Mechanistic Insights into the Plant Disease Resistance Mediated by NPR1

NPR1 介导的植物抗病性的机制见解

基本信息

批准号：
10390811
负责人：
Pei Zhou
金额：
$ 36.62万
依托单位：
DUKE UNIVERSITY
依托单位国家：
美国
项目类别：
财政年份：
2022
资助国家：
美国
起止时间：
2022-08-01 至 2026-05-31
项目状态：
未结题

来源：
https://reporter.nih.gov/project-details/10390811
关键词：
Achievement Address Agriculture Ankyrin Repeat Arabidopsis Architecture Aspirin BTB/POZ Domain Binding Biochemical Biological Process Biological Response Modifiers Biology C-terminal CUL3 gene Cardiovascular Diseases Cell Nucleus Cell Survival Cells Cessation of life Circadian Rhythms Complex Cytoplasm DNA Binding Domain Dimerization Disease Disease Resistance Dissociation Electron Microscopy Endoplasmic Reticulum Ensure Event Fever Gene Activation Gene Expression Genes Genetic Genetic Engineering Genetic Transcription Goals Health Benefit Human Immune response Immunity Investigation Knowledge Length Malignant Neoplasms Masks Mediating Molecular Molecular Conformation Mouse-ear Cress N-terminal Natural Immunity Nature Nuclear Nuclear Translocation Oxidation-Reduction Pathogenesis Pathogenicity Pesticides Plant Diseases Plants Polyubiquitination Process Proteins Recombinants Regulation Resistance Resolution Rest Role Salicylic Acids Signal Pathway Signal Transduction Stress Structure Testing Transcription Coactivator Transcription Repressor Ursidae Family Wing analog base circadian regulation cofactor cryogenics cullin-3 dimer disulfide bond fitness genome-wide human disease insight mutant pain relief particle pathogen pesticide resistance pressure prevent proteotoxicity public health relevance receptor recruit response success transcription factor transcriptional reprogramming ubiquitin-protein ligase

项目摘要

Project Summary/Abstract NPR1 (NONEXPRESSOR OF PATHOGENSIS-RELATED GENES 1) is a master immune regulator in plants. It orchestrates systemic acquired resistance (SAR) by activating PATHOGENESIS-RELATED (PR) genes in response to induction of salicylic acid (SA) during the plant response to pathogenic challenges. Extensive genetic and biochemical studies have shown that NPR1 is a receptor of SA. SA activation of NPR1 triggers genome- wide transcriptional reprograming via NPR1 interactions with a variety of transcription activators and repressors. NPR1 itself is regulated by redox agents, and its proteolytic turnover has profound implications in a wide range of biological functions, including circadian rhythm and resistance to proteotoxic stress in the endoplasmic reticulum. Despite the essential role of NPR1 in plant biology, the molecular details underlying the myriad of NPR1 functions have remained largely unknown. Building upon our initial success in elucidating the structure of apo NPR1 using single-particle cryoEM, here we propose to elucidate the molecular basis of the NPR1 function in plants. Specifically, we will address (1) how SA activates NPR1, (2) how NPR1 interacts with transcription factors and regulators, and (3) how NPR1 is degraded. Information gained from these studies will provide the much-needed mechanistic insights into the SA-NPR1 signaling cascade in plants and help develop disease- resistant crops. As SA is the principle metabolite of aspirin, such knowledge may also contribute to a better understanding of the well-documented medicinal benefits of SA and analogs in humans.

项目摘要/摘要 NPR1（病原体相关基因1）是植物中的主要免疫调节剂。它通过激活与发病机理相关的基因（PR）基因来策划系统性获得的抗性（SAR）在植物对致病挑战的反应期间，对诱导水杨酸（SA）的反应。广泛的遗传生化研究表明NPR1是SA的受体。 NPR1激活触发基因组 - 通过NPR1相互作用与各种转录激活剂和阻遏物通过NPR1相互作用进行广泛的转录重编程。 NPR1本身受氧化还原剂的调节，其蛋白水解周转率在广泛的范围内具有深远的影响生物学功能，包括昼夜节律和对内质中蛋白毒性应激的抗性网状。尽管NPR1在植物生物学中起着至关重要的作用，但分子细节是无数的基础 NPR1功能在很大程度上尚不清楚。基于我们在阐明结构的最初成功的基础上 APO NPR1使用单粒子冷冻素质，在这里我们建议阐明NPR1函数的分子基础在植物中。具体而言，我们将解决（1）SA如何激活NPR1，（2）NPR1如何与转录相互作用因素和调节剂，以及（3）NPR1如何降解。从这些研究中获得的信息将提供对植物中SA-NPR1信号级联的急需的机械见解，并有助于发展疾病 - 抗性作物。由于SA是阿司匹林的主要代谢物，因此这种知识也可能有助于更好了解人类中有据可查的SA和类似物的药物益处。