Zhang Liqing, Huang Xin, He Chengyong, Zhang Qing-Yu, Zou Xiaohua, Duan Ke, Gao Qinghua
Shanghai Key Laboratory of Protected Horticultural Technology, Forestry and Fruit Tree Research Institute, Shanghai Academy of Agricultural Sciences, Shanghai, China.
College of Food Science, Shanghai Ocean University, Shanghai, China.
Front Plant Sci. 2018 Apr 25;9:434. doi: 10.3389/fpls.2018.00434. eCollection 2018.
, which is part of the species complex, can cause anthracnose diseases in strawberries worldwide. However, the molecular interactions between and strawberry are largely unknown. A deep RNA-sequencing approach was applied to gain insights into the pathogenicity mechanisms of and the defense response of strawberry plants at different stages of infection. The transcriptome data showed stage-specific transcription accompanied by a step-by-step strawberry defense response and the evasion of this defense system by fungus. Fungal genes involved in plant cell wall degradation, secondary metabolism, and detoxification were up-regulated at different stage of infection. Most importantly, infection was accompanied by a large number of highly expressed effectors. Four new identified effectors function in the suppression of Bax-mediated programmed cell death. Strawberry utilizes pathogen-associated molecular patterns (PAMP)-triggered immunity and effector-triggered immunity to prevent invasion, followed by the initiation of downstream innate immunity. The up-regulation of genes related to salicylic acid provided evidence that salicylic acid signaling may serve as the core defense signaling mechanism, while jasmonic acid and ethylene pathways were largely inhibited by . The necrotrophic stage displayed a significant up-regulation of genes involved in reactive oxygen species activation. Collectively, the transcriptomic data of both and strawberry shows that even though plants build a multilayered defense against infection, employs a series of escape or antagonizing mechanisms to successfully infect host cells.
属于该物种复合体一部分的[具体物种名称未给出],可在全球范围内引发草莓炭疽病。然而,[具体物种名称未给出]与草莓之间的分子相互作用在很大程度上尚不清楚。应用深度RNA测序方法来深入了解[具体物种名称未给出]的致病机制以及草莓植株在感染不同阶段的防御反应。转录组数据显示了阶段特异性转录,伴随着草莓逐步的防御反应以及真菌对该防御系统的逃避。参与植物细胞壁降解、次生代谢和解毒的真菌基因在感染的不同阶段上调。最重要的是,[具体物种名称未给出]感染伴随着大量高表达的效应子。四个新鉴定的效应子在抑制Bax介导的程序性细胞死亡中发挥作用。草莓利用病原体相关分子模式(PAMP)触发的免疫和效应子触发的免疫来防止[具体物种名称未给出]入侵,随后启动下游固有免疫。与水杨酸相关基因的上调提供了证据,表明水杨酸信号传导可能作为核心防御信号机制,而茉莉酸和乙烯途径在很大程度上被[具体物种名称未给出]抑制。坏死营养阶段显示参与活性氧激活的基因显著上调。总体而言,[具体物种名称未给出]和草莓的转录组数据表明,尽管植物建立了多层防御来抵御感染,但[具体物种名称未给出]采用了一系列逃避或拮抗机制来成功感染宿主细胞。