Understanding local and systemic signaling pathways in plant immunity

植物具有抵抗微生物感染的抗病途径。每年，尽管作物品种和杀虫剂具有抗性，但估计仍有10%至40%的世界粮食产量因疾病而损失。鉴于这些损失，我的研究目标是了解植物的免疫反应，为操纵植物免疫以提高作物抗病性的努力提供信息。在局部受感染的叶片中，单个植物细胞感知称为PAMP的病原体相关分子，以启动PAMP触发免疫（PTI）。局部防御可以诱导系统获得抗性（SAR），其中移动的信号从诱导的叶片产生并传递到远距离叶片以建立对未来病原体攻击的抗性。一些植物随着年龄的增长对特定病原体的抗性越来越强，并表现出与病原体相关的抗性（ARR）。例如，3至4周龄的幼小拟南芥属植物对细菌病原体番茄假单胞菌致病变种（pv）番茄（P. lagingae）敏感，但表现出对与6至7周龄的成熟植物相同的病原体的抗性。我的研究团队试图了解植物免疫的分子遗传和生化基础，使用模式系统，拟南芥和P.我们证明，植物激素水杨酸（SA）执行一个以前未知的功能，作为一种抗菌剂，抑制生长和生物膜形成的植物细胞间隙中的P. pallingae在ARR和PTI。生物膜由被细胞外基质包围的粘附细菌细胞组成，细胞外基质被认为可以保护细菌免受宿主防御。据我们所知，我们是第一个表明P. dingae在叶细胞间隙形成生物膜的实验室，并证明生物膜的形成有助于P. dingae的成功。我们将对植物和病原体进行平行转录组学分析，以了解成熟植物如何感知正常毒性病原体，以及PTI和ARR响应植物如何抑制P. erichingae生物膜形成。我的实验室在理解SAR移动的信号（包括DIR 1）如何进入韧皮部，从诱导的叶子移动到远处的叶子，并鉴定出在韧皮部积累并有助于SAR的蛋白质方面取得了重大进展，可能是通过与DIR 1相互作用。我们将利用DIR 1在SAR诱导和远距离叶片中的作用来鉴定负责SAR诱导叶片中DIR 1运动的分子组分，并通过使用SAR突变体和蛋白质-蛋白质测定（TurboID，co-IP + LC-MS/MS）进行DIR 1运动测定来鉴定在非诱导条件下限制其运动和/或在SAR激活后促进DIR 1运动的DIR 1相互作用物。还将通过有条件地阻断进入韧皮部来检查SAR期间DIR 1的细胞途径，以观察对DIR 1-iLOV（iLOV：荧光肽）运动的影响，使用荧光显微镜进行监测，以揭示SAR期间DIR 1所采取的路径的基本细胞信息。

Plants possess disease resistance pathways to combat microbial infections. Each year an estimated 10 to 40% of world food production is lost to disease despite resistant crop varieties and pesticide application. In view of these losses, the goal of my research is to understand plant immune responses to inform efforts to manipulate plant immunity to improve disease resistance in crops. In locally infected leaves, individual plant cells perceive pathogen-associated molecules called PAMPs to initiate PAMP-Triggered Immunity (PTI). Local defense can induce Systemic Acquired Resistance (SAR), in which mobile signals are produced and transported from induced to distant leaves to establish resistance to future pathogen attack. Some plants become more resistant to a particular pathogen as they age and exhibit Age-Related Resistance (ARR). For example, young 3 to 4 week-old Arabidopsis plants are susceptible to the bacterial pathogen, Pseudomonas syringae pathovar (pv) tomato (P.syringae), but exhibit resistance to the same pathogen as mature 6 to 7 week-old plants. My research team seeks to understand the molecular genetic and biochemical basis of plant immunity using the model system, Arabidopsis and P. syringae. We demonstrated that the plant hormone salicylic acid (SA) performs a previously unknown function as an antimicrobial agent that suppresses the growth and biofilm formation of P.syringae in plant intercellular spaces during ARR and PTI. Biofilms consist of adherent bacterial cells surrounded by an extracellular matrix that are thought to protect bacteria from host defense. To our knowledge, we are the first lab to show that P. syringae forms biofilms in leaf intercellular spaces and demonstrate that biofilm formation contributes to P.syringae success. We will perform parallel transcriptomic analysis of the plant and pathogen to understand how mature plants perceive normally virulent pathogens and how PTI- and ARR-responding plants inhibit P.syringae biofilm formation. My lab has made significant progress in understanding how SAR mobile signals including DIR1 access the phloem for movement from induced to distant leaves and identified proteins that accumulate in the phloem and contribute to SAR, perhaps by interacting with DIR1. We will take advantage of DIR1's role in both SAR-induced and distant leaves to identify the molecular components responsible for DIR1 movement out of SAR-induced leaves and identify DIR1 interactors that restrict its movement under non-inductive conditions and/or facilitate DIR1 movement upon SAR activation by performing DIR1 movement assays using SAR mutants and protein-protein assays (TurboID, co-IPs + LC-MS/MS). DIR1's cellular route during SAR will also be examined by conditionally blocking access to the phloem to observe the effect on movement of DIR1-iLOV (iLOV:fluorescent peptide), monitored using fluorescence microscopy, to reveal fundamental cellular information about the path taken by DIR1 during SAR.