小立碗藓转录因子PpTF66调控离子通道PpSOT1在盐胁迫应答中的作用机制

全球6%以上土地盐碱化严重。约5亿年前陆地先锋苔藓植物从水登陆便可能面临干旱高盐等不良环境的胁迫，演化出应对机制的藓类就可能在盐碱地生长繁衍。但是，对藓类植物盐胁迫应答的分子调控机制并不清楚。前期研究我们发现，模式植物小立碗藓转录因子PpTF66激活了一条独立于ABI3介导的逆境应答途径；用CHIP技术等分离到PpTF66的靶基因，并对其中一些候选基因进行“敲除或过表达”遗传操作，发现一个编码“未知功能蛋白”的PpSOT1基因缺失或过表达的突变体植株在盐（NaCl）胁迫下有明显的敏感或耐受表型。实验结果显示，PpSOT1是膜蛋白并可定位于细胞质膜，具有“阳离子转运活性”。该申请项目将聚焦于：分析PpTF66调控PpSOT1在盐胁迫应答中的分子作用机制。拟采用遗传、细胞和生理生化等技术，分析PpTF66对PpSOT1的转录调控特点、表征PpSOT1对离子转运的分子作用机制。

More than 6% of the world's land is seriously salinized. About 500 million years ago, when the land pioneer bryophytes landed from water, they might face the stress of drought, high salinity and other adverse environments, and the mosses that evolved the coping mechanism might grow and multiply in saline-alkali land. However, the molecular regulatory mechanism of salt stress response in mosses is not clear. Previous studies have shown that PpTF66, a transcriptional factor in moss model Physcomitrella Patens, activates a stress response pathway independent of ABI3. Target genes of PpTF66 have been isolated by CHIP technology, and some of them have been "knocked out or overexpressed" by genetic manipulation. A mutant plant, when the PpSOT1 coding for "unknown functional protein" was deleted or overexpressed, showed obvious phenotype of sensitivity or tolerance under the Salt (NaCl) stress condition. Preliminary results showed that PpSOT1 encoded a membrane protein and could be localized in the plasma membrane, which had "cationic transport activity". The application project will focus on: revealing the mechanism of how the transcriptional factor PpTF66 regulates PpSOT1 to respond the Salt Stress in Physcomitrella Patens