Plasmodesmata: genetic control of cell-to-cell communication during plant defence

像动物一样，植物也会遭受各种真菌、细菌和病毒病原体引起的各种疾病。当真菌或细菌病原体攻击植物时，前线最初发生在单个细胞上。植物可以对抗病原体的一种方法是启动一个过程，导致被攻击的细胞死亡，阻止病原体从该细胞获得营养并传播。这个过程涉及许多有毒分子的产生，关键是被攻击细胞周围的细胞不会遭受同样的命运。植物细胞通过称为胞间连丝的通道与相邻细胞相连。这些通道就像是通向邻近细胞的大门，小分子可以简单地从一个细胞传递到另一个细胞。那么问题就来了，一个垂死的细胞是如何阻止有毒分子泄漏到它的邻居中的？牢房是否关上了通往邻居的门？我们知道，当植物暴露于寒冷或植物经历发育过渡时，胞间连丝可以打开和关闭，以控制细胞之间的信号移动。我们想研究当病原体攻击时这些门是否关闭以及这是如何发生的。最近，许多位于胞间连丝的新蛋白质被鉴定出来。其中之一是真菌几丁质的受体，当检测到真菌时，它会导致胞间连丝关闭。我将通过对受到不同病原体攻击的活组织进行显微分析，来研究为什么当病原体被感知时，胞间连丝会闭合。我还将通过对这种反应所需的蛋白质的生化和遗传鉴定来确定胞间连丝是如何闭合的。通过确定当病原体攻击时胞间连丝何时以及如何打开和关闭，我们将能够理解植物用于对抗疾病的非常重要的机制。该计划的最后一个目标将开始探索水稻中的这一现象，目的是了解这种全球粮食作物如何利用这一机制来对抗病原体。了解这些机制将使我们能够利用它们来帮助植物对抗疾病，使我们处于有利地位，以应对可能因全球气候变化而引起的植物疾病流行率增加的影响。

Like animals, plants suffer all manner of diseases caused by various fungal, bacterial and viral pathogens. When a fungal or bacterial pathogen attacks a plant, the battlefront occurs initially at a single cell. One means by which a plant can fight off the pathogen is to initiate a process that results in death of the cell that is being attacked, preventing the pathogen from gaining nutrients from this cell and spreading. This process involves the generation of many toxic molecules and it is crucial that the cells surrounding the attacked cell do not suffer the same fate. Plant cells are connected to their neighbouring cells by channels called plasmodesmata. These channels are like open doorways into neighbouring cells and small molecules can simply pass from cell to cell. The question then is how a dying cell stops toxic molecules leaking out into its neighbours? Does the cell close the doors into its neighbours? We know that plasmodesmata can open and close to control the movement of signals between cells when a plant is exposed to cold or when the plant undergoes a developmental transition. We want to investigate whether these doors close when a pathogen attacks and how this happens.Recently, many new proteins that are located at plasmodesmata have been identified. One of these is a receptor for fungal chitin and causes plasmodesmata to close when a fungus is detected. I will examine why plasmodesmata close when a pathogen is perceived by microscopic analysis of living tissue that is under attack from different pathogens. I will also determine how plasmodesmata close by biochemical and genetic identification of proteins that required for this response. By establishing when and how plasmodesmata open and close when a pathogen attacks we will be able to understand a very important mechanism that a plant uses to fight disease. The last objective of this programme will begin to explore this phenomenon in rice with the aim of understanding how this global food crop uses this mechanism to fight off pathogens. Understanding these mechanisms will enable us to exploit them to help plants fight disease, placing us in a strong position to combat the impact of increased prevalence of plant disease that is likely to arise from global climate changes.