Moderate NaCl modulates tomato fruit sugar-acid ratio via SlSR3-mediated regulation of SlPFK

Soil salinity, a prevalent environmental stress, has been shown to enhance fruit quality to some extent. Signal-responsive/calmodulin-binding transcription activators (SR/CAMTAs) are known to regulate plant growth and stress responses, yet their role in salt-mediated improvement of fruit organoleptic quality remains largely unexplored. Here, we investigated the involvement of SlSR3 in NaCl-induced enhancement of the sugar-acid ratio in tomato (Solanum lycopersicum L.) fruit. All tomato fruits used in this study were harvested at the identical developmental stage. Treatment with 50 mM NaCl significantly increased the sugar-acid ratio in wild-type and SlSR3-overexpressing fruits by elevating soluble sugars (glucose, fructose, sucrose) and reducing titratable acids (malic acid, tartaric acid). NaCl also enhanced the activities of sucrose synthase (SUS), phosphofructokinase (PFK), and citrate synthase (CS). In contrast, these effects were largely abolished in SlSR3 knockout lines, indicating that SlSR3 is required for the NaCl-induced improvement. Mechanistically, NaCl treatment upregulated fructose and citric acid-metabolism genes. Yeast one-hybrid, dual-luciferase reporter and chromatin immunoprecipitation quantitative PCR assays further demonstrated that SlSR3 directly binds to the SlPFK promoter and represses its transcriptional expression, while NaCl treatment significantly relieves this inhibitory effect. Moreover, SlPFK is indispensable for the regulatory function of SlSR3 in modulating NaCl-induced sugar-acid ratio. Collectively, our findings uncover that NaCl promotes the sugar‑acid ratio by alleviating SlSR3‑mediated transcriptional repression of SlPFK, a module in which SlSR3 otherwise negatively modulates this ratio. This work reveals a novel mechanism by which salt stress improves fruit quality via modulation of a SR/CAMTA transcription factor.