ABA treatment mitigates chilling injury in cucumber fruit by modulating purine metabolism

Chilling injury (CI) severely impacts the quality of cucumber fruit during cold storage. This study identified 0.1 mM abscisic acid (ABA) as optimal for mitigating CI in cucumber fruit, with integrative metabolomics, transcriptomic and physiological analyses employed to unveil its protective effects. Integrated metabolomics and transcriptomic analysis revealed a significant enrichment of purine metabolism in both differentially abundant metabolites (DAMs) and differentially expressed genes (DEGs) upon ABA treatment, with strong correlations observed between 9 DAMs and 16 DEGs in the purine metabolism pathway. This suggests purine metabolism may be central to ABA-induced chilling tolerance. Physiological analysis suggested that ABA treatment enhanced energy supply, while reducing H 2 O 2 level by enhancing the activities of two key antioxidant enzymes (CAT and APX) in cucumber fruit. Furthermore, metabolomics profiling revealed that ABA treatment also modulated the levels of several endogenous hormones or their precursors. Further integrative analyses revealed a connection between purine metabolism and potential transcription factors (TFs) (e.g., MYB, ERF, bHLH). We, therefore, propose that ABA treatment may regulate purine metabolism via the induced TFs, thereby modulating energy supply, ROS levels, and hormone balance to mitigate CI. This work provides critical insights into ABA-mediated mitigation of CI in cucumber fruit during cold storage. • 0.1 mM abscisic acid (ABA) was optimal in reducing chilling injury in cucumber fruit. • Purine metabolism pathway may be a key hub for ABA-induced chilling tolerance. • Purine metabolism mediates ABA-regulated ROS homeostasis and energy supply. • ABA amplifies defense signals by modulating endogenous hormone dynamics.