刘杰等《Plant Physiology》2023年

论文题目：Stripe rust effector Pst21674 compromises wheat resistance by targeting transcription factor TaASR3

论文作者：Peijing Zheng, Mengxue Liu, Lijing Pang, Ruyi Sun, Mohan Yao, Xiaojie Wang, Zhensheng Kang, Jie Liu

论文摘要：Pathogens compromise host defense responses by strategically secreting effector proteins. However, the molecular mechanisms by which effectors manipulate disease-resistance factors to evade host surveillance remain poorly understood. In this study, we characterized a Puccinia striiformis f. sp.tritici (Pst) effector Pst21674 with a signal peptide. Pst21674 was significantly up-regulated during Pst infections in wheat (Triticumaestivum L.), and knocking down Pst21674 by host-induced gene silencing led to reduced Pst pathogenicity and restricted hyphal spread in wheat. Pst21674 interaction with the abscisic acid-, stress- and ripening-induced protein TaASR3 was validated mainly in the nucleus. Size exclusion chromatography, bimolecular fluorescence complementation, and luciferase complementation imaging assays confirmed that TaASR3 could form a functional tetramer. Virus-induced gene silencing and overexpression demonstrated that TaASR3 contributes to wheat resistance to stripe rust by promoting accumulation of reactive oxygen species (ROS) and cell death. Additionally, transcriptome analysis revealed that the expression of defense-related genes was regulated in transgenic wheat plants overexpressing TaASR3. Interaction between Pst21674 and TaASR3 interfered with the polymerization of TaASR3 and suppressed TaASR3-mediated transcriptional activation of defense-related genes. These results indicate that Pst21674 serves as an important virulence factor secreted into the host nucleus to impede wheat resistance to Pst, possibly by targeting and preventing polymerization of TaASR3.

病原体侵染植物时可通过分泌效应蛋白来破坏宿主的防御反应。然而，关于效应子调控抗病因子以逃避寄主监视的分子机制仍然知之甚少。本研究鉴定了一个含有信号肽的小麦条锈菌(Pst)效应子Pst21674。Pst21674在条锈菌侵染早期显著上调表达，利用寄主诱导的基因沉默技术（HIGS）沉默Pst21674，条锈菌的致病性降低，菌丝发育受到明显抑制。Pst21674与脱落酸、胁迫和成熟诱导蛋白TaASR3在细胞核中相互作用。分子凝胶过滤层析技术、双分子荧光互补和荧光素酶互补成像技术确定TaASR3可以形成一个功能性的四聚体。病毒诱导的基因沉默技术（VIGS）和转基因过表达表明，TaASR3通过活性氧(ROS)的积累和细胞死亡增强小麦对条锈病的抗性。此外，转录组分析显示，在过表达TaASR3的转基因小麦植株中，防御相关基因的表达受到调控。Pst21674与TaASR3的相互作用干扰了TaASR3的聚合，抑制了TaASR3介导的防御相关基因的转录激活。这些结果表明，Pst21674作为一个重要的毒力因子分泌到寄主细胞核中，通过靶向和干扰TaASR3的聚合来抑制小麦对条锈菌的抗性。

论文链接：https://doi.org/10.1093/plphys/kiad497