Golovinomyces cichoracearum effector‐associated nuclear‐localisation of RPW8 .2 amplifies its expression to boost immunity in Arabidopsis
Golovinomyces cichoracearum effector‐associated nuclear‐localisation of RPW8 .2 amplifies its expression to boost immunity in Arabidopsis
复制标题
Golovinomyces cichoracearum 效应子 - 相关核 - RPW8 .2 的定位放大其表达以增强拟南芥中的免疫力
DOI：
10.1111/nph.18682
复制
发表时间：
2022
期刊：
影响因子：
9.4
通讯作者：
Li, Guo‐Bang
中科院分区：
文献类型：
--
作者：
Zhao, Jing‐Hao;Huang, Yan‐Yan;Wang, He;Yang, Xue‐Mei;Li, Yan;Pu, Mei;Zhou, Shi‐Xin;Zhang, Ji‐Wei;Zhao, Zhi‐Xue;Li, Guo‐Bang
拟南芥抗白粉病 8.2 (RPW8.2) 是由受感染表皮细胞中的白粉病 (PM) 真菌 (Golovinomyces cichoracearum) 特异性诱导的，可激活免疫力。然而，RPW8.2诱导的机制尚不清楚。在这里，我们鉴定了aG。通过对拟南芥 cDNA 文库进行酵母双杂交筛选，发现了与 RPW8.2 相互作用的菊苣效应子，称为 Gc-RPW8.2 相互作用蛋白 1 (GcR8IP1)。GcR8IP1 与 RPW8.2 具有物理关联，其真正有趣的新基因指结构域对于这种关联是必要且充分的。 GcR8IP1 被分泌并转移到感染 PM 的宿主细胞的细胞核中。 GcR8IP1 与 RPW8.2 的结合导致细胞核中 RPW8.2 的增加。反过来，核定位的 RPW8.2 促进了 RPW8.2 启动子的活性，导致 RPW8.2 的转录自我扩增，从而增强感染部位的免疫力。此外，GcR8IP1 的异位表达或宿主诱导的基因沉默支持其作为 PM 毒力因子的作用。总之，我们的结果揭示了通过改变 RPW8.2 的分配和 PM 真菌效应子触发的转录自我扩增来增强 RPW8.2 依赖性防御的机制，这例证了效应器触发免疫的非典型形式。
ArabidopsisRESISTANCE TO POWDERY MILDEW 8.2 (RPW8.2) is specifically induced by the powdery mildew (PM) fungus (Golovinomyces cichoracearum) in the infected epidermal cells to activate immunity. However, the mechanism of RPW8.2‐induction is not well understood.Here, we identify aG. cichoracearumeffector that interacts with RPW8.2, named Gc‐RPW8.2 interacting protein 1 (GcR8IP1), by a yeast two‐hybrid screen of anArabidopsiscDNA library.GcR8IP1 is physically associated with RPW8.2 with its REALLY INTERESTING NEW GENE finger domain that is essential and sufficient for the association. GcR8IP1 was secreted and translocated into the nucleus of host cell infected with PM. Association of GcR8IP1 with RPW8.2 led to an increase in RPW8.2 in the nucleus. In turn, the nucleus‐localized RPW8.2 promoted the activity of theRPW8.2promoter, resulting in transcriptional self‐amplification ofRPW8.2to boost immunity at infection sites. Additionally, ectopic expression or host‐induced gene silencing ofGcR8IP1supported its role as a virulence factor in PM.Altogether, our results reveal a mechanism of RPW8.2‐dependent defense strengthening via altered partitioning of RPW8.2 and transcriptional self‐amplification triggered by a PM fungal effector, which exemplifies an atypical form of effector‐triggered immunity.