Delayed senescence of apple leaves by exogenous melatonin treatment: toward regulating the ascorbate–glutathione cycle
Article first published online: 12 OCT 2011
© 2011 John Wiley & Sons A/S
Journal of Pineal Research
Volume 53, Issue 1, pages 11–20, August 2012
How to Cite
Wang, P., Yin, L., Liang, D., Li, C., Ma, F. and Yue, Z. (2012), Delayed senescence of apple leaves by exogenous melatonin treatment: toward regulating the ascorbate–glutathione cycle. Journal of Pineal Research, 53: 11–20. doi: 10.1111/j.1600-079X.2011.00966.x
- Issue published online: 5 JUL 2012
- Article first published online: 12 OCT 2011
- Accepted manuscript online: 14 SEP 2011 06:48PM EST
- Received July 26, 2011; Accepted September 9, 2011.
- ascorbate–glutathione cycle;
- chlorophyll degradation;
- leaf senescence;
Abstract: The objectives of this study were to test the effects of exogenous melatonin on apple (Malus domestica Borkh. cv. Golden Delicious) leaves and investigate its possible physiological role in delaying leaf senescence. Detached leaves treated with 10 mm melatonin solutions clearly showed a slowing in their process of dark-induced senescence, as evidenced by both biochemical and molecular parameters. Melatonin delayed the normal reduction in chlorophyll content and maximum potential photosystem II efficiency (Fv/Fm). It also suppressed the transcript levels of a key chlorophyll degradation gene, pheide a oxygenase (PAO), and the senescence-associated gene 12 (SAG12). This outcome was thought to be because of the enhanced antioxidant capabilities of melatonin. Indeed, H2O2 accumulation was inhibited by exogenous melatonin, which might have resulted from direct reactive oxygen species scavenging by melatonin and a great enhancement of ascorbate peroxidase (APX; EC 220.127.116.11), which acted on both mRNA and protein activity levels. Melatonin treatment led to the maintenance of higher contents of ascorbic acid (AsA) and glutathione (GSH) but less dehydroascorbate (DHA) and oxidized glutathione (GSSG) compared with the control, possibly through its regulation of the AsA–GSH cycle.