Postharvest waste and loss of horticultural crops exacerbates the agricultural problems facing humankind and will continue to do so in the next decade. Fruits and vegetables provide us with a vast spectrum of healthful nutrients, and along with ornamentals, enrich our lives with a wide array of pleasant sensory experiences. These commodities are, however, highly perishable. Approximately 33% of the produce that is harvested is never consumed since these products naturally have a short shelf-life, which leads to postharvest loss and waste. This loss, however, could be reduced by breeding new crops that retain desirable traits and accrue less damage over the course of long supply chains. New gene-editing tools promise the rapid and inexpensive production of new varieties of crops with enhanced traits more easily than was previously possible. Our aim in this review is to critically evaluate gene editing as a tool to modify the biological pathways that determine fruit, vegetable, and ornamental quality, especially after storage. We provide brief and accessible overviews of both the CRISPR–Cas9 method and the produce supply chain. Next, we survey the literature of the last 30 years, to catalog genes that control or regulate quality or senescence traits that are “ripe” for gene editing. Finally, we discuss barriers to implementing gene editing for postharvest, from the limitations of experimental methods to international policy. We conclude that in spite of the hurdles that remain, gene editing of produce and ornamentals will likely have a measurable impact on reducing postharvest loss and waste in the next 5–10 years.

Paradoxically, refrigerating many fruits and vegetables destroys their quality, and may even accelerate their spoilage. This phenomenon, known as postharvest chilling injury (PCI), affects produce from tropical and subtropical regions and leads to economic and postharvest loss and waste. Low temperatures are used to pause the physiological processes associated with senescence, but upon rewarming, these processes may resume at an accelerated rate. Chilling-injured produce may be discarded for not meeting consumer expectations or may prematurely deteriorate. In this review, we describe progress made in identifying the cellular and molecular processes underlying PCI, and point to advances in biotechnological approaches for ameliorating symptoms. Further, we identify the gaps in knowledge that must be bridged to develop effective solutions to PCI.

Postharvest chilling injury (PCI) reduces fruit quality and shelf-life in tomato (Solanum lycopersicum L.). PCI has been traditionally studied in the pericarp, however its development is likely heterogeneous in different fruit tissues. To gain insight into PCI’s spatio-temporal development, we used postharvest biomarkers e.g. respiration and ethylene rates, ion leakage etc., to confirm the occurrence of PCI, and compared these data with molecular (gene expression), biophysical (MRI data) and biochemical parameters (Malondialdehyde (MDA) and starch content) from the pericarp or columella. Tissues were stored at control (12.5 °C) or PCI-inducing temperatures (2.5 or 5 °C) followed by rewarming at 20 °C. MRI and ion leakage revealed that cold irreversibly impairs ripening-associated membrane liquefaction; MRI also showed that the internal and external fruit tissues responded differently to cold. MDA and especially starch contents, were affected by chilling in a tissue-specific manner. The expression of the six genes studied: ACO1 and ACS2 (ripening), CBF1 (cold response), DHN, AOX1a and LoxB (stress-related) showed non-overlapping temporal and spatially-specific responses. Overall, the data highlighted the interconnectedness of fruit cold response and ripening, and showed how cold stress reconfigures the latter. They further underscored that multidimensional spatial and temporal biological studies are needed to develop effective solutions to PCI.

Tomato fruit ripening is triggered by the demethylation of key genes, which alters their transcriptional levels thereby initiating and propagating a cascade of physiological events. What is unknown is how these processes are altered when fruit are ripened using postharvest practices to extend shelf-life, as these practices often reduce fruit quality. To address this, postharvest handling-induced changes in the fruit DNA methylome and transcriptome, and how they correlate with ripening speed, and ripening indicators such as ethylene, abscisic acid, and carotenoids, were assessed. This study comprehensively connected changes in physiological events with dynamic molecular changes. Ripening fruit that reached ‘Turning’ (T) after dark storage at 20°C, 12.5°C, or 5°C chilling (followed by 20°C rewarming) were compared to fresh-harvest fruit ‘FHT’. Fruit stored at 12.5°C had the biggest epigenetic marks and alterations in gene expression, exceeding changes induced by postharvest chilling. Fruit physiological and chronological age were uncoupled at 12.5°C, as the time-to-ripening was the longest. Fruit ripening to Turning at 12.5°C was not climacteric; there was no respiratory or ethylene burst, rather, fruit were high in abscisic acid. Clear differentiation between postharvest-ripened and ‘FHT’ was evident in the methylome and transcriptome. Higher expression of photosynthetic genes and chlorophyll levels in ‘FHT’ fruit pointed to light as influencing the molecular changes in fruit ripening. Finally, correlative analyses of the -omics data putatively identified genes regulated by DNA methylation. Collectively, these data improve our interpretation of how tomato fruit ripening patterns are altered by postharvest practices, and long-term are expected to help improve fruit quality.