Liu Jie, Guan Tao, Zheng Peijing, Chen Liyang, Yang Yang, Huai Baoyu, Li Dan, Chang Qing, Huang Lili, Kang Zhensheng
State Key Laboratory of Crop Stress Biology for Arid Areas and College of Life Sciences, Northwest A&F University, Yangling, People's Republic of China.
State Key Laboratory of Crop Stress Biology for Arid Areas and College of Plant Protection, Northwest A&F University, Yangling, People's Republic of China.
Environ Microbiol. 2016 Nov;18(11):4118-4135. doi: 10.1111/1462-2920.13451. Epub 2016 Aug 1.
Accumulation of reactive oxygen species (ROS) following plant-pathogen interactions can trigger plant defence responses and directly damage pathogens. Thus, it is essential for pathogens to scavenge host-derived ROS to establish a parasitic relationship. However, the mechanisms protecting pathogens from host-derived oxidative stress remain unclear. In this study, a superoxide dismutase (SOD) gene, PsSOD1, was cloned from a wheat-Puccinia striiformis f. sp. tritici (Pst) interaction cDNA library. Transcripts of PsSOD1 were up-regulated in the early infection stage. Heterologous mutant complementation and biochemical characterization revealed that PsSOD1 encoded a Zn-only SOD. The predicted signal peptide was functional in an invertase-mutated yeast strain. Furthermore, immunoblot analysis of apoplastic proteins in Pst-infected wheat leaves and bimolecular fluorescence complementation suggested that PsSOD1 is a secreted protein that potentially forms a dimer during Pst infection. Overexpression of PsSOD1 enhanced Schizosaccharomyces pombe resistance to exogenous superoxide. Transient expression of PsSOD1 in Nicotiana benthamiana suppressed Bax-induced cell death. Knockdown of PsSOD1 using a host-induced gene silencing (HIGS) system reduced the virulence of Pst, which was associated with ROS accumulation in HIGS plants. These results suggest that PsSOD1 is an important pathogenicity factor that is secreted into the host-pathogen interface to contribute to Pst infection by scavenging host-derived ROS.
植物与病原体相互作用后活性氧（ROS）的积累可触发植物防御反应并直接损伤病原体。因此，病原体清除宿主来源的ROS以建立寄生关系至关重要。然而，保护病原体免受宿主来源氧化应激的机制仍不清楚。在本研究中，从一个小麦-条锈菌（Puccinia striiformis f. sp. tritici，Pst）相互作用的cDNA文库中克隆了一个超氧化物歧化酶（SOD）基因PsSOD1。PsSOD1的转录本在感染早期上调。异源突变体互补和生化特性分析表明，PsSOD1编码一种仅含锌的SOD。预测的信号肽在一个转化酶突变的酵母菌株中具有功能。此外，对Pst感染的小麦叶片质外体蛋白的免疫印迹分析和双分子荧光互补表明，PsSOD1是一种分泌蛋白，在Pst感染期间可能形成二聚体。PsSOD1的过表达增强了粟酒裂殖酵母对外源超氧化物的抗性。PsSOD1在本氏烟草中的瞬时表达抑制了Bax诱导的细胞死亡。使用宿主诱导基因沉默（HIGS）系统敲低PsSOD1降低了Pst的毒力，这与HIGS植物中ROS的积累有关。这些结果表明，PsSOD1是一种重要的致病因子，它被分泌到宿主-病原体界面，通过清除宿主来源的ROS促进Pst感染。
