SlWRKY81 regulates Spd synthesis and Na⁺/K⁺ homeostasis through interaction with SlJAZ1 mediated JA pathway to improve tomato saline‐alkali resistance

Abstract

SUMMARYSaline‐alkali stress is an important abiotic stress factor affecting tomato (Solanum lycopersicum L.) plant growth. Although the involvement of the tomato SlWRKY gene family in responses to saline‐alkali stress has been well established, the mechanism underlying resistance to saline‐alkali stress remains unclear. In this study, we investigated the role of SlWRKY81 in conferring saline‐alkali stress resistance by using overexpression and knockout tomato seedlings obtained via genetic modification. We demonstrated that SlWRKY81 improves the ability of tomato to withstand saline‐alkali stress by enhancing antioxidant capacity, root activity, and proline content while reducing malondialdehyde levels. Saline‐alkali stress induces an increase in jasmonic acid (JA) content in tomato seedlings, and the SlWRKY81 promoter responds to JA signaling, leading to an increase in SlWRKY81 expression. Furthermore, the interaction between SlJAZ1 and SlWRKY81 represses the expression of SlWRKY81. SlWRKY81 binds to W‐box motifs in the promoter regions of SlSPDS2 and SlNHX4, thereby positively regulating their expression. This regulation results in increased spermidine (Spd) content and enhanced potassium (K+) absorption and sodium (Na+) efflux, which contribute to the resistance of tomato to saline‐alkali stress. However, JA and SlJAZ1 exhibit antagonistic effects. Elevated JA content reduces the inhibitory effect of SlJAZ1 on SlWRKY81, leading to the release of additional SlWRKY81 protein and further augmenting the resistance of tomato to saline‐alkali stress. In summary, the modulation of Spd synthesis and Na+/K+ homeostasis mediated by the interaction between SlWRKY81 and SlJAZ1 represents a novel pathway underlying tomato response to saline‐alkali stress.