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.
摘要：
盐度阻碍植物生长和发育，导致作物产量下降和作物质量下降。一氧化氮（NO）和油菜素内酯（BR）是植物生长调节剂，可协调过多的植物生理反应。尽管如此，这些因素相互作用影响耐盐性的方式尚不清楚。BR被BR受体胆碱酯酶不敏感1（BRI1）及其共受体BRI1相关激酶1（BAK1）感知形成受体复合物，最终诱导BR调节的反应。为了应对压力，在真核细胞中经历了广泛的NO介导的蛋白质修饰。这里,我们表明，BR参与了番茄幼苗（Solanumlycopersicumcv。Micro-Tom)和NO可能在盐胁迫下激活BR信号，这与NO介导的S-亚硝基化有关。Further,体外和体内结果表明，BAK1（SERK3A和SERK3B）是S-亚硝基化的，在盐条件下受到抑制，并被NO增强。因此，SERK3A和SERK3B的敲低降低了BAK1的S-亚硝基化，并导致BR反应受损，从而消除NO诱导的耐盐性。此外,我们为BRI1和SERK3A/SERK3B之间的相互作用提供了证据。同时,没有增强BRI1-SERK3A/SERK3B相互作用。这些结果表明，NO介导的BAK1的S-亚硝基化增强了BRI1-BAK1的相互作用，促进了BR反应并随后提高了番茄的耐盐性。我们的发现说明了氧化还原信号和BR信号协调植物生长以响应非生物胁迫的机制。
