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Ash trees (genus. Here we sequence the genome of a low-heterozygosity Fraxinus excelsior tree from Gloucestershire, UK, annotating 38,852 protein-coding genes of which 25% appear ash specific when compared with the genomes of ten other plant species. Analyses of paralogous genes suggest a whole-genome duplication shared with olive (Olea europaea, Oleaceae). We also re-sequence 37 F. excelsior trees from Europe, finding evidence for apparent long-term decline in effective population size. Using our reference sequence, we reanalyse association transcriptomic data 3 , yielding improved markers for reduced susceptibility to ash dieback. Surveys of these markers in British populations suggest that reduced susceptibility to ash dieback may be more widespread in Great Britain than in Denmark. We also present evidence that susceptibility of trees to H. fraxineus is associated with their iridoid glycoside levels. This rapid, integrated, multidisciplinary research response to an emerging health threat in a non-model organism opens the way for mitigation of the epidemic.

Over the last two decades, ash dieback has become a major problem in Europe, where the causative fungus has invaded the continent rapidly. The disease is caused by the invasive pathogenic fungus Hymenoscyphus pseudoalbidus (anamorph Chalara fraxinea), which causes severe symptoms and dieback in common ash, Fraxinus excelsior. It is becoming a significant threat to biodiversity in forest ecosystems and the economic and aesthetic impacts are immense. Despite the presence of the disease for at least 10 years in Scandinavia, a small fraction of F. excelsior trees have remained vigorous, and these trees exhibit no or low levels of symptoms even where neighbouring trees are very sick. This gives hope that a fraction of the ash trees will retain a sufficiently viable growth to survive. Following a period of high mortality in natural populations, selection and breeding of remaining viable ash trees could therefore provide a route for restoring the role of ash in the landscape. This paper reviews the available data on disease dissemination, and the consequences thereof in terms of symptom severity and mortality, and appraises studies that have tested the hypothesis that less-affected trees have genetically based resistance. The implications of the results for the adaptive potential of common ash to respond to the disease through natural or assisted selection are discussed. The risks of adverse fitness effects of population fragmentation due to high mortality are considered. Finally, it is recommended that resistant trees (genotypes) should be selected to facilitate conservation of the species.

An emerging infectious pathogen Hymenoscyphus pseudoalbidus has spread across much of Europe within recent years causing devastating damage on European common ash trees (Fraxinus excelsior) and associated plant communities. The present study demonstrates the presence of additive genetic variation in susceptibility of natural F. excelsior populations to the new invasive disease. We observe high levels of additive variation in the degree of susceptibility with relatively low influence of environmental factors (narrow-sense heritability = 0.37–0.52). Most native trees are found to be highly susceptible, and we estimate that only around 1% has the potential of producing offspring with expected crown damage of <10% under the present disease pressure. The results suggest that the presence of additive genetic diversity in natural F. excelsior populations can confer the species with important ability to recover, but that low resistance within natural European populations is to be expected because of a low frequency of the hypo-sensitive trees. Large effective population sizes will be required to avoid genetic bottlenecks. The role of artificial selection and breeding for protection of the species is discussed based on the findings.

The European common ash (Fraxinus excelsior) is currently threatened by a pathogenic fungus, Hymenoscyphus pseudoalbidus, which seems to enter the trees through the leaves. Continuous assessments of 39 clones in Danish field trials have shown that there are significant differences in the susceptibility of clones to the new disease. Interestingly, clones that showed early leaf senescence in the autumn were in general less susceptible to the disease than late-senescing clones. Thus, variation in susceptibility could be owing to phenological differences associated with the infection biology. To test whether differences in susceptibility are driven by genetically based factors other than phenology, we compared inoculations with H. pseudoalbidus on four highly susceptible clones with those of four less susceptible clones. Development of necrosis was hereafter followed regularly. The growth of the fungus in the inner bark was further detected with species-specific PCR primers. The severity of the response to infection shows significant differentiation among clones and significant correlation with clone susceptibility, as assessed from natural infections in field trials. The fungus was detected in tissues immediately surrounding the necrosis but showed some signs of endophytic growth. The results suggest that healthier clones are able to limit the growth and spread of the fungus and thereby minimize the occurrence of symptoms. This gives hope for the future preservation of F. excelsior in Europe through selection and breeding.

In Europe, common ash (Fraxinus excelsior) is being decimated because of the invasive fungus Hymenoscyphus fraxineus.

Tree disease epidemics are a global problem, impacting food security, biodiversity and national economies. The potential for conservation and breeding in trees is hampered by complex genomes and long lifecycles, with most species lacking genomic resources. The European Ash tree Fraxinus excelsior is being devastated by the fungal pathogen Hymenoscyphus fraxineus, which causes ash dieback disease. Taking this system as an example and utilizing Associative Transcriptomics for the first time in a plant pathology study, we discovered gene sequence and gene expression variants across a genetic diversity panel scored for disease symptoms and identified markers strongly associated with canopy damage in infected trees. Using these markers we predicted phenotypes in a test panel of unrelated trees, successfully identifying individuals with a low level of susceptibility to the disease. Co-expression analysis suggested that pre-priming of defence responses may underlie reduced susceptibility to ash dieback.

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