Abstract

Saline-alkaline stress is one of several major abiotic stresses in crop production. Exogenous spermidine (Spd) can effectively increase tomato saline-alkaline stress resistance by relieving membrane lipid peroxidation damage. However, the mechanism through which exogenous Spd pre-treatment triggers the tomato antioxidant system to resist saline-alkaline stress remains unclear. Whether H2O2 and polyamine oxidase (PAO) are involved in Spd-induced tomato saline-alkaline stress tolerance needs to be determined. Here, we investigated the role of PAO and H2O2 in exogenous Spd-induced tolerance of tomato to saline-alkaline stress. Results showed that Spd application increased the expression and activities of superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), glutathione reductase (GR), and the ratio of reduced ascorbate (AsA) and glutathione (GSH) contents under saline-alkaline stress condition. Exogenous Spd treatment triggered endogenous H2O2 levels, SlPAO4 gene expression, as well as PAO activity under normal conditions. Inhibiting endogenous PAO activity by 1,8-diaminooctane (1,8-DO, an inhibitor of polyamine oxidase) significantly reduced H2O2 levels in the later stage. Moreover, inhibiting endogenous PAO or silencing the SlPAO4 gene increased the peroxidation damage of tomato leaves under saline-alkaline stress. These findings indicated that exogenous Spd treatment stimulated SlPAO4 gene expression and increased PAO activity, which mediated the elevation of H2O2 level under normal conditions. Consequently, the downstream antioxidant system was activated to eliminate excessive ROS accumulation and relieve membrane lipid peroxidation damage and growth inhibition under saline-alkaline stress. In conclusion, PAO triggered H2O2-mediated Spd-induced increase in the tolerance of tomato to saline-alkaline stress.

Highlights

  • Plants regularly face a variety of abiotic stresses, including salt [1], drought [2], and extreme temperatures stress [3] throughout their life; these stresses seriously affect their growth, development, and productivity [4,5]

  • H2 O2 is primarily formed in chloroplasts, mitochondria, peroxisomes, cytosol, and apoplast, which are mediated by NADPH oxidases (RBOH), diamine, and apoplastic polyamine oxidases (PAO)

  • Short-term salinealkaline stress stimulated tomato’s antioxidant system by increasing the gene expression and activities of superoxide dismutase (SOD), CAT, ascorbate peroxidase (APX), and glutathione reductase (GR) as well as the GSH content, which indicates that the SOD, CAT, and AsA-GSH cycles were involved in antioxidant activity in response to saline-alkaline stress (Figures 2 and 3)

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Summary

Introduction

Plants regularly face a variety of abiotic stresses, including salt [1], drought [2], and extreme temperatures stress [3] throughout their life; these stresses seriously affect their growth, development, and productivity [4,5]. Saline-alkaline stress-induced osmotic stress and ion toxicity result in metabolic disorders, increased electrolyte leakage, cell membrane permeability, excessive accumulation of reactive oxygen species (ROS), DNA damage, protein degradation, and inhibition of plant growth and development [8,9]. Plants perceive and defend against saline-alkaline stress through complex signal transduction pathways [10,11] to activate molecular, physiological, and biochemical responses, such as accumulating low molecular weight osmolytes (proline and PAs) [12], regulation of ion absorption and homeostasis [11,13], and activation of an antioxidant system to maintain internal redox homeostasis [2,12]. H2 O2 is the most abundant and relatively stable ROS in plant cells; it regulates redox signaling and metabolic pathways in response to salinity stress [2]. H2 O2 is primarily formed in chloroplasts, mitochondria, peroxisomes, cytosol, and apoplast, which are mediated by NADPH oxidases (RBOH), diamine, and apoplastic polyamine oxidases (PAO)

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