Department of Biology, Heinrich Heine University Düsseldorf, Universitätsstraße 1, 40225 Düsseldorf, Germany; Cluster of Excellence on Plant Sciences (CEPLAS), Heinrich Heine University Düsseldorf, Universitätsstraße 1, D-40225 Düsseldorf, Germany.
Plant Biology Section, University of Fribourg, Route Albert Gockel 3, 1700 Fribourg, Switzerland.
Mol Plant. 2016 May 2;9(5):662-681. doi: 10.1016/j.molp.2016.01.005. Epub 2016 Jan 20.
Tryptophan-derived, indolic metabolites possess diverse functions in Arabidopsis innate immunity to microbial pathogen infection. Here, we investigate the functional role and regulatory characteristics of indolic metabolism in Arabidopsis systemic acquired resistance (SAR) triggered by the bacterial pathogen Pseudomonas syringae. Indolic metabolism is broadly activated in both P. syringae-inoculated and distant, non-inoculated leaves. At inoculation sites, camalexin, indol-3-ylmethylamine (I3A), and indole-3-carboxylic acid (ICA) are the major accumulating compounds. Camalexin accumulation is positively affected by MYB122, and the cytochrome P450 genes CYP81F1 and CYP81F2. Local I3A production, by contrast, occurs via indole glucosinolate breakdown by PEN2- dependent and independent pathways. Moreover, exogenous application of the defense hormone salicylic acid stimulates I3A generation at the expense of its precursor indol-3-ylmethylglucosinolate (I3M), and the SAR regulator pipecolic acid primes plants for enhanced P. syringae-induced activation of distinct branches of indolic metabolism. In uninfected systemic tissue, the metabolic response is more specific and associated with enhanced levels of the indolics I3A, ICA, and indole-3-carbaldehyde (ICC). Systemic indole accumulation fully depends on functional CYP79B2/3, PEN2, and MYB34/51/122, and requires functional SAR signaling. Genetic analyses suggest that systemically elevated indoles are dispensable for SAR and associated systemic increases of salicylic acid. However, soil-grown but not hydroponically -cultivated cyp79b2/3 and pen2 plants, both defective in indolic secondary metabolism, exhibit pre-induced immunity, which abrogates their intrinsic ability to induce SAR.
色氨酸衍生的吲哚代谢物在拟南芥对微生物病原体感染的先天免疫中具有多种功能。在这里，我们研究了吲哚代谢在拟南芥由细菌病原体丁香假单胞菌引发的系统获得性抗性（SAR）中的功能作用和调节特征。吲哚代谢在接种和远离接种的叶片中广泛激活。在接种部位，累积的主要化合物是独脚金内酯、吲哚-3-基甲胺（I3A）和吲哚-3-羧酸（ICA）。独脚金内酯的积累受 MYB122 和细胞色素 P450 基因 CYP81F1 和 CYP81F2 的正向影响。相比之下，局部 I3A 的产生是通过 PEN2 依赖和独立途径吲哚葡糖苷分解产生的。此外，防御激素水杨酸的外源应用以牺牲其前体吲哚-3-基甲基葡糖苷（I3M）为代价刺激 I3A 的产生，并使植物对植保素和哌啶酸的反应增强，以增强 P. syringae 诱导的吲哚代谢不同分支的激活。在未感染的系统组织中，代谢反应更具特异性，与吲哚 I3A、ICA 和吲哚-3-甲醛（ICC）的水平升高有关。系统性吲哚积累完全依赖于功能 CYP79B2/3、PEN2 和 MYB34/51/122，并且需要功能性 SAR 信号。遗传分析表明，系统性升高的吲哚对于 SAR 和相关的系统性水杨酸增加是可有可无的。然而，在土壤中生长而不是在水培中生长的 cyp79b2/3 和 pen2 植株，它们在吲哚次生代谢中都有缺陷，表现出预先诱导的免疫，从而消除了它们诱导 SAR 的内在能力。
