Differential regulation of plant innate immunity

植物先天免疫的差异调节

基本信息

批准号：
10179410
负责人：
Ping He
金额：
$ 29.69万
依托单位：
TEXAS A&M AGRILIFE RESEARCH
依托单位国家：
美国
项目类别：
财政年份：
2010
资助国家：
美国
起止时间：
2010-04-01 至 2023-06-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/10179410
关键词：
Address Animals Apoptosis Arabidopsis Architecture BAK1 gene Binding Biochemical Biological Biological Assay Biological Models Biology Carbohydrates Catharanthus roseus Cell Death Cell membrane Cell surface Cells Collection Complement Complex Defect Event Evolution Flagellin GPI Membrane Anchors Genes Genetic Genetic Screening Genomics Immune Immune response Immune signaling Immunity Immunologic Receptors Infection Infection prevention Innate Immune System Insecta Knock-out Laboratories Leucine-Rich Repeat Ligands Light Link Luciferases MAP Kinase Gene MAP2K1 gene MAP3K1 gene Mammals Mediating Medical Research Mission Modeling Molecular Natural Immunity Nucleotides Pathogen detection Pattern Pattern recognition receptor Peptides Perception Phosphotransferases Physiological Plant Model Plants Proteins RNA Interference Receptor Activation Receptor Signaling Regulation Reporter Research Resources Role Series Signal Transduction Site Toll-like receptors United States National Institutes of Health Ursidae Family base design extracellular immune activation indexing leucine-rich repeat protein microbial multicatalytic endopeptidase complex mutant pathogen receptor response trafficking ubiquitin-protein ligase whole genome

项目摘要

Differential regulation of plant innate immunity Project Summary The innate immune system detects pathogen-derived molecules to prevent infections via specialized immune receptors. The immune receptors include cell surface-resident pattern recognition receptors (PRRs), such as Toll-like receptors (TLRs) in mammals and receptor-like kinases (RLKs) in plants, and intracellular NOD-like receptors (NLRs), such as plant nucleotide-binding domain leucine-rich repeat proteins. Plant plasma membrane-localized RLKs function as PRRs that sense pathogen-associated molecular patterns (PAMPs) and collectively contribute to host immunity against a broad-spectrum of pathogens. Plant intracellular NLRs detect pathogen specific effector proteins that are translocated into host cells and trigger pathogen-specific immunity, often accompanied with programmed cell death. The genetic tractability of plants made it possible to identify many plant PRR and NLR immune receptors. However, how the signaling networks underlying PRR- and NLR- mediated immunity are interconnected remains largely unknown. The PI’s laboratory has developed a series of sensitive and high-throughput genetic screens to reveal the complex activation and signaling mechanisms in plant PRR- and NLR-mediated immunity. The screens point to an unexpected role of a group of RLKs with an extracellular malectin-like domain in plant immunity. The ample preliminary evidence supports a tantalizing hypothesis that specific malectin-like RLKs regulate two-tiered plant immunity and cell death by differential modulation of PRR and NLR immune receptor complexes. Specifically, this project seeks to elucidate: how malectin-like RLKs, LET1 and LET2, inversely regulate PRR and NLR complex formation and activation; how LET1/2 are modulated by glycosylphosphatidylinositol (GPI)-anchored LLG1 as an adaptor and secreted peptide RALF9 as a ligand; and how NLR protein SUMM2 stability is inversely regulated by two distinct E3 ubiquitin ligases. By elucidating cell surface-resident malectin-like RLK module as a molecular link of PRR and NLR immune receptors, the project has the potential to change the dogma of the interconnection of PRR and NLR- mediated immunity, which was previously thought to function independently at the receptor level and only converge in downstream signaling events. Plant PRR- and NLR-mediated immunity is analogous to mammalian TLR- and NLR-mediated innate immunity respectively. Uniquely, the enriched genetic and genomic resources, including the collection of whole-genome knockout lines, as well as the well-established cellular and biochemical assays present Arabidopsis as a tractable model system to understand the host immune mechanism at the whole organismal and physiological level. Thus, the impacts of the project will reach beyond plant biology and provide complementary views to the general understanding of innate immune signaling.

植物先天免疫的差异调节项目概要先天免疫系统检测病原体衍生分子，通过专门的免疫来预防感染免疫受体包括细胞表面驻留的模式识别受体（PRR），例如哺乳动物中的 Toll 样受体 (TLR) 和植物中的受体样激酶 (RLK) 以及细胞内 NOD 样受体（NLR），例如植物核苷酸结合域富含亮氨酸的重复蛋白。膜定位的 RLK 发挥 PRR 的作用，感知病原体相关分子模式 (PAMP) 并共同促进宿主对植物细胞内 NLR 检测的广谱病原体的免疫力。病原体特异性效应蛋白易位到宿主细胞中并触发病原体特异性免疫，通常伴随着程序性细胞死亡，植物的遗传易处理性使得识别成为可能。许多植物 PRR 和 NLR 免疫受体然而，PRR- 和 NLR- 的信号网络如何。介导的免疫之间的相互关联仍然很大程度上未知。PI 的实验室已经开发了一系列的方法。敏感和高通量的遗传筛选，揭示复杂的激活和信号传导机制植物 PRR 和 NLR 介导的免疫作用植物免疫中细胞外malectin样结构域的充分初步证据支持了诱人的结果。假设特定的 malectin 样 RLK 通过差异调节两级植物免疫和细胞死亡具体而言，该项目旨在阐明：如何调节 PRR 和 NLR 免疫受体复合物。 malectin 样 RLK、LET1 和 LET2 如何反向调节 PRR 和 NLR 复合物的形成和激活； LET1/2 由糖基磷脂酰肌醇 (GPI) 锚定的 LLG1 作为衔接子和分泌肽进行调节 RALF9 作为配体；以及 NLR 蛋白 SUMM2 稳定性如何受到两种不同 E3 泛素的反向调节通过阐明细胞表面驻留的 malectin 样 RLK 模块作为 PRR 和 NLR 的分子连接。免疫受体，该项目有可能改变 PRR 和 NLR 互连的教条- 介导的免疫，以前被认为在受体水平上独立发挥作用，并且仅汇聚在下游信号事件中。植物 PRR 和 NLR 介导的免疫类似于哺乳动物 TLR 和 NLR 介导的先天免疫独特的是，丰富的遗传和基因组资源，包括全基因组的收集。敲除系以及成熟的细胞和生化测定表明拟南芥是一种易于处理的植物模型系统在整个生物和生理水平上了解宿主免疫机制。该项目的影响将超越植物生物学，并为一般科学界提供补充观点。了解先天免疫信号传导。