A functional kinomics approach to dissecting signalling pathways in plant PAMP-triggered immunity

植物也会像动物一样生病。但是植物和动物的免疫系统的工作方式是不同的。我们都知道，如果我们流鼻涕和喉咙痛，一旦我们康复，我们就不会两次生病。这是因为我们的免疫系统有记忆-它学会如何识别使我们生病的病菌，从而阻止它再次感染。这被称为获得性免疫。植物没有获得性免疫，但它们有识别系统来检测病原体。这种方法的原理是，植物不是识别病原体的个体特征，而是识别共性--比如能够区分人和树，但不能区分个人的面孔。植物如何检测病原体是已知的，但接下来发生的事情有点神秘。一般来说，我们可以谈论检测和响应病原体作为传递信号的练习-科学家称之为“信号转导”。因此，病原体的存在是一个信号，这个信号必须在植物细胞的特定部位传递，以协调通过各种细胞反应的免疫反应。这是怎么回事？我们知道一些关于病原体识别的知识，其中虫子的部分被位于植物细胞壁中的所谓“受体”蛋白检测到。通常，受体与一种称为蛋白激酶的开关相连。蛋白激酶激活一系列的中继（或术语中的“信号转导途径”），其中可能包含更多的蛋白激酶。这些激活细胞反应，协调信号的输出，在这种情况下是防御反应。我们知道蛋白激酶是这个信号传递过程中非常重要的一部分。在这里，我们建议从细胞中去除每种蛋白激酶，看看这如何影响细胞反应和免疫力。我们可以使用基因技术来做到这一点，这种技术可以沉默负责每个激酶存在的每个基因的表达。这些激酶中的一些将在信号传导过程中具有一般或特定的作用，我们希望使用这种策略来识别它们。这将为植物免疫的信号通路提供许多新的重要信息。此外，我们知道病原体有自己的技巧来破坏信号转导。我们已经确定了病原体制造的许多蛋白质。这些蛋白质中的一些将“靶向”植物蛋白激酶，通过与它们结合并使它们失活。我们提出了一个额外的屏幕，以确定病原体蛋白结合的蛋白激酶在这里发现。这将提供病原体如何能够通过停止信号转导来感染植物的重要信息。

Plants get sick with diseases just like animals do. But there are differences in the way the immune systems of plants and animals work. We all know that if we come down with a runny nose and a sore throat, once we recover, we won't get sick to the same bug twice. This is because our immune system has a memory - it learns how to recognise the bug that made us sick, which stops it infecting again. This is called acquired immunity. Plants don't have acquired immunity, but they do have recognition systems to detect pathogens. The way this works is that instead of recognising individual characteristics of pathogens, plants recognise generalities - like being able to distinguish people from trees, but not individual faces. Something is known about how plants detect pathogens, but what happens next is a bit of a mystery. In general terms, we can talk about detecting and responding to a pathogen as an exercise in relaying signals - what scientists call 'signal transduction'. So, the presence of the pathogen is one signal, and this signal must be relayed around particular parts of the plant cell to coordinate the immune response through various cellular responses. How does this work? We know something about pathogen recognition, where parts of the bug are detected by so called 'receptor' proteins that sit in the plant cell wall. Often, the receptors are linked to a type of switch called a protein kinase. The protein kinase activates a series of relays (or a 'signal transduction pathway', in the jargon), which may contain more protein kinases. These activate the cellular responses which coordinate the output of the signal, in this case the defence response. So, we know that protein kinases are a very important part of this signalling process. Here, we propose to remove each protein kinase from the cell, and see how this affects cellular responses and immunity. We can do this using genetic techniques which silence the expression of each gene responsible for the existence of each kinase. Some of these kinases will have general or specific roles in the signalling process, and we hope to identify them using this strategy. This will provide a lot of new, important information on the signalling pathways that underlie plant immunity. Also, we know that pathogens have their own tricks to disrupt signal transduction. We have already identified many of the proteins that pathogens make to do this. Some of these proteins will 'target' plant protein kinases, by binding to them and inactivating them. We propose an additional screen to identify pathogen proteins that bind to the protein kinases discovered here. This will provide important information on how the pathogen is able to infect the plant by stopping signal transduction.