Molecular Plant-Microbe Interactions

分子植物-微生物相互作用

• 批准号: 262236-2013
• 负责人: Bouarab, Kamal
• 金额: $ 3.42万
• 依托单位: Université de Sherbrooke
• 依托单位国家: 加拿大
• 项目类别: Discovery Grants Program - Individual
• 财政年份: 2017
• 资助国家: 加拿大
• 起止时间: 2017-01-01 至 2018-12-31
• 项目状态: 已结题
• 来源: https://www.nserc-crsng.gc.ca/ase-oro/Details-Detailles_eng.asp?id=630380
• 关键词: Molecular; Plant; Microbe; Interactions

Plants fight microbial attacks using both constitutive and induced defenses which include RNA silencing, basal and highly specific resistance. Basal resistance (PTI, for PAMP Triggered Immunity) is very often mediated via the detection of pathogen-associated molecular patterns (PAMPs). However, adapted microbes express a suite of effector proteins that often act to suppress these defenses. Plants have evolved other receptors called resistance proteins (R proteins) that detect these pathogen effectors and activate strong defenses called Effector Triggered Immunity (ETI). RNA silencing is a nucleotide sequence-specific RNA turnover mechanism that is highly conserved among eukaryotes. Common features of the RNA silencing in different organisms are the involvement of double-stranded (ds)RNA as initiator molecule and the presence of small (s)RNAs of 21-25nt that are processed from dsRNA by an RNAse III-like enzyme named Dicer. The sRNAs confer sequence specificity to a RNA-induced silencing complex (RISC) featuring a nuclease that degrades any RNA-sharing sequence homology to the activating dsRNA molecules. During the last funding period we showed that plant pathogens use several strategies, including suppression of immunity, manipulation of host genes, to enable disease. We also showed that plant is able to sense a suppressor of RNAi pathway as a counter-counter defense strategy to induce ETI. In the next funding, I will focus on how salicylic acid induces virulence of some pathogens, how plant pathogens manipulate host genes to suppress innate immunity and how plant sense a suppressor of RNAi pathway leading to activation of ETI. The knowledge obtained will contribute to the development of new strategies to better manage the disease problems not only in Canada, but around the world.

植物利用自身和诱导防御来对抗微生物的攻击，包括RNA沉默、基础和高度特异性抗性。基础耐药（PTI， PAMP触发免疫）通常是通过检测病原体相关分子模式（PAMP）介导的。然而，适应的微生物表达了一套效应蛋白，经常抑制这些防御。植物进化出了其他受体，称为抗性蛋白（R蛋白），可以检测这些病原体效应物，并激活强大的防御，称为效应触发免疫（ETI）。RNA沉默是一种在真核生物中高度保守的核苷酸序列特异性RNA转换机制。在不同的生物体中，RNA沉默的共同特征是双链RNA作为启动分子的参与，以及21-25nt的小RNA的存在，这些小RNA由一种名为Dicer的RNAse iii样酶从dsRNA加工而来。srna赋予rna诱导沉默复合体（RISC）序列特异性，该复合体具有一种核酸酶，可以降解任何与激活dsRNA分子同源的rna共享序列。在上一个资助期间，我们表明植物病原体使用几种策略，包括抑制免疫，操纵宿主基因，使疾病发生。我们还发现植物能够感知RNAi通路的抑制因子，作为诱导ETI的反制防御策略。在接下来的资助中，我将重点研究水杨酸如何诱导一些病原体的毒力，植物病原体如何操纵宿主基因抑制先天免疫，以及植物如何感知RNAi途径的抑制因子导致ETI的激活。所获得的知识将有助于制定新的战略，以便不仅在加拿大，而且在全世界更好地管理疾病问题。