Induction of ethylene in avocado fruit in response to chilling stress on tree.

Chilling of avocado fruit (Persea americana cv. Arad) in the orchard caused a dramatic induction of fruit ripening and a parallel increase in ethylene biosynthesis and receptor genes' expression during shelf life. In-orchard chilling stress stimulated ethylene and CO(2) production already in fruit attached to the tree, and these reduced thereafter during 20 degrees C storage. In non-chilled control fruit, ethylene and CO(2) production started after 3d at 20 degrees C and exhibited a climacteric peak. In-orchard chilling stress also led to membrane destruction expressed as higher electrical conductivity (EC) in chilling stressed (CS) fruit and accelerated softening compared with control fruit. The increase in ethylene production on the day of harvest in CS fruit was accompanied by high expression of two 1-aminocyclopropane-1-carboxylic aCSd (ACC) synthase genes: PaACS1 and PaACS2, and ACC oxidase PaACO. The initial gene expressions of PaACS1, PaACS2, and PaACO in the CS fruit at the day of harvest was similar to the levels reached by the control fruit after 4d at 20 degrees C. The expression levels of both PaETR and PaERS1 in CS fruit on tree were 25 times higher than the control. In control fruit, expression of ethylene receptor genes was very low at harvest and increased in parallel to the onset of the climacteric ethylene peak. PaCTR1 transcript levels were less affected by chilling stress, and small changes (less than 3-fold) were observed in CS fruit on the day of harvest. Together, our results suggest that ethylene biosynthesis and ethylene response-pathway genes are involved in regulation of ethylene responsiveness in response to in-orchard chilling stress and during ripening.