Abstract
Kiwifruit (Actinidia spp.), celebrated for its unique flavor and rich nutritional content, is a globally popular fruit. This fruit requires post-harvest ripening before consumption. However, the unpredictable ripening pace significantly impacts consumer acceptance and sales, thereby hindering the commercial growth of kiwifruit. To address this, understanding the key molecular mechanisms and metabolites governing postharvest ripening and senescence could offer valuable insights for developing storage strategies and breeding techniques in yellow-fleshed kiwifruits. We constructed two models that integrated these findings with existing theories. The first model suggests that, unlike the T6P-sucrose regulatory mechanism observed in plant leaves, the separation of harvested kiwifruit from the mother plant leads to an insufficient supply of T6P, which activates the SnRK1 kinase. This, in turn, inhibits the TOR kinase signaling pathway, regulating starch metabolism. The T6P-SnRK1-TOR-starch metabolism pathway plays a regulatory role during postharvest ripening, limiting excessive starch degradation that could accelerate aging and decay in yellow-fleshed kiwifruit. The second model highlights the role of abscisic acid (ABA), cytokinins (CKs), and ethylene in regulating the process, inducing the activation of ERFs and cell wall-degrading enzymes, promoting fruit postharvest softening. These findings indicate that at least two models, the T6P-SnRK1-TOR-starch metabolism model and the ABA-CKs-ethylene-cell wall degradation model, regulate postharvest fruit ripening, offering new insights into the artificial regulation of yellow-fleshed kiwifruit ripening speed.