盐碱地是限制作物生产的重要因素之一。膜蛋白激酶参与了盐等逆境应答途径，对提高植物耐盐性发挥重要作用。本课题鉴定了一批耐盐相关基因，其中包括明显提高转基因水稻耐盐性的膜蛋白激酶TPK1。TPK1具有Ser/Thr和Tyr磷酸化的性质，是典型的双特异性蛋白激酶。本课题发现抑制TPK1基因的表达明显降低了小麦的耐盐性，而过表达TPK1可显著提高小麦的耐盐性，初步阐明了TPK1参与耐盐应答的作用模式。进一步发现，TPK1蛋白参与油菜素内酯BR和Ca2+信号传递，可能对盐胁迫信号传递起重要作用。然而，目前对双特异性蛋白激酶功能研究较少，本项目旨在鉴定BR和Ca2+信号对TPK1活性的调控机制，阐明TPK1介导的信号途径。这对深入了解小麦耐盐分子机制有重要意义，同时为作物抗逆育种提供理论依据。

Salt is one of the main factors limiting crop production. Member protein kinases are involved in salt-responsive pataway, which play improtant roles in improving salt tolerance in plants. The project applicant identified a series of salt-responsive genes from wheat, including membrane protein kinase gene TPK1. TPK1 is a typical dual specificity protein kinase with Ser/Thr and Tyr activity. The project team found that TaTPK1-RNAi decrease the salt tolerance; on the contrary, overexpression of TaTPK1 increased the salt tolerance in transgenic wheat. Furthermore, it was proved that TaTPK1 might be involved in brassinosteroid (BR) and Ca2+ signaling pathway. However, a few dual-specificity kinases were investigated in plants. To further investigate the TaTPK1-mediated salt stress signal pathway, the project aim was to identify the activity regulation of BR and Ca2+ signals to the TPK1, and to clarify the role of TaTPK1-mediated salt stress signal pathway. It is of great significance in in-depth understanding the TaTPK1-mediated signaling transduction network. At the same time, it is to provide important theoretical basis for crop stress-resistant breeding.