Deciphering the mechanisms of non-host resistance to Zymoseptoria tritici

破译小麦发酵壳孢非宿主抗性机制

• 批准号: 2270840
• 金额: --
• 依托单位: University of Nottingham
• 依托单位国家: 英国
• 项目类别: Studentship
• 财政年份: 2019
• 资助国家: 英国
• 起止时间: 2019 至 无数据
• 项目状态: 已结题
• 来源: https://gtr.ukri.org/projects?ref=studentship-2270840
• 关键词: Deciphering; mechanisms; non; host; resistance

The air- and water-borne spores of plant pathogenic fungi are ubiquitous in nature and will often encounter many diverse plant species. However, plants remain immune to the majority of would be invaders. This highly effective and broad-spectrum immunity, termed non-host resistance (NHR), is thought to be under polygenic control and is therefore highly durable. Despite the paramount importance of NHR to interactions between plants and microbes, in most cases the precise mechanisms involved are poorly understood. The fungus Zymoseptoria tritici is only able to cause disease on leaves of wheat, and is the causal agent of Septoria tritici blotch (STB) disease. This disease is of global importance and currently one of the foremost threats, and economic constraints, to wheat production in the UK and Western Europe. Z. tritici does not physically penetrate plant cells during infection. Instead it colonises the intercellular space between plant cells (apoplast) and, thus, likely relies on the functions of apoplastic small secreted proteins (effectors) to manipulate plant defences and enable infection. This infection strategy is shared by many other species of plant pathogenic fungi causing globally important plant diseases. What prevents Z. tritici and fungi with similar lifestyles from causing disease on the non-host plant species they encounter remains virtually unknown. We recently discovered a dozen of Z. tritici effectors that trigger strong, defence reactions in the form of cell death, when infiltrated into Nicotiana benthamiana (tobacco), which is a non-host for Z. tritici. Most of these effectors required secretion into the apoplast to elicit cell death responses, and induction of cell death depended on the plant regulatory receptor-like kinases BAK1 and SOBIR1. Because the latter are known to be required for defence signalling following activation of cell surface pattern recognition immune receptors we hypothesised that tobacco possesses numerous receptors that can recognise different Z. tritici apoplastic effectors and initiate defence signalling. We also hypothesised that these multiple, likely distinct receptors play an important role in NHR against Z. tritici, and might be deployed for engineering disease resistance in wheat (New Phytologist 213: 7-9 [2017]; New Phytologist 213: 338-350 [2017]). The principal aim of the proposed PhD studentship project is to identify the putative immune receptor(s) that facilitate recognition of Z. tritici effectors in tobacco, functionally characterise these proteins, and assess their contribution to the NHR phenomenon. This will be done using a combination of functional genomics and biochemical approaches including Virus-induced gene silencing of cell surface receptor encoding genes (Nature Communications 9:594 [2018]) and proteomic screening to identify tobacco receptors interacting /binding to Z. tritici effectors (Proceedings National Academy Sciences USA 113:3389-94 [2016]).

植物病原真菌的空气和水传播孢子在自然界中普遍存在，并且经常会遇到许多不同的植物物种。然而，植物对大多数入侵者保持免疫。这种高效和广谱的免疫，称为非宿主抗性（NHR），被认为是在多基因控制下，因此是高度持久的。尽管NHR对植物和微生物之间的相互作用至关重要，但在大多数情况下，对所涉及的精确机制知之甚少。三孢发酵壳针孢菌（Zymoseptoria triangulae）是小麦叶斑病的病原菌，仅在小麦叶片上发生。这种疾病具有全球重要性，目前是英国和西欧小麦生产的最大威胁和经济制约因素之一。Z.在感染过程中，三唑醇不物理地穿透植物细胞。相反，它定殖在植物细胞之间的细胞间隙（质外体），因此可能依赖于质外体小分泌蛋白（效应子）的功能来操纵植物防御并使感染成为可能。许多其他引起全球重要植物疾病的植物病原真菌也采用这种感染策略。是什么阻止了Z。具有相似生活方式的真菌和真菌对它们遇到的非宿主植物物种造成疾病的可能性几乎仍然未知。我们最近发现了一打Z当渗透到本氏烟草（Nicotianabenthamiana）（烟草）中时，触发细胞死亡形式的强烈防御反应的三肽效应物，本氏烟草是Z.三个月。大多数这些效应物需要分泌到质外体中才能引发细胞死亡反应，而细胞死亡的诱导依赖于植物调节受体样激酶BAK 1和SOBIR 1。因为后者已知是细胞表面模式识别免疫受体激活后防御信号所需的，我们假设烟草具有许多可以识别不同Z的受体。三倍体质外体效应子并启动防御信号传导。我们还假设这些多个可能不同的受体在NHR抗Z中起重要作用。trips，并可能用于小麦的工程抗病性（New Phytologist 213：7-9 [2017]; New Phytologist 213：338-350 [2017]）。本博士研究生项目的主要目的是鉴定促进Z识别的假定免疫受体。烟草中的三磷酸腺苷效应物，功能性地抑制这些蛋白质，并评估它们对NHR现象的贡献。这将使用功能基因组学和生物化学方法的组合来完成，包括病毒诱导的细胞表面受体编码基因的基因沉默（Nature Communications 9：594 [2018]）和蛋白质组学筛选，以鉴定与Z相互作用/结合的烟草受体。trivalent effectors（Proceedings National Academy Sciences USA 113：3389-94 [2016]）。