GmSNAT1 enhances cold tolerance in soybean by promoting melatonin biosynthesis and interacting with GmPSYR1.
The GmSNAT1 gene, which encodes a key enzyme involved in soybean melatonin biosynthesis, is crucial for abiotic stress tolerance. In the present study, the molecular mechanism by which GmSNAT1 enhances cold tolerance is elucidated. The cold tolerance of plants was significantly increased by GmSNAT1 overexpression and reduced by CRISPR/Cas9-mediated knockout, a phenotype that was effectively rescued by exogenous melatonin. Integrated transcriptomic, physiological, and biochemical analyses revealed that the GmSNAT1-mediated melatonin pathway activates calcium signaling; coordinates the crosstalk between auxin, abscisic acid, and ethylene; and mobilizes transcription factor networks to orchestrate bidirectional physiological responses. Additionally, the activation of antioxidant systems for reactive oxygen species scavenging and the upregulation of photosynthesis-related genes to maintain photosynthetic stability were explored. The physical interaction between GmSNAT1 and the plant sulfotyrosine peptide receptor GmPSYR1 was confirmed using co-immunoprecipitation, bimolecular fluorescence complementation, and yeast two-hybrid assays. This interaction may be involved in cold stress signal transduction, regulation of root development, and redox homeostasis through GmPSYR1. Collectively, these findings demonstrate that cold adaptation in soybeans is synergistically enhanced by GmSNAT1 via a multidimensional axis encompassing melatonin synthesis, signal transduction, and physiological protection, thereby providing a novel molecular target for breeding cold-tolerant crops.