Hymenoscyphus fraxineus

Hymenoscyphus fraxineus is an ascomycete fungus that causes ash dieback, a chronic fungal disease of ash trees in Europe characterised by leaf loss and crown dieback in infected trees. The fungus was first scientifically described in 2006 under the name Chalara fraxinea. Four years later it was discovered that Chalara fraxinea is the asexual (anamorphic) stage of a fungus that was subsequently named Hymenoscyphus pseudoalbidus and then renamed as Hymenoscyphus fraxineus.

The first recognised report of this disease was in 1992 after a large number of ash trees had died in Poland. The disease is now widespread in Europe, with up to 85% mortality rates recorded in plantations and 69% in woodlands. It is closely related to a native fungus Hymenoscyphus albidus, which is harmless to European ash trees. A 2016 report published in the Journal of Ecology posited that a combination of H. fraxineus and emerald ash borer attacks could result in the extinction of European ash trees.

The fungus Hymenoscyphus fraxineus was first identified and described in 2006 under the name Chalara fraxinea. In 2009, based on morphological and DNA sequence comparisons, Chalara fraxinea was suggested to be the asexual stage (anamorph) of the ascomycete fungus Hymenoscyphus albidus. However, Hymenoscyphus albidus has been known from Europe since 1851 and is not regarded as pathogenic. In 2010, through molecular genetic methods, the sexual stage (teleomorph) of the fungus was recognized as a new species and named Hymenoscyphus pseudoalbidus. Four years later it was determined that "under the rules for the naming of fungi with pleomorphic life-cycles", the correct name should be Hymenoscyphus fraxineus. Hymenoscyphus fraxineus is "morphologically virtually identical" to Hymenoscyphus albidus, but there are notable genetic differences between the two species.

The lifecycle of Hymenoscyphus fraxineus comprises two phases: sexual and asexual. The asexual stage (anamorph) grows in affected trees attacking the bark and encircling twigs and branches. The sexual, reproductive stage, (teleomorph) grows during summer on ash petioles in the previous year's fallen leaves. The ascospores are produced in asci and are transmitted by wind, which may explain the rapid spread of the fungus. The origins of the disease are uncertain, but researchers are investigating the theory that the fungus originated in Asia, where ash trees are immune to the disease. Genetic analysis of the fungus Lambertella albida which grows harmlessly on petioles of the Manchurian ash (Fraxinus mandschurica) in Japan, has shown that it is likely to be the same species as Hymenoscyphus fraxineus.

In December 2012, teams from The Sainsbury Laboratory (TSL) and the John Innes Centre in Norwich sequenced the genome of the fungus. The sequence has been published on the website OpenAshDieBack and offers insights into the mechanisms of infection in trees by the fungus. The study identified toxin genes and other genes that may be responsible for the virulence of the fungus. In the long term researchers aim to find the genes that confer resistance to the pathogen in some ash trees.

Trees now believed to have been infected with this pathogen were reported dying in large numbers in Poland in 1992. By the mid 1990s, the fungus had also been identified in Lithuania, Latvia and Estonia. However, it was not until 2006 that the fungus's asexual stage, Chalara fraxinea, was first described by scientists, and 2010 before its sexual stage was described. By 2008, the disease had also been discovered in Scandinavia, the Czech Republic, Slovenia, Germany, Austria and Switzerland. By 2012, it had spread to Belgium, France, Hungary, Italy, Luxembourg, the Netherlands, Romania, Russia, Britain and Ireland. By 2016, it was already identified in central Norway, the northernmost distribution area of the ash tree.

Up to 85% mortality rates due to H. fraxineus have been recorded in plantations and 69% in woodlands. The disease has caused a large-scale decline of ash trees across Poland, with evidence suggesting that in the long term "15 to 20 per cent of trees may survive without exhibiting symptoms." In 2012, it was reported that the disease was reaching its peak in Sweden and Denmark, and that it was entering a post-decline (or chronic) phase in Latvia and Lithuania. The disease was first observed in Denmark in 2002, and had spread throughout the country by 2005. In 2009 it was estimated that 50 per cent of Denmark's ash trees were affected by crown dieback, and a 2010 estimate stated that 60–90% of ash trees in Denmark were affected and may eventually disappear. The disease was first reported in Sweden in 2003. A survey conducted in Götaland in 2009 found that more than 50% of the trees had noticeable thinning and 25% were severely injured.

A Danish study found that substantial genetic variation between ash trees resulted in significant differences in their susceptibility to the disease. However, the proportion of trees with a high level of natural resistance seemed to be very low, probably less than 5%. A Lithuanian trial based on the planting of trees derived from both Lithuanian and foreign populations of European ash found 10% of trees survived in all progeny trials to the age of eight years. Mass screening trials in Britain found that less than 5% of trees were healthy after three years. Subsequent genetic analysis of these trials found a highly polygenic basis to ash dieback resistance, and allowed genomic prediction models for tree health to be trained. Use of these genomic prediction models on adult and juvenile trees in a woodland in Surrey, England, gave evidence that natural selection is acting to increase resistance to ash dieback in ash populations.