Endogenous melatonin deficiency aggravates high temperature-induced oxidative stress in Solanum lycopersicum L

Melatonin is a natural biostimulating molecule that occurs in a number of plant species. Despite a short history of phytomelatonin research, the critical roles of melatonin in plant stress responses have extensively been documented. However, the majority of such studies constitute ‘pharmacological approach’ and studies exploring the relevance of endogenous melatonin are scanty. As an attempt to unmask the role of endogenous melatonin in plant thermotolerance, we generated melatonin deficient tomato plants by silencing a gene, CAFFEIC ACID O-METHYLTRANSFERASE 1 (COMT1), involved in melatonin biosynthesis. We first examined the effect of exogenous melatonin and then performed a detailed analysis of the effect of melatonin deficiency on oxidative stress markers, enzymatic and non-enzymatic antioxidants, and redox homeostasis in tomato plants. The results showed that suppression of endogenous melatonin had an opposite effect of exogenous melatonin on tomato tolerance to high temperature stress. Endogenous melatonin deficiency aggravated high temperature-induced oxidative stress as evidenced by increased electrolyte leakage percentage, malondialdehyde concentration, and oxidized and insoluble protein accumulation in tomato leaves. These changes were accompanied with the significant reductions in the activity of ascorbate peroxidase and catalase, two key antioxidant enzymes that play prominent role in plant thermotolerance. Furthermore, silencing of COMT1 altered redox balance as reflected by the significantly decreased ratios of GSH:GSSG and AsA:DHA under high temperature stress. In contrast, exogenous melatonin augmented the endogenous melatonin level in COMT1-silenced plants and alleviated the heat-induced oxidative stress. Our results suggest that an optimal endogenous melatonin level is critical, not only for its self-antioxidant capacity, but also for maintaining an efficient enzymatic antioxidant system and redox homeostasis under perturbed environmental conditions.