in peach fruit.

Nitric oxide (NO) is an important regulator of plant response to cold stress. In this study, NO treatment delayed the development of chilling injury (CI), inhibited the increase in H2O2 content, O2- production rate and decrease in firmness of postharvest peach fruit. Meanwhile, through RNA-seq analysis, NO treatment up-regulated gene expression of PpG-6-PDH, Pp6-PGDH and PpAOX while it down-regulated the expression of PpGPI and PpHK, suggesting that the pentose phosphate respiratory pathway and cyanide-resistant respiratory pathway were promoted and the glycolysis pathway was inhibited. Furthermore, the PpAOX expression was consistent with the trend of PpPOD1/2 expression and H2O2 content, indicating that AOX may play a role in reducing oxidative damage of peach fruit by scavenging H2O2. Thus, it was concluded that NO treatment could induce the cyanide-resistant respiration pathway to enhance antioxidant ability and chilling tolerance in post-harvest peach fruit.

Salicylic acid treatment mitigates chilling injury in peach fruit by regulation of sucrose metabolism and soluble sugar content.

Peach fruit stored in the cold are susceptible to chilling injury. A pre-storage treatment with the natural hormone salicylic acid can alleviate chilling damage, although the mechanism is unclear. We found that a treatment with 1 µmol L-1 salicylic acid for 15 min prior to storage at 4 °C delayed and reduced fruit internal browning, a symptom of chilling injury. Salicylic acid had a large effect on sugar metabolism, increasing total soluble sugars via a substantial increase in sucrose content. The transcript abundance of genes related to sucrose biosynthesis and degradation was significantly regulated by salicylic acid, consistent with the changes in sucrose content. Salicylic acid treatment also increased the expression of two DREB cold stress-related proteins, transcriptional activators that regulate cold resistance pathways. The results show that salicylic acid alleviates chilling injury in peach by multiple mechanisms, including an increased content of sucrose and activation of cold response genes.

Jasmonic acid and salicylic acid induce the accumulation of sucrose and increase resistance to chilling injury in peach fruit.

BACKGROUND: Salicylic acid (SA) and jasmonic acid (JA) can both enhance resistance of chilling injury (CI) in cold-storage peach fruit, but the regulatory mechanisms involved and whether there is a coordinated regulation between them is unclear. In this study, postharvest peach fruit were treated with an aqueous SA solution for 15 min or an aqueous JA solution for 30 s before storage at 4 °C for 35 days. RESULTS: SA and JA treatments both delayed and reduced development of internal browning (a symptom of CI) and induced the accumulation of hydrogen peroxide and sucrose. The SA and JA also reduced catalase and peroxidase activities, which are involved in hydrogen peroxide generation. The SA and JA treatments significantly regulated the transcript abundance of genes related to sucrose biosynthesis and degradation consistent with the observed increase in sucrose content. CONCLUSION: These results intimate that JA and SA may be involved in coordinating the alleviation of CI via increased accumulation of sucrose. © 2021 Society of Chemical Industry.

Jasmonic acid treatment alleviates chilling injury in peach fruit by promoting sugar and ethylene metabolism.

Peach (Prunus persica L.) fruit are highly susceptible to chilling injury during cold storage, resulting in internal flesh browning and a failure to soften normally. We have examined the effect of a postharvest treatment consisting of a brief (30 s) dip in the natural plant hormone jasmonic acid, prior to storage at 4 °C. Jasmonic acid treatment reduced the severity of internal flesh browning and did not inhibit fruit softening over a 35 d storage period. Two major physiological effects of jasmonic acid on the fruit were observed, an increase in ethylene production and a prevention of the decline in soluble sugar content seen in controls. An increased soluble sugar content may have multiple benefits in resisting chilling stress, scavenging reactive oxygen species and acting to stabilize membranes. Our results show that a treatment with jasmonic acid can enhance chilling tolerance of peach fruit by regulating ethylene and sugar metabolism.