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We must develop the genetic tools to fight ash dieback

Ash dieback - wilting our leaves since September 2012. Gareth Fuller/PA

Ashwellthorpe Lower Wood in Norfolk, England has been managed by coppicing, an ancient form of forestry, for more than a thousand years. It was recorded as coppiced woodland in the Domesday Book published in 1068 and, as implied from its name, ash trees are a major constitutent species. In fact the name Ashwellthorpe comes from the Vikings, for whom Yggdrasil, the giant ash tree, was sacred.

In 1992 the wood was purchased by the Norfolk Wildlife Trust as a nature reserve and Site of Special Scientific Interest. Since then the coppice rotation has been managed by local volunteers to maintain the amazing biodiversity there.

So we were devastated when, in September 2012, we realised that many ash trees in the wood were diseased with what we suspected was ash dieback fungus that had spread from mainland Europe. We tested extracted DNA from the pith of diseased branches, and confirmed the fungal pathogen was present.

Ash dieback had already arrived in the UK in imported trees, but no trees have been planted in Ashwellthorpe, an ancient wood that could have existed since the last Ice Age. This must have been a substantial natural infection, implying that ash trees in Britain will become infected, and that the inexorable spread of the disease from the east to the west of Europe would not been halted by the English Channel. The only questions now are how long the disease will take to establish itself across the country and what proportion of trees will be tolerant to the disease and will survive.

Faced with this scenario, what can be done? European scientists had already established a great deal. The cause of ash dieback was identified in 2006, the fungus named Chalara fraxinea, later realised to actually be a stage of the fungus Hymenoscyphus pseudoalbidus. DNA techniques were established that could confirm the presence of the fungus, and researchers had identified several aspects of its lifecycle, including how the disease is spread by spores fired into the air from small fruiting bodies (mushrooms) that sprout in July and August from rotting leaf stems.

The ash dieback disease fungal cycle. A Edwards

We need to gain more understanding of how the fungal pathogen works. For example, how can we establish laboratory-based tests to discover how it causes the disease? These could be used rapidly to identify resistant trees; they could also be used to establish if and how trees could be inoculated against the disease. For instance species of Trichoderma - ubiquitous, largely harmless fungi found in the soil - have been cultured as biological control agents against some plant fungal diseases.

Establishing and laying out the pathogen’s genome sequence and identifying the genes used for infection can give us real insight into how the disease functions. Those working with us have sequenced H. pseudoalbidus using a variety found in Britain. By comparing it with the genes of European varieties, it’s clear that the variation between samples cannot be due to crossbreeding with H. albidus, the closely related, but harmless, fungus usually found on ash leaves.

The key to the long term survival of ash trees lies in the observations of Erik Dahl Kjaer and colleagues in Denmark. Using trees grafted several years ago, they found that one tree, Tree 35 out of 39 trees tested, showed tolerance to the fungus in a number of different environments.

This showed that this lower susceptibility to infection is not due to environmental influences, so it must be genetically determined. This means we can breed ash that can withstand the disease. We can be optimistic of some level of genetic resistance among UK ash trees too, and the Department for the Environment, Food and Rural Affairs is undertaking a long-term breeding programme as part of its Chalara Management Plan.

Can we help nature by identifying regions of the ash genome associated with tolerance to the disease? This could be done using genetic crosses with resistant trees, but this would take years. An alternative approach is to try to undertake association genetics. A recently described modification of association genetics is to identify genetic markers using RNA sequencing, a method recently pioneered in crop plants. But genetic approaches require a detailed genetic map, and there is no map for ash or any close relatives yet. Sequencing the ash genome would help greatly in generating a map.

Such a genetic project can provide the tools to help identify the most promising crosses to make between tolerant ash trees. But at this stage nothing is known about whether tolerance is due to one or many genes, whether there are different types of tolerance, whether tolerance is recessive or dominant, or whether combinations of different genes can enhance tolerance. It will take many years to establish, but for those countries facing decimation of their ash forests, it is certainly worth trying.

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