Spermidine mediated endogenous nitric oxide coordinately boosts stability through antioxidant capacity and Na+/K+ transporters in tomato under saline-alkaline stress

Spermidine (Spd) and nitric oxide (NO) are closely intertwined in their synthesis and play a significant role in plant responses to saline-alkaline stress. However, the specific interactions between Spd and NO in alleviating the toxicity of saline-alkaline stress in plants remain poorly understood. In this study, we aimed to elucidate the involvement of NO in the regulation of saline-alkaline stress tolerance by spermidine (Spd). To achieve this, we employed exogenous Spd treatment, NO synthesis inhibitors, and NO scavengers. We found that exogenous Spd stimulates NO synthesis in the leaves and roots of tomato seedlings by upregulating the nitrate reductase (NR) activities and the expression of its coding gene SlNR1. Importantly, when NO synthesis is inhibited or NO is scavenged, the regulatory effects of Spd on proline content, antioxidant enzyme system, ionic homeostasis, and the expression of genes involved in Na+/K+homeostasis in tomato seedlings are compromised under saline-alkaline stress. These observations suggest that NO plays a pivotal role in the defensive mechanisms induced by Spd against saline-alkaline stress in tomato seedlings. Consequently, Spd enhances the tolerance of tomato plants to saline-alkaline stress by regulating the nitrate reductase (NR) signaling pathway and mediating NO synthesis.