ASHS 2024 Conference

Hardy kiwifruit (Actinidia arguta) is highly sensitive to low temperatures, which can cause chilling injury (CI) as a physiological disorder. Peel surface pitting with black/dark brown spots was developed as CI symptoms in cold-stored hardy kiwifruit. In this study, we performed transcriptomic and lipidomic analyses to elucidate the potential mechanism of CI symptoms in cold-stored hardy kiwifruit. The peel tissues of hardy kiwifruit were collected after harvest (HV) and after cold storage; pitted peel tissues from CI-damaged fruit (PT) and healthy peel tissues from CI-unaffected fruit (HT) were also collected. Transcriptomic analysis identified 10,612 differential expressed genes (DEGs) between HV and HT tissues, and 3,206 DEGs were detected between HT and PT tissues. Among the 3,206 DEGs, 1,322 transcripts were up-regulated in HT tissues, while 1,874 transcripts were up-regulated in PT tissues. The KEGG pathway enriched by up-regulated DEGs in HT indicated protein modification, L-valine degradation, and polyol metabolism, while up-regulated DEGs in PT enriched alkaloid biosynthesis, protein modification, and lipid metabolism. In lipidomics analysis, a total of 101 lipids clustered into 14 subgroups were detected in peel tissues of cold-stored hardy kiwifruit. Based on the results of VIP scores (> 1.5), the levels of triacylglycerol (TAG) 54:8, TAG 54:9, phosphatidylcholine (PC) 36:4, PC 34:2, PC 36:5, PC 34:3, and TAG 54:7 were higher in PT tissues, but the levels of phosphatidylethanolamine (PE) 36:2, phosphatidylserine (PS) 38:3, PS 36:0, PC 36:1, PE 34:1, and PE 36:1, were higher in HT tissues, compared with the other tissues. Therefore, the results indicated that the CI symptoms in cold-stored hardy kiwifruit would be derived from integrated transcriptomic and lipidomic results.