Postharvest senescence limits the storability and market value of sand pear, yet the role of aldo-keto reductases (AKRs) in this process remains unclear. Here, we conducted a genome‑wide analysis of the PpAKR superfamily and functionally characterized PpAKR1, previously identified as salicylic acid (SA) responsive in ‘Whangkeumbae’ fruit. A total of 50 PpAKR genes were identified and categorized into four families-AKR2, AKR4, AKR6, and AKR13-based on phylogenetic analysis. The PpAKR1 gene, which belongs to the AKR13 family, exhibited the highest homology with PpAKR40. The PpAKR1 was localized in the cytoplasm and nucleus. Furthermore, RT-qPCR analysis demonstrated that PpAKR1 is predominantly expressed during the postharvest stage and responds to treatments with SA, auxin, ethylene, and 1-aminocyclopropane-1-carboxylic acid in ‘Whangkeumbae’ fruit. Silencing of the PpAKR1 gene in pear fruit resulted in a marked reduction in fruit firmness and SA content, accompanied by significant increases in ethylene production, MDA, H2O2, and O2- levels. Concurrently, the activities of antioxidant enzymes, including SOD, POD, and CAT, were substantially decreased. In contrast, the activities of cell wall-degrading enzymes—PG, PME, and CX—were significantly elevated. Notably, exogenous application of SA effectively mitigated the fruit senescence symptoms induced by PpAKR1 silencing. Overexpression of PpAKR1 in sand pear callus resulted in increased SA content, a reduction in the accumulation of MDA, H₂O₂, and O₂⁻, while enhancing the activities of SOD, POD, and CAT, and reducing the activities of PG, PME, and CX, thereby delaying callus senescence. In response to SA, the senescence of PpAKR1-overexpressing callus was further delayed, whereas ethylene accelerated the senescence process. These findings provide valuable insights into the PpAKR gene superfamily and offer preliminary evidence supporting the role of the SA-induced PpAKR1 gene in delaying senescence in sand pear fruit.
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