SlNAP1-SlGAI-SlAOS1 module regulates jasmonic acid biosynthesis mediating the low-temperature stress response in tomato.

Abstract

Low-temperature stress is a widespread form of abiotic stress globally, affecting all stages of plant growth and development and significantly impairing crop yield and quality. During the evolutionary process of plants adapting to environmental stress, the NAM, ATAF, and CUC (NAC) transcription factor (TF) family has gradually evolved into one of the core regulators of plant responses to abiotic stress. This study demonstrates that the NAC TF family member SlNAP1 responds significantly to low-temperature and jasmonic acid (JA) signals. It directly targets and regulates SlAOS1, promoting JA biosynthesis and positively regulating low-temperature tolerance in tomatoes. Under low-temperature stress, SlAOS1 overexpression leads to a significant rise in JA accumulation and alleviates reactive oxygen species (ROS) overproduction, whereas its knockout elicits the opposite phenotypic responses. Further investigation confirmed that SlGAI interacts with SlNAP1 and enhances its regulation of SlAOS1. Overexpression of SlGAI has a phenotype consistent with that of SlNAP1, significantly increasing JA accumulation and reducing ROS levels. Our findings demonstrate that the SlNAP1-SlGAI-SlAOS1 module plays a central role in JA biosynthesis and further define its function in mediating tomato responses to low-temperature stress via the regulation of JA accumulation.