Using genomics to understand tree rust biology and epidemiology

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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.**