Understanding the priming response in Systemic Acquired Resistance and Age-Related Resistance

植物具有许多抵抗微生物感染的抗病途径。每年估计有40%的世界粮食产量因昆虫、杂草和疾病而损失，尽管作物品种和杀虫剂具有抗药性。鉴于这些损失，我的研究团队的目标是了解系统性获得性抵抗(SAR)和年龄相关抵抗(ARR)。SAR和ARR都涉及启动阶段，在这个阶段，最初的生物、化学或发育刺激允许植物对随后的病原体感染做出快速而有效的反应。了解这些启动机制将为遗传和育种战略提供见解，使作物能够快速有效地对疾病做出反应。*SAR是由一片叶子中产生SAR信号的“免疫”感染诱导的，这些信号会转移到未受感染的叶片上，以启动植物对未来感染的抗性反应。SAR的结果类似于哺乳动物的疫苗接种，但SAR更有效，因为它保护植物免受多种不同病原体的侵袭。我们研究了合成孔径雷达中的一个关键角色--DIR1。DIR1编码一种脂转移蛋白(LTP)，在体外它能在其疏水结合腔内结合脂类。我们假设DIR1与一个脂类和/或疏水分子结合，这个复合体移动到远处的组织，为远处的叶片做好准备，以抵御未来的病原体感染。我们发现DIR1移动到远处的组织来启动启动，并创建了一些工具来识别DIR1的S结合伙伴。我们能够理解DIR1及其结合伙伴在遥远的叶片中是如何被感知的，从而为植物抵御下一次感染做好准备。这些信息将为未来提高作物抗病能力的操作提供信息。*我们还研究了ARR，在ARR中，与成熟度相关的发育触发器启动成熟植物以高度抗病的方式对通常致病的病原体做出反应。我们确定了ARR所需的基因，包括开花调节基因SVP。在植物与细菌病原菌的相互作用中，许多病原菌都进化出了抑制植物防御的能力。我们的数据支持这样的假设，即SVP在防止细菌病原体紫丁香假单胞菌抑制抗微生物水杨酸(SA)积累方面发挥作用。通过检测SA在野生型和SVP突变体中的积累，结合下一代RNA测序、芯片定量聚合酶链式反应、遗传抑制基因筛选和酵母双杂交，我们将发现SVP是如何控制ARR的。我们的研究表明，在ARR期间，植物使用一种新的机制来防御自己，通过靶向和防止病原体抑制防御的能力。了解这一新的防御机制将提供基本信息，增强我们操纵这一途径的能力，从而将高效的ARR反应延伸到作物幼苗。

Plants possess a number of disease resistance pathways to combat microbial infections. Each year an estimated 40% of world food production is lost due to insects, weeds and disease despite resistant crop varieties and pesticide application. In view of these losses, the goal of my research team is to understand Systemic Acquired Resistance (SAR) and Age-related Resistance (ARR). Both SAR and ARR involve a priming stage in which an initial biological, chemical or developmental stimulus allows a plant to respond rapidly and effectively to subsequent pathogen infections. Understanding these priming mechanisms will provide insights for genetic and breeding strategies to allow crops to respond rapidly and effectively to disease. *** SAR is induced by an "immunizing" infection in one leaf producing SAR signals that move to uninfected leaves to prime plants to respond in a resistant manner to future infections. The outcome of SAR is similar to vaccination in mammals, however SAR is more effective as it protects plants against many different pathogens. We study a key player in SAR called DIR1. DIR1 encodes a lipid transfer protein (LTP) and in vitro it binds lipids in its hydrophobic binding cavity. We hypothesize that DIR1 binds a lipid and/or hydrophobic molecule and this complex moves to distant tissues to prime distant leaves to resist future pathogen infections. We discovered that DIR1 moves to distant tissue to initiate priming and created a number of tools to identify DIR1's binding partners. We are in position to understand how DIR1 and its binding partners are perceived in distant leaves to prepare plants to resist the next infection. This information will inform future manipulations to improve crop disease resistance.*** We also study ARR, in which a maturity-associated developmental trigger primes mature plants to respond in a highly resistant manner to normally virulent pathogens. We identified genes required for ARR including the flowering regulator SVP. In the interaction between plants and bacterial pathogens, many pathogens have evolved the ability to suppress plant defense. Our data support the hypothesis that SVP plays a role in preventing the bacterial pathogen, Pseudomonas syringae from suppressing the accumulation of anti-microbial salicylic acid (SA). By examining SA accumulation in wild type and svp mutants, combined with next generation RNA-sequencing, ChIP-qPCR, genetic suppressor screening and yeast-2-hybrid, we will discover how SVP controls ARR. Our research suggests that during ARR, plants use a novel mechanism to defend themselves by targeting and preventing the pathogen's ability to suppress defense. Understanding this novel defense mechanism will provide fundamental information enhancing our ability to manipulate this pathway to extend the highly effective ARR response to young crop plants.********