The SlbHLH92 transcription factor enhances salt stress resilience by fine-tuning hydrogen sulfide biosynthesis in tomato.

Ongoing soil salinization severely hampers plant growth and the sustainability of global crops production. Hydrogen sulfide (H₂S), acting as a critical gaseous signaling molecule, plays a vital role in plant response to various environmental cues such as salt stress. Nonetheless, it is not well understood how the transcriptional network regulates H₂S production in response to salt stress in tomato. Herein, we determine that the bHLH transcription factor SlbHLH92 functions as a transcriptional activator in tomato (Solanum lycopersicum L.), upregulating the expression of the L-CYSTEINE DESULFHYDRASE 1 (SlLCD1) gene involved in H₂S biosynthesis, thereby enhancing the plants' tolerance to salt stress. When exposed to salt stress, overexpression of SlbHLH92 in tomato leads to enhanced salt tolerance compared to wild-type plants. In contrast, suppression of SlbHLH92 expression with RNAi silencing results in increased sensitivity to salt stress. Subsequent molecular and biochemical investigations confirm that the salt-induced SlbHLH92 upregulates the expression of SlLCD1, leading to an increase in H₂S levels, as well as other salt-responsive genes (SlCBL10 and SlVQ16), by directly binding to specific cis-elements in their promoter regions. Furthermore, the VQ-motif containing protein SlVQ16 physically interacts with SlbHLH92, thereby promoting an increase in its transcriptional activity. Taken together, our study reveals an emerging mechanism in which the SlbHLH92-SlVQ16-H₂S signaling cascade contributes to enhancing salt tolerance in tomato, presenting potential genetic targets for breeding salt-tolerant tomato cultivars.