Lester Workshop

Superfi cial scald of apples and pears, which manifests as brown or black patches on the fruit skin, results from necrosis of the hypodermal cortical tissue (Bain and Mercer, 1963) and is thought to be induced by oxidation products of the sesquiterpene (E,E)-α-farnesene (Anet, 1972a; Huelin and Coggiola, 1970a, 1970b; Huelin and Murray, 1966). Synthesis of sesquiterpenes in plant tissues occurs mainly via the cytosolic mevalonic acid (MVA) pathway, which is initiated by the enzyme 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR) (Eisenreich et al., 2001). Studies utilizing radiolabeled precursors (Rupasinghe et al., 2001) or a statin inhibitor of HMGR (Ju and Curry, 2000a) indicated that in apple peel α-farnesene is synthesized almost exclusively via the MVA pathway, rather than the chloroplastic deoxyxylulose phosphate pathway. Fruit of scald-susceptible apple cultivars such as ‘Granny Smith’, ‘Law Rome’, and ‘Red Delicious’ typically exhibit a burst of α-farnesene synthesis shortly after they are placed in low-temperature storage, which results in a marked accumulation of the sesquiterpene in the skin and epicuticular coating during the fi rst 8 to 12 weeks (Fig. 1a) (Anet, 1972a; Huelin and Coggiola, 1968; Whitaker et al., 1997, 1998). The concentration of α-farnesene subsequently plateaus and then declines as its conjugated triene oxidation products increase to a maximum at ≈20 to 28 weeks (Fig. 1b) (Anet, 1972a; Huelin and Coggiola, 1970a; Whitaker et al., 1997, 1998). The primary in vivo oxidation products of α-farnesene that accumulate in apple epicuticular wax and peel tissue during cold storage have been identifi ed as conjugated trienols, 9E and 9Z isomers of 2,6,10-trimethyldodeca-2,7,9,11-tetraen-6-ol (Rowan et al., 1995; Whitaker et al., 1997). A recent study showed that application of these conjugated trienols and their corresponding hydroperoxides to apple fruit before storage induced symptoms indistinguishable from naturally occurring superfi cial scald (Rowan et al., 2001). Prestorage treatment of apples with the antioxidant diphenylamine (DPA) inhibits oxidation of α-farnesene and largely prevents development of scald (Huelin and Coggiola, 1970a). Moreover, exposure of apple fruit to the blockers of ethylene action diazocyclopentadiene and 1-methylcyclopropene (1-MCP) greatly curtails α-farnesene production and markedly reduces scald incidence and severity (Gong and Tian, 1998; Fan et al., 1999; Rupasinghe et al., 2000a; Shaham et al., 2003; Watkins et al., 2000). Results from the studies with 1-MCP as well as several previous reports (Du and Bramlage, 1994a; Watkins et al., 1993, 1995; Whitaker and Solomos, 1997) show that ethylene perception, production, and responsiveness are clearly involved in regulation of α-farnesene synthesis and induction of scald in apple fruit. This paper presents and overview of α-farnesene biosynthesis and oxidation in apple fruit in relation to the longstanding hypothesis that oxidation products of this sesquiterpene are directly involved in induction of superfi cial scald. Progress toward understanding regulation of α-farnesene synthesis in apple by specifi c genes and enzymes is reviewed, and strategies for molecular genetic suppression of α-farnesene synthesis are discussed. In addition, an alternative hypothesis that apple scald is caused by more general oxidative stress and the inability to detoxify reactive oxygen species and free radicals is briefl y elaborated.