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Heat stress and abscisic acid (ABA) induce leaf senescence, whereas melatonin (MT) and gibberellins (GA) play critical roles in inhibiting leaf senescence. Recent research findings confirm that plant tolerance to diverse stresses is closely associated with foliage lifespan. However, the molecular mechanism underlying the signaling interaction of MT with GA and ABA regarding heat-induced leaf senescence largely remains undetermined. Herein, we investigated putative functions of melatonin in suppressing heat-induced leaf senescence in tomato and how ABA and GA coordinate with each other in the presence of MT. Tomato seedlings were pretreated with 100 μM MT or water and exposed to high temperature (38/28°C) for 5 days (d). Heat stress significantly accelerated senescence, damage to the photosystem and upregulation of reactive oxygen species (ROS), generating RBOH gene expression. Melatonin treatment markedly attenuated heat-induced leaf senescence, as reflected by reduced leaf yellowing, an increased Fv/Fm ratio, and reduced ROS production. The Rbohs gene, chlorophyll catabolic genes, and senescence-associated gene expression levels were significantly suppressed by MT addition. Exogenous application of MT elevated the endogenous MT and GA contents but reduced the ABA content in high-temperature-exposed plants. However, the GA and ABA contents were inhibited by paclobutrazol (PCB, a GA biosynthesis inhibitor) and sodium tungstate (ST, an ABA biosynthesis inhibitor) treatment. MT-induced heat tolerance was compromised in both inhibitor-treated plants. The transcript abundance of ABA biosynthesis and signaling genes was repressed; however, the biosynthesis genes MT and GA were upregulated in MT-treated plants. Moreover, GA signaling suppressor and catabolic gene expression was inhibited, while ABA catabolic gene expression was upregulated by MT application. Taken together, MT-mediated suppression of heat-induced leaf senescence has collaborated with the activation of MT and GA biosynthesis and inhibition of ABA biosynthesis pathways in tomato.

In recent years, research on spermine (Spm) has turned up a lot of new information about this essential polyamine, especially as it is able to counteract damage from abiotic stresses. Spm has been shown to protect plants from a variety of environmental insults, but whether it can prevent the adverse effects of drought has not yet been reported. Drought stress increases endogenous Spm in plants and exogenous application of Spm improves the plants’ ability to tolerate drought stress. Spm’s role in enhancing antioxidant defense mechanisms, glyoxalase systems, methylglyoxal (MG) detoxification, and creating tolerance for drought-induced oxidative stress is well documented in plants. However, the influences of enzyme activity and osmoregulation on Spm biosynthesis and metabolism are variable. Spm interacts with other molecules like nitric oxide (NO) and phytohormones such as abscisic acid, salicylic acid, brassinosteroids, and ethylene, to coordinate the reactions necessary for developing drought tolerance. This review focuses on the role of Spm in plants under severe drought stress. We have proposed models to explain how Spm interacts with existing defense mechanisms in plants to improve drought tolerance.

Ozone (O3) is a gaseous environmental pollutant that can enter leaves through stomatal pores and cause damage to foliage. It can induce oxidative stress through the generation of reactive oxygen species (ROS) like hydrogen peroxide (H2O2) that can actively participate in stomatal closing or opening in plants. A number of phytohormones, including abscisic acid (ABA), ethylene (ET), salicylic acid (SA), and jasmonic acid (JA) are involved in stomatal regulation in plants. The effects of ozone on these phytohormones’ ability to regulate the guard cells of stomata have been little studied, however, and the goal of this paper is to explore and understand the effects of ozone on stomatal regulation through guard cell signaling by phytohormones. In this review, we updated the existing knowledge by considering several physiological mechanisms related to stomatal regulation after response to ozone. The collected information should deepen our understanding of the molecular pathways associated with response to ozone stress, in particular, how it influences stomatal regulation, mitogen-activated protein kinase (MAPK) activity, and phytohormone signaling. After summarizing the findings and noting the gaps in the literature, we present some ideas for future research on ozone stress in plants