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Ash dieback damage was assessed and analysed on 16–22 year-old grafts in two ash seed orchards (Fraxinus excelsiorL.). The grafts originated from 106 plus-tree clones selected from 27 stands in southern Sweden based on their phenotypes. The results obtained indicate that ash dieback disease is strongly genotypically controlled. There was considerable genotypic variation among individuals. None of the clones seemed to be totally resistant, but some exhibited reduced susceptibility and retained this resistance after 6 years under heavy infection pressure. Autumn phenology based on leaf coloration was subject to moderate genetic control (H2= 0.19). The genetic correlation between autumn phenology and damage was weak to moderate (rGfrom 0.38 to 0.60) and positive, indicating that susceptible clones have a prolonged growing season. There was no evidence suggesting that stands differed in susceptibility. Together with the high heritability of resistance, strong age×age correlations and weak genotype×environment interactions, this suggests there is good scope for breeding less susceptible trees for the future. [ABSTRACT FROM AUTHOR]

Abstract: The ascomycete fungus Hymenoscyphus pseudoalbidus (anamorph Chalara fraxinea) is responsible for ash dieback currently expanding over large parts of Europe. Our objective was to investigate the genetic structure of H. pseudoalbidus and to examine its relationship to the species H. albidus, known as a saprotroph. The study comprised 181 isolates of H. pseudoalbidus collected within the diseased area, 17 H. albidus isolates from six apothecia, collected outside the diseased area in Norway, and nine apothecia of H. pseudoalbidus collected in Sweden. By analysis of microsatellite markers developed for this study, combined with AP-PCR using the M13 primer, we demonstrated sexual heterothally in H. pseudoalbidus, detected high gene flow and low geographic structure of the H. pseudoalbidus population and found indications of a founder effect. Also, substantial genetic differences were detected between the two species of fungi; only four of seven microsatellite markers developed for H. pseudoalbidus were amplified for H. albidus, and no alleles were shared among the species. Furthermore, AP-PCR banding patterns were distinctly different for the two species. We conclude that even though the two fungi have a similar habitat and are morphologically virtually identical, they do not share a recent common ancestor. [Copyright &y& Elsevier]