Pipecolic Acid Orchestrates Plant Systemic Acquired Resistance and Defense Priming via Salicylic Acid-Dependent and -Independent Pathways
Pipecolic Acid Orchestrates Plant Systemic Acquired Resistance and Defense Priming via Salicylic Acid-Dependent and -Independent Pathways
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DOI：
10.1105/tpc.15.00496
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发表时间：
2016-01-01
期刊：
影响因子：
11.6
通讯作者：
Zeier, Juergen
中科院分区：
文献类型：
--
作者：
Bernsdorff, Friederike;Doering, Anne-Christin;Zeier, Juergen
我们研究了两种免疫调节植物代谢产物水杨酸（SA）和哌啶酸（Pip）在植物系统获得性抗性（SAR）、SAR相关防御引发和基础免疫建立中的关系。使用SA-缺陷的ald 1，ald 1和ald 2植物缺乏SA和Pip，我们表明，SA和Pip的行为都是独立的，彼此之间的协同作用，在拟南芥的基础免疫假单胞菌。转录组分析表明，SAR建立在拟南芥的特点是一个强大的转录反应系统诱导的叶子，准备植物未来的病原体攻击，通过预激活多个阶段的防御信号和SA积累后，SAR激活导致下调光合作用和衰减茉莉酸响应系统内的植物。而系统的Pip海拔是必不可少的SAR和必要的几乎整个转录SAR响应，一个温和的，但显着的SA独立组件的SAR激活和SAR基因表达被揭示。在SAR期间，Pip以黄素依赖性单加氧酶1（FMO 1）依赖性方式协调SA依赖性和SA非依赖性病原体应答的引发。我们的结论是，Pip/FMO 1信号模块作为一个不可或缺的开关激活SAR和相关的防御引发事件，SA放大不同程度的PIP触发的反应，在远端组织的SAR激活的植物。
We investigated the relationships of the two immune-regulatory plant metabolites, salicylic acid (SA) and pipecolic acid (Pip), in the establishment of plant systemic acquired resistance (SAR), SAR-associated defense priming, and basal immunity. Using SA-deficient sid2, Pip-deficient ald1, and sid2 ald1 plants deficient in both SA and Pip, we show that SA and Pip act both independently from each other and synergistically in Arabidopsis thaliana basal immunity to Pseudomonas syringae. Transcriptome analyses reveal that SAR establishment in Arabidopsis is characterized by a strong transcriptional response systemically induced in the foliage that prepares plants for future pathogen attack by preactivating multiple stages of defense signaling and that SA accumulation upon SAR activation leads to the downregulation of photosynthesis and attenuated jasmonate responses systemically within the plant. Whereas systemic Pip elevations are indispensable for SAR and necessary for virtually the whole transcriptional SAR response, a moderate but significant SA-independent component of SAR activation and SAR gene expression is revealed. During SAR, Pip orchestrates SA-dependent and SA-independent priming of pathogen responses in a FLAVIN-DEPENDENT-MONOOXYGENASE1 (FMO1)-dependent manner. We conclude that a Pip/FMO1 signaling module acts as an indispensable switch for the activation of SAR and associated defense priming events and that SA amplifies Pip-triggered responses to different degrees in the distal tissue of SAR-activated plants.