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α α α α -Farnesene was not detectable in preclimacteric fruit peel at harvest. Mevalonic acid lactone (MAL) or farnesyl pyrophosphate (FPP) induced α -farnesene production when fed to preclimacteric peel tissue, but hydroxymethylglutaric acid (HMG) did not. Fruit stored at 0 °C for 30 days (climacteric fruit) produced α -farnesene, and addition of HMG, MAL, or FPP further increased α -farnesene production. When treated at harvest with Lovastatin at 1.25 mmol·L -1 and stored at 0 °C for 30 days, fruit produced ethylene but did not produce α -farnesene. Whereas MAL and FPP induced α α α α -farnesene production in peel sections from these fruit, HMG did not. Induction of α α α α α -farnesene by precursor feeding was concentration-dependent and had no effect on ethylene production. Cortical tissue sections from climacteric fruit did not produce α -farnesene unless HMG, MAL, or FPP were fed during incubation. Including Lovastatin at 0.63 mmol·L -1 in the feeding solution eliminated HMG induced α -farnesene production, but did not affect MAL or FPP-induced α -farnesene production. Neither precursor feeding nor Lovastatin treatment affected ethylene production in cortical tissues. Chemical name used: (1S-(1a (R °), 3α , 7β β β β β, 8β (2S°, 4S°), 8αβ ))-1,2,3,7,8,8α -hexahydro-3,7- dimethyl-8-(2-(tetrahydro-4-hydroxy-6-oxo-2H-pyran-2-yl)ethyl)-1-naphthalnyl 2-methylbutanoate (Lovastatin).

Lovastatin Inhibition of α-Farnesene Production in Ripening Apple: Precursor Feeding Studies