Abstract
The beneficial role of melatonin (MT) as a potent broad-spectrum antioxidant and hormone-like regulator in plant protection against adverse environmental conditions is indisputable. However, the molecular networks underlying its unique scavenging capabilities are still far from understood. Herein, we show the ability of MT to maintain physiological functions under high light stress (HL) is mediated by photoreceptors. Melatonin treatment (50 μM) of the photoreceptor mutants phyA/B and cry1/2 augmented the deleterious effects of excess light (600 μmol m(-2) s(-1), 24 h), as evidenced by increased TBARs levels and electrolyte leakage, as well as decreased photosynthetic efficiency, in contrast to their parental form, Landsberg erecta, in which these parameters were significantly improved. The reduced stress resistance of the mutants was also confirmed by analysis of the transcript accumulation of ROS markers and enzymatic scavengers. Moreover, the increase in melatonin content in the mutants exposed to HL + MT contributed to increased ROS accumulation; therefore, the deleterious effect of MT could not be explained by an imbalance in ROS production below the cytostatic level. We hypothesize that the light-sensitive phenotypes of photoreceptor mutants under MT treatment may be due to the misregulation of stress-related genes that are targets for melatonin action.