Author
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Whitaker, Bruce |
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Submitted to: Acta Horticulturae
Publication Type: Proceedings Publication Acceptance Date: 2/20/2012 Publication Date: N/A Citation: N/A Interpretive Summary: Superficial scald is a disorder of apple and pear fruits that develops during long-term cold storage and intensifies after warming to market temperature. Scald symptoms, brown or black patches on the fruit skin, render the fruit unsalable. Losses can be 20 to 80% for fruit of some varieties after all the expense of growing, harvesting, and cold storage. Susceptibility to scald varies widely among apple and pear varieties, indicating that there is a distinct genetic basis for the disorder. For the last several years, we have sought to identify key genes involved in scald susceptibility. Our studies have singled out a particular gene, a-farnesene synthase (AFS), as a prime target for genetic manipulation to greatly diminish scald incidence in highly susceptible varieties. This could be accomplished by plant molecular biologists using gene-silencing technology or via more classical marker-assisted breeding. Success would eliminate the current scald control measure of a chemical drench that is costly and poses risks to human health and the environment, thus benefitting the pome industry as well as consumers. Technical Abstract: Superficial scald is a physiological storage disorder affecting apple and pear fruits. The disorder develops during cold storage and intensifies after removal to market temperatures. Scald symptoms result from necrosis of a few hypodermal cell layers and manifest as brown or black patches on the fruit skin. Susceptibility to scald varies greatly by cultivar, and is also influenced by preharvest factors such as growing climate and maturity, and postharvest factors including storage atmosphere, ventilation, and temperature. Despite many years of investigation, the biochemical mechanisms underlying scald are still in question. The disorder is thought to be a type of chilling injury induced by oxidative stress. A long-standing hypothesis holds that oxidation products of the sesquiterpene a-farnesene are directly involved via generation of free radicals. Variation in the antioxidant defense mechanisms required to scavenge radicals and combat oxidative stress is postulated to also play a key role in susceptibility or resistance to scald. A marked rise in a-farnesene synthesis typically occurs shortly after scald-susceptible fruit are placed in storage and oxidation of the a-farnesene to conjugated trienols (CTols) proceeds rapidly after about 6-8 weeks, particularly in air storage. High level accumulation of CTols during storage is usually correlated with the incidence and severity of scald. Further evidence supporting a link between a-farnesene oxidation and induction of scald was the finding that prestorage treatment of apples or pears with 1-methylcyclopropene (1-MCP), a blocker of ethylene action, drastically reduced a-farnesene synthesis and scald development. Silencing genes that control a-farnesene biosynthesis or conversion to CTols should prove or disprove a major role of a-farnesene oxidation in the induction of scald. The primary target for gene knockout is AFS1 encoding a-farnesene synthase, which catalyzes the final step in a-farnesene biosynthesis. Enzymatic production of CTols is as yet hypothetical, but possibly a glutathione peroxidase or glutathione S-transferase catalyzes reduction of farnesyl hydroperoxides to the corresponding alcohols. In addition, the precise mechanisms whereby 1-MCP, diphenylamine, UV-visible light irradiation, initial low oxygen stress, and intermittent warming ameliorate or prevent scald are currently being investigated using biochemical, functional genomics, and metabolomics approaches. |
