Going back in time to predict the evolution of future plant pathogen

马铃薯褐腐病是由青枯雷尔氏菌（Ralstonia solanacearum）引起的一种全球性重要作物病害，在英国属于经济风险最高的一类。到目前为止，英国所有的疫情都与来自受污染河流水源的洪水或灌溉马铃薯作物有关，病原体可以通过在其第二宿主植物Woody Nightshade的根部越冬而持续存在。目前，Fera Science通过每年在英国范围内的河流采样来监测病原体的存在，以确定受污染的河流，这些河流将被禁止，不能用于灌溉。该采样程序产生了一个有价值的菌株收集跨越35年的病原体在其自然环境中的演变。该项目将使用基因组学、生物信息学和直接实验来确定R.在过去的三十年里，青枯菌在英国的河流网络中不断进化。2本项目将利用生物信息学、微生物学和植物生物学的结合来确定青枯菌的遗传变化和机制。青枯菌毒力在环境水库中的演变。这项工作将以现有的200株Fera菌株为基础，这些菌株已经与Fera共享并测序。现在将对该集合进行表型表征，并将其链接回元数据（样本位置和年份），特别关注：目标1。利用生物信息学比较关键毒力基因的变异，重点关注SNP、缺失、插入序列和原噬菌体运动的影响。Friman实验室进一步开发了一个基因组规模的模型，可用于模拟不同变异体对毒力基因网络的影响，从而通过计算机模拟预测病原体的表型。比较关键毒力性状的变异，包括运动性、附着性、代谢、趋化性、胁迫耐受性、三型效应蛋白、胞外多糖产生、铁载体等。将使用转录组学在表达水平上对分离株亚组进行表征。该数据将用于验证目标1中获得的计算机模拟表型预测。目标3。植物病原体毒力变异的定量分析。弗利曼实验室已经开发了植物内测定，利用番茄测定来量化病原体毒力的变化，这将用于鉴定整个菌株收集。这将使新的潜在标记基因的毒性病原体基因型在英国，可用于快速流行病学诊断的识别。

Potato brown rot, caused by Ralstonia solanacearum plant pathogenic bacterium, is a globally important crop disease, belonging to the highest economic risk category in the UK. Thus far, all UK outbreaks have been associated with flooding or irrigation of potato crops from contaminated river water sources where the pathogen can persist by overwintering in the roots of its secondary host plant, Woody Nightshade.Pathogen presence is currently monitored through annual, UK-wide river sampling by Fera Science to identify contaminated rivers that will be banned and cannot be used for irrigation. This sampling program has produced a valuable strain collection spanning 35 years of pathogen evolution in its natural environment. This project will use genomics, bioinformatics, and direct experimentation to establish how the virulence of R. solanacearum has evolved in the UK river network during the past three decades.This project will use a combination of bioinformatics, microbiology, and plant biology to identify mechanisms and genetic changes in R. solanacearum virulence when evolving in environmental reservoirs. Work will be based on an existing 200-strain Fera collection, which has already been shared with and sequenced. This collection will now be characterised phenotypically and linked back to metadata (sample location and year) specifically focusing on:Objective 1. Comparing variation in key virulence genes, focusing on effects of SNPs, deletions, and insertion sequence and prophage movement using bioinformatics. Friman lab has further developed a genome-scale model that can be used to model the effect of different variants on virulence gene networks, allowing in silico prediction of pathogen phenotypes.Objective 2. Comparing variation in key virulence traits, including motility, attachment, metabolism, chemotaxis, stress tolerance, type three effector proteins, exopolysaccharide production, siderophores and several others. A subset of isolates will be characterised at the expression level using transcriptomics. This data will be used to validate in silico phenotype predictions obtained in objective 1.Objective 3. Quantifying variation in pathogen virulence in planta. Friman lab has developed in planta assays to quantify changes in pathogen virulence using tomato assays, which will be used to characterise the whole strains collection. This will allow the identification of new potential marker genes for virulent pathogen genotypes in the UK that could be used to rapid epidemiological diagnostics.