条锈菌重要保守效应子PstGSRE1及其m9基序调控小麦免疫机理

小麦条锈病是我国小麦生产上重大致灾病害。前期发现，小麦条锈病菌(Pst)效应子PstGSRE1及其甘氨酸和丝氨酸富集基序m9，通过干扰小麦锌指蛋白转录因子TaLOL2进核而抑制植物免疫。然而，关于它们调控小麦免疫反应的分子机理有待进一步解析。本项目拟截断和点突变m9与TaLOL2，借助瞬时表达明确m9基序抑制寄主PTI和ETI免疫性的功能位点；利用蛋白质互作、荧光素酶互补（LUC）等途径，明确PstGSRE1与TaLOL2互作位点，并解析其与致病性关系。创制TaLOL2抗病过表达材料，通过Chip-seq解析转录因子TaLOL2结合的启动子原件，明确PstGSRE1干扰TaLOL2影响的小麦免疫信号通路。本研究将深入阐明富含甘氨酸和丝氨酸效应子PstGSRE1调控寄主免疫反应的机理，拓展对于小麦-条锈菌互作过程中免疫信号的理解，为开辟持久有效的小麦条锈病防控策略提供基因资源和理论依据。

Stripe rust, caused by Puccinia striiformis f. sp. tritici (Pst), gives great threats to wheat production in China. In our previous studies, we identified an important candidate glycine-serine-rich effector PstGSRE1 from Pst and found that PstGSRE1 and PstGSRE1-m9 motif disrupted nuclear localization of TaLOL2 and suppressed ROS-mediated cell death induced by TaLOL2, thus compromising host immunity. In this project, we will firstly mutate the PstGSRE1-m9 motif and TaLOL2 by peptide fragment and signal amino acid to uncover the functional sites of PstGSRE1, for which are essential for suppressing PTI and ETI of wheat. Secondly, we will reveal the interaction site between PstGSRE1-m9 and TaLOL2 by Pull-down, Co-IP and LUC. Thirdly, we will generate the overexpression transgenic wheat plant of TaLOL2 and find the promoter element of TaLOL2. Furthermore, the immunity pathway of TaLOL2 that disrupted by PstGSRE1 will be revealed by Chip-seq. This project will deeply address the molecular mechanisms of glycine-serine-rich effectors regulating plant immunity and provide gene resources and theoretical foundation for establishing strategies for sustainable control of wheat stripe rust.