Puccinia striiformis f. sp. tritici (Pst), a biotrophic plant pathogen, secretes numerous effectors to modulate host defense systems. Understanding the molecular mechanisms by which Pst effectors regulate wheat immunity is of great importance for the development of novel strategies for durable control of stripe rust. In this study, we identified a glycine-serine-rich effector gene, PstGSRE1, which is highly induced during early infection. Transgenic expression of PstGSRE1 RNAi constructs in wheat significantly reduced virulence of Pst and increased H₂O₂ accumulation in wheat. PstGSRE1 was shown to target the reactive oxygen species (ROS)-associated transcription factor TaLOL2, a positive regulator of wheat immunity. PstGSRE1 disrupted nuclear localization of TaLOL2 and suppressed ROS-mediated cell death induced by TaLOL2, thus compromising host immunity. This work reveals a previously unrecognized strategy whereby rust fungi exploit the PstGSRE1 effector to defeat ROS-associated plant defense by modulating the subcellular compartment of a host immune regulator and facilitate pathogen infection.

小麦条锈菌f。sp。小麦（的Pst），活体营养植物病原体，分泌大量的效应来调节宿主防御系统。理解Pst效应子调节小麦免疫力的分子机制 对于开发持久控制条锈病的新策略非常重要。在这项研究中，我们确定了富含甘氨酸丝氨酸的效应基因PstGSRE1，该基因在早期感染期间被高度诱导。PstGSRE1 RNAi构建体在小麦中的转基因表达显着降低了Pst的毒力并增加了H ₂ O ₂在小麦中积累。已显示PstGSRE1靶向与活性氧（ROS）相关的转录因子TaLOL2，这是小麦免疫力的正调节剂。PstGSRE1破坏TaLOL2的核定位并抑制TaLOL2诱导的ROS介导的细胞死亡，从而损害宿主免疫力。这项工作揭示了一种以前未被认识的策略，在该策略中，锈病真菌利用PstGSRE1效应子通过调节宿主免疫调节剂的亚细胞区室并促进病原体感染来克服ROS相关的植物防御作用。