|Baldwin, Elizabeth - Liz|
Submitted to: Gordon Research Conference Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: 6/14/2010
Publication Date: N/A
Citation: N/A Interpretive Summary:
Technical Abstract: Hexanal, Z-3-hexenal, E-2-hexenal, hexanol and Z-3-hexenol are major tomato (Solanum Lycopersicon) volatile aromas derived from oxygenation of unsaturated fatty acids. Chilling or heating treatments suppress production of these C6 volatiles. The objective of this research was to determine the responses of lipoxygenase (LOX), hydroperoxide lyase (HPL) and alcohol dehydrogenase (ADH), enzymes involved in the oxylipin pathway, to chilling and heating treatments in terms of gene expression and enzyme activity. ‘Tasti Lee’ and ‘Sanibel’ tomatoes, harvested at different maturity stages, were ripened to full (red) ripe stage at ambient temperature. Fruit were then treated by either chilling (5 °C for 5 days) or heating (hot water, 52 °C for 15 min), then cooled with tap water to room temperature, or not-treated as control. Both chilling and heating treatments remarkably reduced C6 aldehyde and alcohol aroma volatiles, directly after treatment, and the levels of aldehydes did not totally recover after 4 days at 20 °C. Chilling treatment down-regulated TomLoxA, B, C, but not D expression, and increased overall LOX activity. Chilling also down-regulated HPL and ADH expression immediately after treatment, however, after 4 days at 20 °C, both genes were up-regulated compared to the control. HPL activity in chilled tomatoes was reduced, but recovered to control levels after 4 days at 20 °C. ADH activity in chilled fruit decreased after 4 days at 20 °C. On the other hand, heating up-regulated TomLoxB and TomLoxC expression greatly even after 4 days at 20 °C, and slightly down-regulated TomLoxA and TomLoxD, while increasing overall LOX activity. Heating up-regulated both HPL and ADH and the effect remained after 4 days at 20 °C. However, heating reduced activities of HPL on day 4 and ADH right after treatment. The results indicate that heating and chilling regulate C6 volatile production by different mechanisms. Chilling-inhibited C6 volatile production may be due to down-regulation of gene expression, except for TomloxD, and subsequent reduction of HPL and ADH enzyme activities in the oxylipin pathway. Heating-inhibition of C6 volatile production, was not due to gene expression, which was upregulated, but there was some suppression of HPL or ADH activities.