Chalara is driven by chemistry

Early claims about genetic resistance to Chalara and present in the Fraxinus excelsior population have not materialised. This was due to confusion between true, gene-based resistance to infection and apparent tolerance shown by some mature ash trees to disease progression and development.

True gene-based resistance to infection means no infection and therefore no disease. Attempts by a pathogen to penetrate genetically resistant plant parts (in this case the leaves) are met by a biochemical response elicited in the host plant by the pathogen. Called a hypersensitive reaction, the response prevents an infection and may leave the foliage with pin-prick spots. Trees initially thought to be resistant were simply showing a degree of tolerance to disease development. This can be underpinned by genetics but is just as likely due to environmental factors. 

Calls from conservation organisations for members of the public to identify and monitor mature ash trees showing resilience to Chalara are essentially a waste of time because there is no way of knowing how these trees would have reacted in the face of infection and disease development decades ago when still in the seedling or sapling stage. I am unaware of any authenticated cases of true genetic resistance in Fraxinus excelsior to infection by Hymenoscyphus fraxineus which essentially means no starting point for a truly conventional plant breeding programme.

The success of systemically acting plant pathogens and diseases like Hymenoscyphus fraxineus/Chalara ash dieback is inspired and driven by chemistry. Such highly efficient and successful plant pathogens synthesise phytotoxic chemicals which precede any physical advance by the fungus to undermine the structural and physiological integrity of the host plant tissue.

There is much evidence to support the contention that the fungally synthesised chemicals associated with manifestation of Chalara ash dieback are viridin and viridiol (furanosteroids). These chemicals are produced by a wide range of fungi and have been known to science since 1945 (Brian and McGowan, 1945).

Viridin is anti-fungal and viridiol is a phytotoxin (herbicide). Viridin is also produced by Trichoderma fungi and in this capacity underpins Trichoderma viride as a commercial biocontrol agent. Trichoderma viride is an antagonistic fungus used to control soil-borne fungal plant pathogens, and as such is called a mycoparasite.

Viridiol was seriously considered for use as a commercial mycoherbicide which is a fungal pathogen used to control weeds (Jones et al. 1988). Such is the potency of these two fungal chemicals.

Research in Sweden has demonstrated necrotic activity by viridiol towards ash seedlings (Andersson et al. 2009). 

You can imagine the scenario. Phytotoxic viridiol disrupts and destroys the ash tree’s living tissue while antifungal viridin stops secondary fungal invaders from muscling in on the action.

With the DNA of Fraxinus excelsior and Hymenoscyphus fraxineus successfully sequenced it should not be too difficult to genetically modify Fraxinus excelsior and thereby confer resistance to infection by Hymenoscyphus fraxineus and the development of Chalara ash dieback disease (Sollars et al. 2017). Chalara is driven by chemistry and can be cured by chemistry.

Such a scenario has already been achieved for a not dissimilar fungal pathogen and disease. The pathogen is Cryphonectria parasitica (chestnut blight disease) and is responsible for the death of some four billion American chestnut trees (Castanea dentata) down the eastern seaboard of the USA, from Maine in the north to Florida in the south. This occurred in the 40 years following introduction of the pathogen from the Far East in the early 20th century.

The phytotoxic chemical produced by Cryphonectria parasitica is oxalic acid. US scientists identified a gene in wheat that directs the synthesis of an enzyme called oxalate oxidase with the capacity to break down oxalic acid. Transgenic trees resistant to Cryphonectria parasitica are now a reality and well on the way to saving North American chestnut from oblivion. 

Projects and programmes to save common ash from Chalara’s clutches now abound, including one funded by DEFRA and optimistically called the Living Ash Project. However, unless future focus is on what can be done (genetic modification), rather than what is apparently impossible (conventional plant breeding), then living ash will become nothing more than a dream.

References:

Andersson, P.F., Johansson, S.B.K., Stenlid, J. and Broberg, A. (2009) ‘Isolation, identification and necrotic activity of viridiol from Chalara fraxinea, the fungus responsible for dieback of ash’. Forest Pathology 40(1). 43–46.

Brian P.W. and McGowan J.G. (1945) ‘Viridin: a Highly Fungistatic Substance Produced by Trichoderma viride’. Nature 156: 144–145.

Jones R.W., Lanini W.T. and Hancock J.G. (1988), ‘Plant growth response to the Phytotoxin Viridiol produced by the fungus Gliocladium virens’. Weed Science 36: 683–687.

Mabbett, T.H. (2015) ‘Last tree standing’. Woodland Heritage 2015 pages 43–56.

Newhouse A.E. et al. (2014) ‘Transgenic American chestnuts show enhanced blight resistance and transmit the trait to T1 progeny’. Plant Science 228: 88–97.