SlSTE1 promotes abscisic acid-dependent salt stress-responsive pathways via improving ion homeostasis and reactive oxygen species scavenging in tomato.

High salinity is one of the major limiting factors that reduces crop productivity and quality. Herein, we report that small SALT TOLERANCE ENHANCER1 (STE1) protein without any known conserved domains is required for tomato salt tolerance. Overexpression (OE) of SlSTE1 enhanced the tolerance to multiple chloride salts (NaCl, KCl, and LiCl) and oxidative stress, along with elevated antioxidant enzyme activities, increased abscisic acid (ABA) and chlorophyll contents, and reduced malondialdehyde (MDA) and reactive oxygen species (ROS) accumulations compared to that of wild-type (WT) plants. Moreover, decreased K efflux and increased H efflux were detected in the OE plants, which induced a higher K /Na ratio. In contrast, SlSTE1-RNAi plants displayed decreased tolerance to salt stress. RNA-seq data revealed 1 330 differentially expressed genes in the OE plants versus WT plants under salt stress, and the transcription of numerous and diverse genes encoding transcription factors, stress-related proteins, secondary metabolisms, kinases, and hormone synthesis/signaling-related proteins (notably ABA and 1-aminocyclopropane-1-carboxylate) was greatly elevated. Furthermore, SlSTE1-OE plants showed increased sensitivity to ABA, and the results suggest that SlSTE1 promotes ABA-dependent salt stress-responsive pathways by interacting with SlPYLs and SlSnRK2s. Collectively, our findings reveal that the small SlSTE1 protein confers salt tolerance via ABA signaling and ROS scavenging and improves ion homeostasis in tomato.