SlNOR interacts with SlMYB60 to regulate the jasmonic acid-mediated low-temperature stress response in tomato

Abstract Low-temperature stress significantly affects plant growth and development. NAM, ATAF, and CUC transcription factors (NAC TFs) play a crucial role in enhancing plant tolerance to low-temperature, drought, and salinity stresses by promoting the initiation of stress responses and signal transduction. In this study, we found that the NAC transcription factor gene NON RIPENING (SlNOR) is significantly induced by low-temperature and jasmonic acid (JA), and it promotes JA biosynthesis by directly targeting and regulating LIPOXYGENASE 10/LIPOXYGENASE 11 (SlLOX10/SlLOX11), thereby positively regulating low-temperature tolerance of tomato (Solanum lycopersicum). Both SlNOR- and SlLOX11-overexpressing lines exhibited a significant increase in JA accumulation under low-temperature stress, reducing excessive reactive oxygen species (ROS) accumulation. SlNOR interacted with V-MYB AVIAN MYELOBLASTOSIS VIRAL ONCOGENE HOMOLOG 60 (SlMYB60) at the protein level, and SlMYB60 directly targeted and regulated SlLOX10/SlLOX11. The phenotype of SlMYB60 overexpression was consistent with SlNOR overexpression. Additionally, MYELOCYTOMATOSIS 2 (SlMYC2), a key transcription factor in the JA signaling pathway, directly bound to SlNOR and promoted SlNOR expression. This study reveals the core function of the SlMYC2-SlNOR-SlMYB60-SlLOX10/11 module in regulating JA synthesis and clarifies the molecular mechanism through which this module regulates JA accumulation to participate in the low-temperature stress response in tomato.