Ash dieback epidemic in Europe: How can molecular technologies help?

An epidemic of ash dieback disease has spread east to west across Europe, first being noted in Poland in 1992 [1]. The disease is caused by the ascomycete fungus Hymenoscyphus fraxineus (also previously known as Chalara fraxinea and H. pseudoalbidus). This is one of several tree pathogens and insect pests that are recent newcomers to Europe caused by worldwide movements of plants and woody materials [2]. H. fraxineus probably arrived in Eastern Europe on Fraxinus mandshurica (Manchurian ash) or F. chinensis (Chinese ash) trees imported to eastern Europe from the Russian Far East [3]. Although it shows few symptoms on its native hosts, H. fraxineus rapidly infects leaves of the European ash (F. excelsior), spreading to the branches and causing symptoms ranging from mild infections (Fig 1) to the death of mature trees [4]. About a quarter of F. excelsior trees in southern Sweden were found to be either dead or severely damaged and it was expected that further severe damage and tree deaths would be observed over time [5]. Here, I briefly outline the life cycle of H. fraxineus, evidence for a founder effect when it arrived in Europe, and the observation that it greatly outnumbers H. albidus, a native saprophyte on European ash. I will also outline a novel approach (associative transcriptomics) that identified genetic markers in ash linked to low disease susceptibility, which is also correlated with changes in secondary metabolites in uninfected ash leaves.