Abstract

Salinity hinders plant growth and development, resulting in reduced crop yields and diminished crop quality. Nitric oxide (NO) and brassinolides (BR) are plant growth regulators that coordinate a plethora of plant physiological responses. Nonetheless, the way in which these factors interact to affect salt tolerance is not well understood. BR is perceived by the BR receptor BRASSINOSTEROID INSENSITIVE 1 (BRI1) and its co-receptor BRI1-associated kinase 1 (BAK1) to form the receptor complex, eventually inducing BR-regulated responses. To response stress, a wide range of NO-mediated protein modifications is undergone in eukaryotic cells. Here, we showed that BR participated in NO-enhanced salt tolerance of tomato seedlings (Solanum lycopersicum cv. Micro-Tom) and NO may activate BR signaling under salt stress, which was related to NO-mediated S-nitrosylation. Further, in vitro and in vivo results suggested that BAK1 (SERK3A and SERK3B) was S-nitrosylated, which was inhibited under salt condition and enhanced by NO. Accordingly, knockdown of SERK3A and SERK3B reduced the S-nitrosylation of BAK1 and resulted in a compromised BR response, thereby abolishing NO-induced salt tolerance. Besides, we provided evidence for the interaction between BRI1 and SERK3A/SERK3B. Meanwhile, NO enhanced BRI1-SERK3A/SERK3B interaction. These results imply that NO-mediated S-nitrosylation of BAK1 enhances the interaction BRI1-BAK1, facilitating BR response and subsequently improving salt tolerance in tomato. Our findings illustrate a mechanism by which redox signaling and BR signaling coordinate plant growth in response to abiotic stress.