Overexpression of StBIN2 Improves Salt Stress Tolerance in Potato

Salt stress has become one of the major abiotic stress factors limiting sustainable crop production worldwide, and potato, as the fourth largest food crop globally, is particularly severely affected by saline and other environmental stresses in terms of its growth, development, yield, and quality. StBIN2 belongs to the GSK3 family of proteins, and numerous studies have confirmed that GSK3 family members widely regulate diverse abiotic stress responses and developmental processes in plants. However, the specific function and underlying mechanism of StBIN2 in the salt stress response of potato remain unclear. In this study, using the potato cultivar 'Chuanyu 10' as experimental material, we successfully isolated and cloned the StBIN2 gene and systematically investigated its biological function under salt stress. Subcellular localization analysis revealed that the StBIN2 protein is localized in the nucleus. Tissue-specific expression pattern analysis showed that StBIN2 transcript levels were significantly higher in leaves and tuber tissues than in other tissues. Under 200 mM NaCl salt stress treatment, StBIN2-overexpressing potato lines exhibited enhanced salt stress tolerance compared with WT plants, whereas gene-silenced lines displayed a hypersensitive phenotype to salt stress. Physiological parameter measurements demonstrated that the activities of superoxide dismutase (SOD) and catalase (CAT) in overexpressing transgenic plants were significantly upregulated relative to those in the WT, whereas the levels of malondialdehyde (MDA) and hydrogen peroxide (H₂O₂) were markedly reduced. Collectively, these experimental results confirm that StBIN2 significantly enhances salt tolerance in transgenic potato, indicating that potato StBIN2 positively participates in the physiological regulation of salt stress. This work lays an important foundation for further elucidation of the functional mechanism of StBIN2 within the plant abiotic stress response network.