Abstract

Postharvest chilling injury (PCI) is a physiological disorder that compromises tomato fruit quality, reducing shelf-life, negatively impacting the fresh market tomato industry, and increasing both consumer dissatisfaction and postharvest losses. PCI has been extensively studied, but practical solutions remain elusive, due in part to its complexity. The domestication of cultivated tomato (Solanum lycopersicum L.) in tropical and subtropical regions explains its cold-sensitivity throughout its life cycle and in all tissues, including fruit. In the cold-tolerant Arabidopsis thaliana, the CBF gene family of transcription factors (AtCBF1-3) plays a critical role in the development of the cold response by regulating the expression of cold-responsive genes. In the cold-tolerant wild tomato relative, Solanum habrochaites, ShCBF1 ectopic overexpression increases the cold-tolerance of Arabidopsis plants. In tomato, AtCBF1 constitutive overexpression increases chilling tolerance but plants show developmental defects. We hypothesize that inducing CBF1 overexpression, specifically in cold-stored fruit, by chemical- or cold-inducible expression systems, will reduce PCI without affecting plant development. To test this hypothesis, cv. Micro-Tom was independently transformed with three transgenic constructs: 1) a chemical-inducible system requiring dexamethasone application to induce AtCBF1 expression and 2) a cold-inducible construct carrying the RD29A promoter to induce ShCBF1, or 3) SlCBF1 expression. Harvested fruit were stored at 2.5°C for up to 4 weeks, to induce PCI. Molecular, physiological and biochemical markers evaluated fruit tolerance to PCI. Results provide insights into the evolutionary nature of this disorder and open opportunities for the development of robust and long-term solutions in the future.