Using genomics to understand tree rust biology and epidemiology

树锈病是北半球一些最重要的森林疾病爆发的原因。白松水疱锈病是一种外来入侵病原体，于19世纪末被引入北美，此后在整个白松分布范围内蔓延。这一疾病系统是动态的，新的发现和观察包括在Orobanchaceae科病原体的新宿主，C. ribicola与本地松锈病的杂交，可以克服商业黑醋栗抗性基因的C. ribicola新种族和亚洲白松上的Cronartium新种。这些发现迫使人们重新审视既定的教条，并可能影响这种疾病的流行。我提出了三个短期目标，以进一步提高我们对树锈病的生物学和流行病学的理解。1)阐明白松水疱锈病病原的起源、传播模式和传入途径。ribicola起源于亚洲并通过欧洲桥头堡种群入侵北美的假设将通过在欧洲，亚洲和北美进行全球抽样来验证。通过在我的实验室建立的测序协议进行基因分型，我们将生成基因组扫描，用于评估病原体的多样性和种群结构，并测试和比较不同的引入方案。2)白松水疱锈病对景观特征、寄主和气候的局部适应性研究。我的假设是，与北美东部相比，北美西部的ribicola受到更大的选择压力，因为它在更广泛的条件下攻击更多的宿主，包括海洋、大陆和高山气候，这将反映在它的种群基因组特征中。为了验证这一假设，我建议在不同的纬度和海拔梯度上对不同的宿主进行取样，并进行基因组扫描，以比较东西方人群中积极选择和罕见变异的程度。然后，我将使用反向生态学方法来识别异常值并进行表型表征。3)锈病种间杂交分析及其流行病学意义评价。我的假设是，杂交松树茎锈病将比亲本物种更具传染性，宿主范围更广。为了验证这一假设，我建议通过评估杂交松锈病在不同寄主（包括新发现的寄主）上的生存能力、发芽率、感染潜力和繁殖来衡量适应度。通过比较纯种和杂交锈病，我们将评估这些杂交是否有可能改变白松水疱锈病的流行。总的来说，这项工作将促进我们对北美最致命的树木病原体之一的了解。

Tree rusts are responsible for some of the most important forest disease outbreaks in the northern hemisphere. White pine blister rust, caused by the fungal pathogen Cronartium ribicola, is an invasive alien pathogen that was introduced into North America in the late 19th century and has since spread throughout the range of distribution of white pines. This pathosystem is dynamic and new findings and observations include new hosts of the pathogen in the family Orobanchaceae, hybridization between C. ribicola and a native pine rust, a new race of C. ribicola that can overcome resistance genes in commercial black currants and new species of Cronartium on white pines in Asia. These findings have forced a reexamination of the established dogma and could impact the disease epidemic. I propose three short-term objectives to further my long-term objective of improving our understanding of the biology and epidemiology of tree rusts. 1) Elucidation of origin, patterns of dispersal, and pathways of introduction of the white pine blister rust pathogen. The hypothesis that C. ribicola originated in Asia and invaded North America via European bridgehead populations will be tested by conducting a global sampling in Europe, Asia and North America. Using genotyping by sequencing protocols established in my lab, we will generate genome scans that will be used to assess diversity and population structure of the pathogen and test and compare different scenarios of introduction. 2) Investigation of local adaptation to landscape features, hosts and climate in white pine blister rust. My hypothesis is that C. ribicola is subjected to stronger selection pressure in western North America, since it attacks more hosts, across broader conditions that include maritime, continental and alpine climates than in eastern North America and that this will be reflected in its population genomic signature. To test this hypothesis, I propose to sample C. ribicola across latitude and altitude gradients on different hosts and generate genome scans to compare the extent of positive selection and rare variants in eastern and western populations. I will then use a reverse ecology approach to identify outliers and conduct phenotypic characterization. 3) Analysis of interspecific hybridization in rusts and evaluation of its epidemiological significance. My hypothesis is that hybrid pine stem rusts will be more infectious and have a broader host range than the parental species. To test this hypothesis, I propose to measure fitness, by assessing viability, germination rates, infection potential, and reproduction of hybrid pine rusts on the different hosts, including the newly discovered hosts. By comparing pure species with hybrid rusts, we will assess whether or not these hybrids have the potential to alter white pine blister rust epidemics. Overall, this work will advance our knowledge of one of North America’s deadliest tree pathogens.