The 2010 ASHS Annual Conference

Postharvest development of fruits harvested at ripening-competent, physiologically mature stages of development typically ensues via orderly expression of ripening- and senescence-associated genes, resulting in changes in pigmentation, volatile production, and carbohydrate modifications that render the commodities suitable for human consumption.  Storage regimes are often designed to delay but not permanently arrest these events. In contrast with ripening-competent fruits, other commodities including immature fruits, leafy crops and floral vegetables are harvested at stages of development in which mitotic activity and/or rapid physical growth are still underway. Once harvested, these commodities are incapable of continuing normal ontogeny and shelf life is maintained using storage conditions designed to strongly suppress global metabolism. The hypothesis under review is that immature commodities are genetically incapable of following a normal course of development upon harvest, and that their deterioration occurs via pathways unlike those exhibited by their fully mature, attached counterparts. Studies of accelerated aging in harvested immature commodities including asparagus spears (elongating, meristematic stem axes), broccoli (immature florets), young lettuce leaves, and immature cucumber fruit and pea carpels (immature, rapidly expanding fruit) have provided evidence that deterioration does not always parallel normal senescence but more so reflects highly specialized cases of programmed cell death (PCD). Triggered by multiple abiotic (environmental) and biotic (developmental) harvest stressors including ethylene, carbon depletion, and temperature extremes, the precise morphologies of cell death in these tissues are variable and dependent on organ type and stage of maturity at harvest. Commonly noted features of salvage-directed PCD include increased nuclease and protease activities, increased electrolyte leakage, vacuolar disruption and DNA laddering.  Tonoplast rupture without DNA laddering was reported for harvested immature lettuce leaves, and distinct morphological and physiological senescence phenotypes were noted for different lettuce varieties.  Differences among organ types are also noted in the timing of PCD events including DNA laddering, which can either precede or follow classic senescence symptoms (wilting, yellowing).  In general, PCD events prior to visible organ deterioration occur in commodities harvested immature, likely due to acutely perturbed homeostasis and remobilization metabolism.  As a corollary, it is proposed that accelerated PCD/senescence in response to biotic and abiotic stressors in stored fruits and vegetables might constitute the underlying basis of some physiological disorders.