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

系统获得性抗性(SAR)是一种由最初的病原菌侵染整个植物所诱导的一种强大的、持久的抗性。这种对健康组织的加强保护是由一套识别系统触发的，这些识别系统引起不同的局部防御反应，并对包括细菌、病毒和卵菌在内的广泛植物病原体有效。水杨酸甲酯(MESA)在烟草中是一种启动SAR的移动信号，在拟南芥中也被认为是一种SAR信号。此外，基于对拟南芥突变体的实验，已提出脂质信号在SAR中发挥作用。这些发现提出了几个问题，包括：i)参与SAR激活的脂质信号(S)的性质是什么；ii)脂质信号和MESA是独立作用的，还是它们在单一的信号通路中联系在一起？这项拟议的研究将调查基于MESA的信号需要特定的脂质预条件的假设，这将通过表征几个与脂质相关的拟南芥突变体中的水杨酸(SA)信号来评估。2D-核磁共振波谱将被用来通过对这些突变植物的韧皮部分泌物的生物测定辅助分析来识别假定的脂类衍生的移动信号。最后，通过对参与脂质代谢的三种可能的SA结合蛋白进行详细分析，我的研究将探索SA和脂质信号之间潜在的新接口。

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.