Differential regulation of plant innate immunity

植物先天免疫的差异调节

• 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
• 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

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 项目摘要 先天免疫系统检测到病原体衍生的分子，以防止通过专门的免疫感染 受体。免疫受体包括细胞表面驻留模式识别受体（PRR），例如 哺乳动物和受体样激酶（RLKS）中的收费受体（TLR），细胞内nod类样 受体（NLR），例如植物核苷酸结合结构域富含亮氨酸的重复蛋白。植物等离子体 膜 - 定位的RLK充当了与病原体相关的分子模式（PAMP）和 统称有助于宿主对广泛的病原体的免疫力。植物内NLR检测 病原体特异性效应蛋白被转移到宿主细胞中并触发病原体特异性免疫， 经常伴有程序性细胞死亡。植物的遗传障碍使您有可能识别 许多植物PRR和NLR免疫受体。但是，如何信号网络是如何基础的prr-和nlr- 介导的免疫力是相互联系的，仍然在很大程度上未知。 PI的实验室已经开发了一系列 敏感和高通量遗传筛选，以揭示复杂的激活和信号传导机制 植物PRR和NLR介导的免疫力。屏幕指向一组RLK的意外角色 植物免疫中的细胞外恶性蛋白样结构域。充足的初步证据支持诱人 假设特异性恶素样RLK调节差异的两层植物免疫组织化学和细胞死亡 PRR和NLR免疫受体复合物的调节。具体而言，该项目旨在阐明： MaLectin样RLK，LET1和LET2反向调节PRR和NLR复合物的形成和激活；如何 LET1/2通过糖基磷脂酰肌醇（GPI）锚定为衔接子和分泌的肽调节 ralf9作为配体；以及NLR蛋白Summ2的稳定性如何由两个不同的E3泛素负责 连接酶。通过阐明细胞表面居民恶素样RLK模块作为PRR和NLR的分子链接 免疫接收器，该项目有可能改变PRR和NLR-互连的教条 介导的免疫力，以前被认为在接收器水平上独立起作用，仅 在下游信号事件中收敛。 植物PRR和NLR介导的免疫史与哺乳动物TLR和NLR介导的先天性免疫史类似 独特的是丰富的遗传和基因组资源，包括全基因组的收集 敲除线，以及良好的蜂窝和生化测定，将拟南芥作为一种诱因 在整个有机和物理水平上了解宿主免疫机制的模型系统。那， 该项目的影响将超越植物生物学，并为一般提供完整的看法 了解先天免疫信号。