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

植物拥有许多抗病途径来对抗微生物感染。尽管有抗性作物品种和使用杀虫剂，但每年估计有40%的世界粮食产量因昆虫、杂草和疾病而损失。鉴于这些损失，我的研究小组的目标是了解系统性获得性抗性（SAR）和年龄相关抗性（ARR）。SAR和ARR都涉及一个启动阶段，在这个阶段，最初的生物、化学或发育刺激使植物能够迅速有效地对随后的病原体感染作出反应。了解这些启动机制将为遗传和育种策略提供见解，使作物能够快速有效地对疾病作出反应。*** SAR是由一个叶片的“免疫”感染引起的，产生SAR信号，这些信号移动到未感染的叶片，以抵抗未来感染的方式向主要植物作出反应。SAR的结果与哺乳动物的疫苗接种相似，但SAR更有效，因为它可以保护植物免受许多不同病原体的侵害。我们研究了SAR中的一个关键角色DIR1。DIR1编码脂质转移蛋白（LTP），并在体外通过疏水结合腔与脂质结合。我们假设DIR1结合脂质和/或疏水分子，该复合体移动到远处的组织，使远处的叶子抵抗未来的病原体感染。我们发现DIR1移动到远处组织启动启动，并创建了许多工具来识别DIR1的结合伙伴。我们能够理解DIR1及其结合伙伴如何在远处的叶片中被感知，从而使植物做好抵抗下一次感染的准备。这些信息将为今后提高作物抗病性的操作提供信息。***我们还研究了ARR，其中成熟相关的发育触发启动成熟植物以高度抗性的方式响应通常毒性病原体。我们确定了ARR所需的基因，包括开花调节因子SVP。在植物与病原菌的相互作用中，许多病原菌进化出了抑制植物防御的能力。我们的数据支持SVP在阻止细菌病原体，丁香假单胞菌抑制抗微生物水杨酸（SA）的积累中发挥作用的假设。通过检测野生型和svp突变体的SA积累，结合下一代rna测序、ChIP-qPCR、基因抑制因子筛选和酵母-2杂交，我们将发现svp如何控制ARR。我们的研究表明，在ARR过程中，植物利用一种新的机制来防御自己，通过靶向和阻止病原体抑制防御的能力。了解这种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反应扩展到年轻作物。********

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.********