Metabolic Integration and Cell Signaling Group, Plant Physiology Section, Department of Ciencias Agrarias y del Medio Natural, Universitat Jaume I, Avenida Vicente Sos Baynat, E-12071, Castellón, Spain.
Plant J. 2014 Apr;78(2):227-40. doi: 10.1111/tpj.12465. Epub 2014 Mar 26.
Priming is a physiological state for protection of plants against a broad range of pathogens, and is achieved through stimulation of the plant immune system. Various stimuli, such as beneficial microbes and chemical induction, activate defense priming. In the present study, we demonstrate that impairment of the high-affinity nitrate transporter 2.1 (encoded by NRT2.1) enables Arabidopsis to respond more quickly and strongly to Plectosphaerella cucumerina attack, leading to enhanced resistance. The Arabidopsis thaliana mutant lin1 (affected in NRT2.1) is a priming mutant that displays constitutive resistance to this necrotroph, with no associated developmental or growth costs. Chemically induced priming by β-aminobutyric acid treatment, the constitutive priming mutant ocp3 and the constitutive priming present in the lin1 mutant result in a common metabolic profile within the same plant-pathogen interactions. The defense priming significantly affects sugar metabolism, cell-wall remodeling and shikimic acid derivatives levels, and results in specific changes in the amino acid profile and three specific branches of Trp metabolism, particularly accumulation of indole acetic acid, indole-3-carboxaldehyde and camalexin, but not the indolic glucosinolates. Metabolomic analysis facilitated identification of three metabolites in the priming fingerprint: galacturonic acid, indole-3-carboxylic acid and hypoxanthine. Treatment of plants with the latter two metabolites by soil drenching induced resistance against P. cucumerina, demonstrating that these compounds are key components of defense priming against this necrotrophic fungus. Here we demonstrate that indole-3-carboxylic acid induces resistance by promoting papillae deposition and H2 O2 production, and that this is independent of PR1, VSP2 and PDF1.2 priming.
启动是一种保护植物免受广泛病原体侵害的生理状态，是通过刺激植物免疫系统实现的。各种刺激物，如有益微生物和化学诱导，可激活防御启动。在本研究中，我们证明了高亲和力硝酸盐转运体 2.1（由 NRT2.1 编码）的损伤使拟南芥能够更快、更强地对 Plectosphaerella cucumerina 的攻击做出反应，从而增强抗性。拟南芥突变体 lin1（受 NRT2.1 影响）是一种启动突变体，对这种坏死营养体表现出组成型抗性，没有相关的发育或生长成本。通过 β-氨基丁酸处理进行化学诱导启动、组成型启动突变体 ocp3 和 lin1 突变体中存在的组成型启动导致在相同的植物-病原体相互作用中出现相同的代谢谱。防御启动显著影响糖代谢、细胞壁重塑和莽草酸衍生物水平，并导致氨基酸谱和色氨酸代谢三个特定分支的特定变化，特别是吲哚乙酸、吲哚-3-乙醛和独脚金内酯的积累，但不包括吲哚类硫代葡萄糖苷。代谢组学分析有助于鉴定启动指纹中的三种代谢物：半乳糖醛酸、吲哚-3-羧酸和次黄嘌呤。通过土壤淋洗用后两种代谢物处理植物可诱导对 P. cucumerina 的抗性，表明这两种代谢物是防御启动对抗这种坏死真菌的关键成分。在这里，我们证明吲哚-3-羧酸通过促进乳突沉积和 H2 O2 的产生来诱导抗性，并且这与 PR1、VSP2 和 PDF1.2 的启动无关。
