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

马铃薯褐腐病是由青枯病病原菌引起的一种全球性农作物病害，在英国属于经济风险最高的类别。到目前为止，英国所有的疫情都与洪水或灌溉来自受污染的河流水源的马铃薯作物有关，在那里病原体可以通过在其第二宿主植物Woody Nightshade的根中越冬而持续存在。目前，病原体的存在是通过Fera Science在全英国范围内的年度河流采样来监测的，以确定将被禁止且不能用于灌溉的受污染河流。这一采样计划产生了一个有价值的菌株集合，跨越了病原体在其自然环境中35年的进化。本项目将使用基因组学、生物信息学和直接实验来确定青枯病菌在过去30年中在英国河网中的毒力是如何进化的。本项目将结合生物信息学、微生物学和植物生物学来确定青枯菌在环境水库中进化时的毒力机制和遗传变化。这项工作将基于现有的200株FERA收集，这些收集已经与人分享并进行了测序。现在将对这一集合进行表型描述，并将其与元数据(样本位置和年份)联系起来，特别侧重于：目标1.利用生物信息学比较关键毒力基因的变异，重点研究SNPs、缺失以及插入序列和前噬菌体运动的影响。Friman实验室进一步开发了一个基因组规模的模型，可以用来模拟不同变异对毒力基因网络的影响，从而允许对病原菌表型的电子预测。目的2.比较关键毒力性状的差异，包括运动性、依附性、新陈代谢、趋化性、逆境耐受性、类型3效应蛋白、胞外多糖的产生、铁载体等。分离株的一个子集将使用转录组学在表达水平上进行表征。这些数据将用于验证在目标1中获得的电子表型预测。目的3.量化植物病原菌毒力的变异。弗里曼实验室已经开发了植物试验，使用番茄试验来量化病原菌毒力的变化，这将被用来表征整个菌株集合。这将允许在英国识别新的毒力病原体基因型的潜在标记基因，这些基因可以用于快速流行病学诊断。

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.