水稻耐盐新基因ST1的克隆与耐盐机制解析

盐胁迫是制约水稻产业发展的重要因素。申请人前期鉴定到一个新的耐盐突变体st1 (salt tolerance 1)，盐胁迫下st1表现出很强的耐盐性，耐盐相关生理指标也发生显著变化。进一步研究发现，ST1调控的水稻耐盐性与其蛋白含量负相关，盐胁迫可显著诱导ST1磷酸化。通过多种蛋白相关技术分析发现，蛋白激酶MAPK4与ST1存在物理互作，并能够磷酸化ST1，影响ST1蛋白的稳定性，推测ST1调控耐盐与其蛋白磷酸化修饰机制密切相关。为此，本项目拟以st1突变体及其相关转基因水稻为试材，深入解析磷酸化修饰在ST1调控水稻耐盐中的作用。在此基础上，厘清ST1参与水稻耐盐调控的具体信号通路，最终阐明磷酸化机制调控ST1耐盐性的分子机理。该研究有助于我们深入了解蛋白修饰机制在水稻耐盐性中的作用和机理，同时可为系统解析水稻耐盐的分子机理，利用分子设计育种获得耐盐、优质的水稻新材料奠定理论基础。

Salt stress is an important factor that restricts rice production. The applicant's previous study discovered a new salt-tolerant mutant st1 (salt tolerance 1). Under salt stress, the mutant exhibited a strong salt-tolerant phenotype, and the physiological indexes related to salt tolerance significantly changed. Further studies showed that ST1-regulated salt tolerance in rice was negatively correlated with its protein content, and salt stress could significantly induce ST1 phosphorylation. Through a variety of protein-related techniques, we found that the protein kinase MAPK4 can physically interact with and phosphorylate ST1, thereby affecting the protein stability of ST1, suggesting that ST1-regulated salt tolerance was closely related to its protein modification mechanism. Therefore, this project intends to use st1 mutants and their related transgenic rice as materials to deeply analyze the role of phosphorylation modification in ST1 regulation of rice salt tolerance. On this basis, the study will clarify the specific signaling pathways that ST1 regulates the salt tolerance, and finally clarify the molecular mechanism of the phosphorylation in ST1 regulated salt tolerance. This research will help us to deeply understand the role and mechanism of protein modification mechanism in rice salt tolerance, and at the same time, it can lay a theoretical foundation for systematically analyzing the molecular mechanism of rice salt tolerance and using molecular design and breeding to obtain salt-tolerant and high-quality materials.