Laboratory study demonstrates that melatonin delays leaf senescence in Arabidopsis thaliana, suggesting targeted suppression of WRKY75 and salicylic acid signaling.
Leaf senescence is regulated by a number of physiological and genetic factors including the production of reactive oxygen species (ROS), salicylic acid (SA), and WRKY transcription factors. Although previous studies suggested that melatonin can delay leaf senescence, its mechanism of action has reminded unclear. Here, we report that melatonin delays WRKY75-mediated leaf senescence. Exogenous melatonin increased chlorophyll content and reduced ROS accumulation. It also up-regulated the serotonin N-acetyltransferase gene leading to elevated melatonin levels. In parallel, melatonin treatment decreased SA levels, and down-regulated the expression of salicylic acid induction deficient 2. In addition, expression of senescence-associated genes 13 and WRKY75, both positively associated with senescence, was reduced after melatonin treatment. Together, these findings suggest that melatonin delays leaf senescence by modulating ROS, SA, and WRKY75 signaling pathways.
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Wang et al. (2025) studied this question.
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