LAND: Ash dieback in Norway - causes, impact and control

Ash dieback are caused by Hymenoscyphus fraxineus (earlier named H. pseudoalbidus), an invasive species from northeastern part of Asia. The disease is increasingly spreading in Norway and is now well established were ash is natural from the Swedish border to Romsdal. The disease is now well established in Sunnmøre, and the northermost locations are in Rauma on the Southern side of Isfjorden. Targeted management of ash (Fraxinus excelsior) will benefit from information on their population genetic history. Such information is lacking for the northern range margin populations which can be especially important to characterize and conserve in the face of climate change. First we used chloroplast (cp) and nuclear microsatellite markers to investigate population genetic history of the northern range margins of common ash. Second, we investigated fine scale spatial genetic structure in four populations with contrasting disease history, two Norwegian and two Lithuanian populations, to evaluate the effects ash dieback may have on the genetic structure of ash. We find that northern ash populations bare the same cp haplotypes as south-eastern European populations suggesting shared glacial refugia. Based on our microsatellite data, we find that the population genetic history of the northern range is coherent with a leading edge colonization model. Populations in the north diverged during colonization producing a complex pattern of population genetic structures accompanied by a decrease in genetic diversity. On the monitoring plots the situation for the big and small trees are different. On the plots in the southeastern part of Norway the crown density is steadily being worse, but relatively few trees are dead. Up to now only 10% of the big trees have died, but still many are nearly without symptoms, which look promising for the future of ash. The small trees are much more affected, and more than half of them are dead. At the west coast, the situation is worse this year, and the first symptoms has been observed at the northernmost plot, at Stryn. Mode of infection of the ash dieback pathogen in naturally infected ash stems was followed by a qPCR assay specific to DNA of the ash dieback pathogen and by microscopy. The data suggest that axial spread of H. fraxineus in ash stems takes place through hyphal growth primarily within the starch containing perimedullary pith and paratracheal parenchyma associated with xylem vessels, whereas bark infection originates through the radially spanning rays that bridge phloem with xylem and pith. We have continued sampling of ash leaves during the growth season to study the dynamics of fungal establishment in ash leaves. This year we have also sampled leaves of rowan from the same stand to get a reference of pathogen growth on a non-host substrate. These materials will be analysed later this autumn by a qPCR assay specific to DNA of the ash dieback pathogen and will form the basis of a manuscript of its own.

Dieback of European ash, caused by a fungus presumably introduced to Europe relatively recently, is threatening the tree on a continental scale. Norway represents the currently expanding frontier of the disease, and the aim of this proposal is to provide key information about ash dieback, the causative agent, genetic structure and disease resistance of Norwegian ash populations. No prior information is available about the genetic structure of Norwegian ash populations. Therefore, characterizing the presen t genetic resources, on a genome wide basis, and comparison with other European populations will provide us vital information to evaluate conservation efforts. By sampling primarily within the nature reserves present in Norway, the survey will yield valua ble data for evaluation of migration and gene flow among these populations, as well as estimation of effective population size to avoid inbreeding within these fragmented populations. Danish field trials have implicated a genetic component in host resista nce towards ash dieback. As there is clustering of relatives in many ash populations, we will also test if spatial variation in susceptibility to ash dieback is related to certain family groups. Identification of such superior families can be employed in breeding programmes. In addition the proposal includes molecular characterization of the causative pathogen and establishment of the host developmental stage and tissue through which the infection takes place. We will also develop a high-throughput diagno stic assay for detection of the fungus in diseased trees and propagation material. In cooperation with the Norwegian genetic resource centre, the data will be passed down to the management authorities to be used in developing sustainable management plans for ash in nature reserves in Norway. In conclusion, the project will contribute to maintenance of ash-associated biodiversity, sustainable management of ash stands and disease-free propagation of the tree.