Long distance signaling during pathogen-induced systemic acquired resistance in plants: lipid requisites and their interface(s) with salicylates

系统性获得性抗性（SAR）是一种强有力的长期抗性，是由最初的病原体感染在整个植物中诱导的。这种对健康组织的增强保护是由一系列识别系统触发的，这些识别系统引发了不同的局部防御反应，并对广泛的植物病原体（包括细菌、病毒和卵菌）有效。水杨酸甲酯（MeSA）是烟草中激活SAR的移动信号；它也被认为是拟南芥的SAR信号。此外，基于拟南芥突变体的实验，脂质信号已被提出在SAR中起作用。这些发现提出了几个问题，包括：i)参与SAR激活的脂质信号的性质是什么？ ii)脂质信号和MeSA是独立作用还是在单一信号通路中连接？该研究将探讨mesa信号通路需要特定的脂质前提条件的假设，这将通过在几种脂质相关的拟南芥突变体中表征水杨酸（SA）信号通路来评估。二维核磁共振波谱将通过对这些突变植物韧皮部渗出物的生物测定辅助分析来识别假定的脂质来源的移动信号。最后，通过对三种可能参与脂质代谢的SA结合蛋白进行详细分析，我的研究将探索SA与脂质信号传导之间潜在的新界面。

Systemic acquired resistance (SAR) is a potent long-lasting resistance that is induced throughout the plant by an initial pathogen infection. This increased protection of healthy tissue is triggered by a set of recognition systems that elicit distinct local defense responses and is effective against a broad spectrum of plant pathogens, including bacteria, viruses, and oomycetes. Methyl salicylate (MeSA) was identified as a mobile signal initiating SAR in Nicotiana tabacum; it also has been implicated as an SAR signal in Arabidopsis thaliana. In addition, lipid signaling has been proposed to have a role in SAR, based on experiments with Arabidopsis mutants. These findings raise several questions, including: i) what is the nature of the lipid signal(s) involved in SAR activation and ii) do the lipid signals and MeSA act independently or are they connected in a single signaling pathway? The proposed research will investigate the hypothesis that MeSA-based signaling requires specific lipid preconditions, which will be assessed by characterizing salicylic acid (SA)-signaling in several lipid-related Arabidopsis mutants. 2D-nuclear magnetic resonance spectroscopy will be used to identify the putative lipid-derived mobile signal through bioassay-aided analysis of the phloem exudates of these mutant plants. Finally, by performing detailed analyses of three putative SA-binding proteins involved in lipid metabolism, my research will explore potential new interfaces between SA and lipid-signaling.