Deciphering the mechanisms of non-host resistance to Zymoseptoria tritici

植物病原真菌的气传和水传孢子在自然界中普遍存在，经常会遇到各种各样的植物物种。然而，植物仍然对大多数可能的入侵者免疫。这种高效和广谱的免疫被称为非宿主抗性(NHR)，被认为是受多基因控制的，因此具有高度的持久性。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，人们对涉及的确切机制知之甚少。小麦发酵菌(ZymosepVictoria Tritici)仅能在小麦叶片上致病，是引起小麦黑斑病的病原。这种疾病具有全球重要性，目前是英国和西欧小麦生产的主要威胁和经济制约因素之一。小麦纹枯病菌在侵染过程中不会穿透植物细胞。相反，它定植于植物细胞(质外体)之间的胞间空间，因此很可能依赖质外体小分泌蛋白(效应器)的功能来操纵植物防御并使其能够感染。这一感染策略被引起全球重要植物疾病的许多其他种类的植物病原真菌所共享。是什么阻止了具有相似生活方式的Z.tritici和真菌在它们遇到的非寄主植物物种上致病仍然几乎是未知的。我们最近发现了十几个小麦纹枯病菌的效应物，当它们渗透到非小麦纹枯病菌寄主的本氏烟草体内时，它们会以细胞死亡的形式触发强烈的防御反应。这些效应器中的大多数需要分泌到质外体中来引发细胞死亡反应，而细胞死亡的诱导依赖于植物调节性受体样激酶BAK1和SOBIR1。因为已知后者在激活细胞表面模式识别免疫受体后是防御信号所必需的，所以我们假设烟草拥有大量的受体，可以识别不同的小麦纹枯病菌质外体效应器并启动防御信号。我们还假设，这些多个、可能的不同受体在抗小麦赤霉菌的NHR中发挥重要作用，并可能被用于工程小麦抗病(新植物学家213：7-9[2017]；新植物学家213：338-350[2017])。拟议的博士研究生项目的主要目的是识别假定的免疫受体(S)，促进烟草中小麦纹枯病菌效应器的识别，从功能上表征这些蛋白质，并评估它们对NHR现象的贡献。这将使用功能基因组学和生化方法的组合来完成，包括病毒诱导的细胞表面受体编码基因的基因沉默(自然通讯9：594[2018])和蛋白质组筛选以确定与小麦纹枯病菌效应器相互作用/结合的烟草受体(美国国家科学院院刊113：3389-94[2016])。

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]).