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: 2015
• 资助国家: 加拿大
• 起止时间: 2015-01-01 至 2016-12-31
• 项目状态: 已结题
• 来源: https://www.nserc-crsng.gc.ca/ase-oro/Details-Detailles_eng.asp?id=571254
• 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.

植物利用结构性和诱导性防御来抵抗微生物的攻击，这些防御包括RNA沉默、基础和高度特异的抗性。基础抗性(PTI，PAMP触发免疫)通常是通过检测病原体相关分子模式(PAMPs)来调节的。然而，适应的微生物表达一套效应器蛋白，这些蛋白通常会抑制这些防御。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器，并激活称为效应器触发免疫(ETI)的强大防御系统。 RNA沉默是一种核苷酸序列特异性的RNA转换机制，在真核生物中高度保守。不同生物中RNA沉默的共同特征是参与双链(DS)RNA作为启动分子，以及存在21-25nt的小(S)RNA，这些RNA是由一种名为DICER的类似RNaseIII的酶加工的。SRNAs赋予RNA诱导沉默复合体(RISC)序列特异性，其特征是一种核酸酶，它能降解与激活的dsRNA分子有任何RNA共享序列同源性。 在上一次资助期间，我们展示了植物病原体使用几种策略，包括抑制免疫，操纵宿主基因，以使疾病发生。我们还表明，植物能够感知RNAi途径的抑制子，作为诱导ETI的一种反防御策略。在下一笔资金中，我将重点研究水杨酸如何诱导某些病原体的毒力，植物病原体如何操纵寄主基因来抑制先天免疫，以及植物如何感知RNAi途径的抑制者导致ETI的激活。所获得的知识将有助于制定新的战略，以更好地管理不仅在加拿大，而且在世界各地的疾病问题。