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杨树中过表达AtGolS与CsRFS增强ROS抗性，并抑制叶片锈病防御响应

已有 3902 次阅读 2017-9-10 09:37 |个人分类:每日摘要|系统分类:科研笔记|关键词:学者

Overexpression of AtGolS3 and CsRFS in poplar enhances ROS tolerance and represses defense response to leaf rust disease

First author:Jonathan La Mantia; Affiliations: University of British Columbia (不列颠哥伦比亚大学): Vancouver, Canada

Corresponding author: Richard Hamelin

Plants respond to pathogens through an orchestration of signaling events that coordinate modifications to transcriptional profiles (转录谱) and physiological processes (生理过程). Resistance to necrotrophic (死体营养的) pathogens often requires jasmonic acid, which antagonizes (拮抗) the salicylic acid dependent biotrophic (活体营养的) defense response. Recently, myo-inositol (肌-肌醇) has been shown to negatively impact salicylic acid (SA) levels and signaling, while galactinol (肌醇半乳糖苷) enhances jasmonic acid (JA)-dependent induced systemic resistance to necrotrophic pathogens. To investigate the function of these compounds in biotrophic pathogen defense, we characterized the defense response of Populus alba × grandidentata (杂种杨) overexpressing Arabidopsis GALACTINOL SYNTHASE3 (AtGolS) and Cucumber sativus RAFFINOSE SYNTHASE (CsRFS) challenged with Melampsora aecidiodes, a causative agent (病原体) of poplar leaf rust disease (锈病). Relative to wild-type leaves, the overexpression of AtGolS3 and CsRFS increased accumulation of galactinol (肌醇半乳糖苷) and raffinose (棉子糖) and led to increased leaf rust infection (感染). During the resistance response, inoculated (接种) wild-type leaves displayed reduced levels of galactinol and repressed transcript abundance of two endogenous GolS genes compared to un-inoculated wild-type leaves prior to the up-regulation of NON-EXPRESSOR OF PR1 and PATHOGENESIS-RELATED1. Transcriptome analysis and qRT-PCR validation also revealed the repression of genes participating in calcium influx (钙离子内流), phosphatidic acid (磷脂酸) biosynthesis and signaling, and salicylic acid signaling in the transgenic lines. In contrast, enhanced tolerance to H2O2 and up-regulation of antioxidant (抗氧化剂) biosynthesis genes were exhibited in the overexpression lines. Thus, we conclude that overexpression of AtGolS and CsRFS antagonizes the defense response to poplar leaf rust disease through repressing reactive oxygen species and attenuating (衰减) calcium and phosphatidic acid signaling events that lead to SA defense.

植物对于病原物的响应会通过一系列的信号转导协调转录谱到生理过程这整个过程的改变。对于死体营养病原物的抗性通常会需要茉莉酸JA的介导，JA会拮抗依赖于水杨酸SA的活体防御响应。最近，对于肌-肌醇的研究显示其会负调控SA的水平及信号转导，而肌醇半乳糖苷则会增强依赖于JA诱导的对于死体营养病原菌的抗性。本文作者在杂种杨树中通过过表达拟南芥的半乳糖苷酶AtGolS基因和黄瓜的棉子糖合成酶CsRFS基因，并用杨树锈病的致病菌Melampsora aecidiodes进行侵染以研究肌-肌醇与肌醇半乳糖苷对于植物的活体营养病原物防御的作用。相比于野生型而言，在AtGolS和CsRFS基因过表达株系中，肌醇半乳糖苷和棉子糖的积累增加，并且导致了叶片锈病感染的增加。在抗性响应中，接种的野生型杂种杨树叶片中表现出肌醇半乳糖苷含量的下降，并且相对于未接种野生型叶片会抑制两个内源GolS基因的转录，且优先于NON-EXPRESSOR OF PR1与PATHOGENESIS-RELATED1的上调表达。转录组分析和qRT-PCR验证揭示了转基因株系中参与钙离子内流、磷脂酸生物合成及信号转导、水杨酸信号转导相关基因收到抑制。相反，在过表达植株中，对于H2O2的抗性增强，且与抗氧化物质生物合成相关基因上调。因此，作者推测AtGolS和CsRFS基因的过表达会通过抑制活性氧物质和衰减钙离子及磷脂酸信号转导来拮抗对杨树锈病的防御响应。