SlNAC63-SlbHLH71 module enhances tomato saline-alkali tolerance via regulating JA biosynthesis and ROS scavenging.

Soil salinization severely limits plant growth and development, posing a significant threat to agriculture. NAC transcription factors are widely involved in the regulation of various abiotic stresses. In this study, we discovered that SlNAC63 responds to both saline-alkali and jasmonic acid (JA) signaling and enhances saline-alkali tolerance in tomato (Solanum lycopersicum L.) by improving the reactive oxygen species (ROS) scavenging capacity. The experiments of Y1H, EMSA, and ChIP-qPCR confirmed that SlNAC63 directly targets and regulates the expression of tomato SlAOS1 and superoxide dismutase SlSOD4. This, in turn, promotes JA biosynthesis and enhances ROS scavenging ability, thereby positively regulating saline-alkali tolerance in tomato. Phenotypic analysis demonstrated that overexpressing SlAOS1 indeed increases JA accumulation, while overexpressing SlSOD4 significantly improves ROS scavenging under saline-alkali stress. Through Y2H, pull-down, and Co-IP assays, we found that SlNAC63 interacts with SlbHLH71. Furthermore, SlbHLH71 enhances the regulatory effects of SlNAC63 on SlAOS1 and SlSOD4 by interacting with SlNAC63 to strengthen its binding affinity to the promoters of SlAOS1 and SlSOD4, thereby promoting JA accumulation and ROS scavenging, which ultimately strengthens saline-alkali tolerance in tomato. This study unveils the central role of the SlNAC63-SlbHLH71 module in the regulation of saline-alkali stress and clarifies the molecular mechanism by which this module participates in the response of tomato to saline-alkali stress through the regulation of JA accumulation and ROS scavenging.