The transcription factor MYB52 regulates salt stress tolerance in tomato by modulating ion homeostasis and proline biosynthesis.

Abstract

Salt stress severely affects tomato (Solanum lycopersicum L.) survival and growth. Although the involvement of the tomato MYB gene family in response to salt stress has been well established, the mechanism underlying resistance to salt stress remains unclear. In this study, we investigated the role of MYB52 in conferring salt stress resistance using overexpression and knockout tomato seedlings obtained via genetic modification. We demonstrated that MYB52 improves the ability of tomato to withstand salt stress by enhancing antioxidant capacity, photosynthetic capacity, and proline content while reducing relative electrolyte leakage (REL) levels. Transcription of MYB52 was induced by salt stress-induced ABA accumulation. Activated MYB52 bound to the promoter of Salt Overly Sensitive 1 (SOS1), Na+/H+ exchanger 1 (NHX1), pyrroline-5-carboxylate synthetase 1 (P5CS1) and Ornithine δ-aminotransferase (OAT), thereby positively regulating their expression. This regulation resulted in enhanced potassium (K+) absorption, sodium (Na+) efflux, and proline content, which contributed to improved salt tolerance in tomato. Furthermore, silencing of SOS1, NHX1, P5CS1 and OAT impaired the salt tolerance of the WT and MYB52-OE plants. These results will refine the mechanistic framework for MYB52 and accelerate its application in crop improvement under increasing soil salinization, thereby advancing the sustainable and efficient production of tomatoes and other vegetable crops.