Differential regulation of plant innate immunity

植物先天免疫的差异性调控 项目摘要 先天免疫系统检测病原体衍生的分子，通过特殊的免疫来预防感染。 感受器。免疫受体包括细胞表面驻留模式识别受体(PRRs)，如 哺乳动物中的Toll样受体(TLRs)和植物中的受体样蛋白(RLK)，以及细胞内的Nod样蛋白 受体(NLR)，如植物核苷酸结合域富含亮氨酸的重复蛋白。植物血浆 膜定位的RLKs作为PRRs，感知病原体相关的分子模式(PAMP)和 共同促进宿主对广泛病原体的免疫力。植物胞内NLRs检测 病原体特异性效应蛋白被转移到宿主细胞并触发病原体特异性免疫， 通常伴随着程序性细胞死亡。植物的遗传适应性使我们有可能识别出 许多植物的PRR和NLR免疫受体。然而，作为PRR和NLR基础的信令网络如何 介导性免疫之间的相互联系在很大程度上仍然是未知的。PI的实验室已经开发出一系列 敏感和高通量的基因筛查，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的意想不到的角色 植物免疫中的胞外Malectin样结构域。充足的初步证据支持一种诱人的 特异类marectin RLKs通过分化调控植物免疫和细胞死亡的假说 PRR和NLR免疫受体复合体的调节。具体地说，这个项目试图阐明：如何 Malectin样RLKs、LET1和LET2反向调节PRR和NLR复合体的形成和激活； 糖基磷脂酰肌醇(GPI)锚定的LLG1作为接头和分泌肽对LET1/2进行调控 RALF9作为配体；以及两种不同的E3泛素如何反向调节NLR蛋白SUMM2的稳定性 连接酶。通过阐明细胞表面驻留的类马来凝集素RLK模块作为PRR和NLR的分子链接 免疫受体，该项目有可能改变PRR和NLR相互联系的教条- 介导性免疫，以前被认为是在受体水平上独立发挥作用，并且只有 汇聚在下行信令事件中。 植物PRR和NLR介导的免疫类似于哺乳动物TLR和NLR介导的天然免疫 分别进行了分析。独特的是，丰富的遗传和基因组资源，包括全基因组的收集 基因敲除系，以及建立良好的细胞和生化分析表明，拟南芥是一种易驯化的 模型系统，从整个生物体和生理水平了解宿主的免疫机制。因此， 该项目的影响将超越植物生物学，并为一般人提供补充意见 了解先天免疫信号。

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.