The SCF component SSK1A mediates degradation of the transcription factor SlWIP2 to regulate salinity stress tolerance in tomato

Salinity stress is a major abiotic stress that impairs growth and lowers yield in tomato (Solanum lycopersicum L.). Enhancing tolerance to salinity stress through breeding requires a comprehensive understanding of the molecular mechanisms underpinning tomato responses to salinity stress. In this study, we characterized the role of the C2H2 zinc-finger protein WIP domain protein 2 (SlWIP2) as a positive regulator of the salinity stress response in tomato. Overexpression of SlWIP2 in tomato led to higher activity of antioxidant enzymes and diminished accumulation of hydrogen peroxide. Conversely, a knockout of SlWIP2 generated by gene editing resulted in impaired antioxidant defenses under salinity stress conditions. We demonstrate that SlWIP2 interacts with SSK1A, the tomato homolog of S-phase kinase-associated protein 1 (SKP1), a component of SCF complexes involved in proteasome-mediated protein degradation. SSK1A mediates the degradation of SlWIP2 via the 26S proteasome pathway. To identify downstream targets of SlWIP2, we performed cleavage under targets and tagmentation (CUT&Tag) analysis, revealing SlUGT8 as a direct target of SlWIP2. We confirmed the direct binding of SlWIP2 to the SlUGT8 promoter via electrophoretic mobility shift assays and reporter assays, leading to higher SlUGT8 expression under salinity stress. In addition, a dual-luciferase reporter assay indicated that SSK1A acts upstream of SlWIP2 to repress its function, modulating SlUGT8 expression and influencing plant responses to salinity stress. Collectively, our findings uncover the SSK1A-SlWIP2-SlUGT8 regulatory module, providing insights into the molecular mechanisms of salinity stress tolerance in tomato and identifying potential targets for breeding salt-tolerant cultivars.