Differential regulation of plant innate immunity

植物天然免疫的差异调节 项目摘要 先天性免疫系统检测病原体衍生的分子，以通过专门的免疫系统预防感染。 受体。免疫受体包括细胞表面驻留的模式识别受体（PRR），如 哺乳动物中的Toll样受体（TLR）和植物中的受体样激酶（RLK），以及细胞内的NOD样 受体（NLR），如植物核苷酸结合结构域富含亮氨酸的重复蛋白。植物血浆 膜定位的RLK作为PRR起作用，其感测病原体相关分子模式（PAMP）， 它们共同有助于宿主对广谱病原体的免疫。植物细胞内NLR检测 病原体特异性效应蛋白，其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我们有可能 许多植物PRR和NLR免疫受体。然而，PRR和NLR的信令网络是如何运作的？ 介导的免疫是相互关联的仍然在很大程度上是未知的。PI的实验室开发了一系列 敏感和高通量的遗传筛选，以揭示复杂的激活和信号机制， 植物PRR和NLR介导的免疫。屏幕指向一组RLK的意外角色， 胞外malectin-like结构域在植物免疫中的作用。充分的初步证据支持了一个诱人的 特异性malectin-like RLKs通过差异表达调控两级植物免疫和细胞死亡假说 调节PRR和NLR免疫受体复合物。具体而言，本项目旨在阐明：如何 malectin-like RLK，LET 1和LET 2，反向调节PRR和NLR复合物的形成和激活;如何 LET 1/2由糖基磷脂酰肌醇（GPI）锚定的LLG 1作为接头和分泌肽调节 RALF 9作为配体;以及NLR蛋白SUMM 2稳定性如何通过两种不同的E3泛素反向调节 连接酶。通过阐明细胞表面驻留的malectin-like 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相互联系的教条- 介导的免疫，这是以前被认为是在受体水平上独立发挥作用， 在下游信号事件中会聚。 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 分别独特的是，丰富的遗传和基因组资源，包括全基因组的收集 敲除系，以及完善的细胞和生化测定目前拟南芥作为一个听话的 模型系统，以了解整个机体和生理水平上的宿主免疫机制。因此，在本发明中， 该项目的影响将超越植物生物学，并提供补充意见， 先天免疫信号的理解。

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.