Abstract
BackgroundMelatonin is a pleiotropic signaling molecule that plays multifarious roles in plants stress tolerance. The polyamine (PAs) metabolic pathway has been suggested to eliminate the effects of environmental stresses. However, the underlying mechanism of how melatonin and PAs function together under heat stress largely remains unknown. In this study, we investigated the potential role of melatonin in regulating PAs and nitric oxide (NO) biosynthesis, and counterbalancing oxidative damage induced by heat stress in tomato seedlings.ResultsHeat stress enhanced the overproduction of reactive oxygen species (ROS) and damaged inherent defense system, thus reduced plant growth. However, pretreatment with 100 μM melatonin (7 days) followed by exposure to heat stress (24 h) effectively reduced the oxidative stress by controlling the overaccumulation of superoxide (O2•−) and hydrogen peroxide (H2O2), lowering the lipid peroxidation content (as inferred based on malondialdehyde content) and less membrane injury index (MII). This was associated with increased the enzymatic and non-enzymatic antioxidants activities by regulating their related gene expression and modulating the ascorbate–glutathione cycle. The presence of melatonin induced respiratory burst oxidase (RBOH), heat shock transcription factors A2 (HsfA2), heat shock protein 90 (HSP90), and delta 1-pyrroline-5-carboxylate synthetase (P5CS) gene expression, which helped detoxify excess ROS via the hydrogen peroxide-mediated signaling pathway. In addition, heat stress boosted the endogenous levels of putrescine, spermidine and spermine, and increased the PAs contents, indicating higher metabolic gene expression. Moreover, melatonin-pretreated seedlings had further increased PAs levels and upregulated transcript abundance, which coincided with suppression of catabolic-related genes expression. Under heat stress, exogenous melatonin increased endogenous NO content along with nitrate reductase- and NO synthase-related activities, and expression of their related genes were also elevated.ConclusionsMelatonin pretreatment positively increased the heat tolerance of tomato seedlings by improving their antioxidant defense mechanism, inducing ascorbate–glutathione cycle, and reprogramming the PAs metabolic and NO biosynthesis pathways. These attributes facilitated the scavenging of excess ROS and increased stability of the cellular membrane, which mitigated heat-induced oxidative stress.
Highlights
Melatonin is a pleiotropic signaling molecule that plays multifarious roles in plants stress tolerance
Heat shock-induced oxidative damage occurs as a result of excess formation of singlet oxygen (1O2), superoxide radical (O2−), hydrogen peroxide (H2O2), and hydroxyl radical (OH) under heat stress [5]; this leads to overproduction of malondialdehyde (MDA) and reduces membrane stability, permeability, and mobility, and impairs protein membrane polymerization [6, 7]
The results showed that superoxide dismutase (SOD) (Fig. 4e), CAT (Fig. 4f), ascorbate peroxidase (APX) (Fig. 4h), and glutathione S-transferase (GST) (Fig. 6h) gene expression levels were upregulated by 1.6, 1.2, 3.2, and 1.3-fold, respectively, in response to their corresponding control groups
Summary
Melatonin is a pleiotropic signaling molecule that plays multifarious roles in plants stress tolerance. We investigated the potential role of melatonin in regulating PAs and nitric oxide (NO) biosynthesis, and counterbalancing oxidative damage induced by heat stress in tomato seedlings. In an unfavorable environment, plants develop an inherent antioxidative defense strategy to detoxify excess ROS, which helps to protect them from oxidative damage [8]. This efficient anti-oxidative defense mechanism consists of different enzymatic antioxidants, such as superoxide dismutase (SOD), catalase (CAT), peroxidase (POD), ascorbate peroxidase (APX), glutathione reductase (GR), monodehydroascorbate reductase (MDHAR), and dehydroascorbate (DHAR), and non-enzymatic antioxidants, such as ascorbate (AsA), glutathione (GSH), carotenoids, and phenols [2, 9, 10]. Heat shock transcription factors A2 (HsfA2) plays a key role in the regulation of expression of heat-shock proteins, ascorbate peroxidase 2 and galactinol synthase 1 and 2 under hightemperature challenged [13]
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