Submitted to: Meeting Proceedings
Publication Type: Proceedings
Publication Acceptance Date: May 5, 2007
Publication Date: January 8, 2008
Citation: Whitaker, B.D. 2008. Genetic and biochemical mechanisms of superficial scald development in apple and pear fruits. Meeting Proceedings. p. 257-268.
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 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, alpha-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.
Superficial scald is a physiological storage disorder of apple and pear fruits. It develops during prolonged cold storage and intensifies after removal to warmer temperatures. Despite many years of investigation, the biochemical mechanism of scald is still unknown. The prevailing hypothesis holds that oxidation products of the sesquiterpene alpha-farnesene are directly involved via generation of free radicals. A sharp rise in alpha-farnesene synthesis occurs shortly after scald-susceptible fruit are placed in air storage, and oxidation of alpha-farnesene to conjugated trienols (CTols) proceeds rapidly after about 6–8 weeks. CTol accumulation during storage is usually correlated with the subsequent incidence and severity of scald. Prestorage treatment of scald-susceptible apples or pears with 1-methylcyclopropene (1-MCP), a blocker of ethylene action, drastically reduced both alpha-farnesene synthesis and scald development. Silencing of genes controlling alpha-farnesene biosynthesis and/or conversion to CTols should prove or disprove the role of alpha-farnesene oxidation in the induction of scald. Logical targets for gene knockouts are genes encoding: 1) an isozyme of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR) committed to sesquiterpene synthesis; 2) alpha-farnesene synthase (AFS), which catalyzes the final rate-limiting step in alpha-farnesene biosynthesis; and 3) a hypothetical enzyme involved in the production of CTols, possibly a glutathione peroxidase (GPX) or glutathione S-transferase. To date we have cloned genes encoding AFS, three isozymes of HMGR, and a GPX from peel tissue of scald-susceptible apple and/or pear fruit. Expression of these genes in relation to the accumulation of alpha-farnesene and CTols and the incidence of scald in untreated and 1-MCP-treated apples and pears has been characterized. Results are discussed with respect to the induction of scald by alpha-farnesene oxidation products, the role of ethylene in scald development, and plans for RNAi suppression of alpha-farnesene synthesis in a scald-susceptible apple or pear cultivar.