Salt-stress-induced tomato sweetening involves an SlSnRK2.6-SlZHD8 sugar accumulation cascade triggered by root-derived abscisic acid.

Crop quality arises from the interplay of genetics and environment. While moderate salt stress is known to enhance fruit sweetness, the underlying molecular mechanisms remain unclear. Using tomato (Solanum lycopersicum) as a model, this study investigates how salt stress promotes fruit sugar accumulation. Root-derived abscisic acid (ABA) transport to fruit acts as the key signal under salt stress. Elevated fruit-ABA activates the kinase SlSnRK2.6, which phosphorylates the SlZHD8 transcription factor. This phosphorylation inhibits SlZHD8 function by reducing its protein stability and DNA-binding, thereby relieving its repression of SlSUS3 and SlSWEET12 to enhance fruit-sugar accumulation. Furthermore, the SlSnRK2.6-SlZHD8-SlSWEET12 module also regulates root-sugar accumulation and confers salt tolerance. Evolutionary analysis revealed a beneficial ZHD8 haplotype, whose reduced promoter-binding affinity promotes fruit-sugar accumulation under normal conditions and enhances salt tolerance. These findings explain how stress enhances quality and highlight the potential of key mutations of ZHD8, particularly the beneficial haplotype, for breeding tomatoes with improved sugar content and salt tolerance.