Thursday, July 24, 2014

Can Genetically Modified Chestnut Trees Fight the Blight? The fifth in a series


More than a century ago, the Appalachian forests from Georgia to Maine contained billions of giant American chestnuts (Castanea dentate). Their nuts supported forest animals and people harvested them by the wagonload to make into flour, beer or to roast. American chestnut wood was abundant, beautiful, and did not rot. These trees are now almost all gone.


The large American chestnut and its nuts (from Google Images).  
What happened? The Asian Chestnut was imported in the 1880s and it carried a fungus to which it had evolved resistance over millennia of human cultivation in China and Japan. The battle between the Asian trees and the fungus (Cryphonectria parasitica) evolved to a near standstill. The Asian trees, which are smaller and grew in orchards, rarely succumbed to the fungus. Yet the fungus still grew on them and formed tough airborne spores by the billions. The American chestnut had evolved no defense and by 1900 the fate of the immense American chestnut forest was blowing in the wind.
 
Billions of chestnuts in this range were affected. The roots and small shoots remain and form the basis of rescue efforts
Imagine this: A spore lands on the trunk of an American tree, perhaps in a small wound where there is a little sap to nourish it. It germinates and makes a fungus that grows and burrows into the tree, forming a canker, a wound that slowly expands around the tree and kills the conducting tissue, the cambium. The infection girdles the tree as effectively as an ax.  Slowly, blowing north and south from the site of the importation on Long Island, the infection spread, killing 4 billion trees and a rich ecosystem and economy.
The growing fungus secretes oxalic acid and creates an acid environment in which it thrives, but the tree's tissue do not. Eventually the conducting elements of the tree die and when the tree is girdled, it dies.
What was to be done? Plant breeders had a strategy – breed the resistant Asian trees with the American trees and select for offspring that are resistant to Cryphonectria parasitica. This continued for generations, always backcrossing to the American tree so that gradually the resistance genes of the Asian trees moved into the American ones. Since breeding started in the1930s, there have been about eight generations and there are now relatively resistant trees whose DNA is 15/16 American.  Each generation takes about eight years - work for patient and dedicated people and fortunately, there were many. One of these researchers is the redoubtable Sandra Anagnostakis, about whom I have written before. Dr. Anagnostakis is in charge of the American chestnut program at the Connecticut Agricultural Research Station.  

There is another approach and that is to study the details of the infection. It turns out that the fungus softens up the tree by secreting a strong acid. Oxalic acid has a benign function in all cells, but in excess, it can also be a nasty piece of work. It is the irritant in Poinsettia leaves and it is the major component of kidney stones. Cryphonectria parasitica secretes it around the site of infection. This acidification blocks the tree’s defenses but allows the fungus to grow because its enzymes evolved to work in acid environments.

Dr. William Powell and Dr. Charles Maynard and their colleagues asked what would happen if an American Chestnut tree had an enzyme that destroyed oxalic acid. A gene from wheat produces such an enzyme, called oxalate oxidase. Enzymes are protein catalysts that carry out chemical reactions. Powell, Maynard and their colleagues engineered the wheat gene into cells of the American chestnut growing in petri dishes. Sure enough, the cells produced oxalate oxidase.

When there were enough cells, they were induced to make small shoots, essentially small plants. The hope was that destroying the parasite’s oxalic acid would give the shoots a fighting chance. So far, the shoots have resisted the fungus. Dr. Powell explains the work in an interesting TEDx talk, while on the same site, Dr. Maynard shows time-lapse videos of infected plants that either have the oxalic acid oxidase gene or do not. The gene seems to protect the few shoots shown. It is too early to claim success - we have to wait a while for trees to test.

The trees produced by decades of plant breeding would be candidates for an oxalate oxidase gene, to create even more resistant trees, since the two mechanisms of resistance may be different and additive.  I have the impression that the two schools do not want to trample on each other’s territory for the moment. The American Chestnut Foundation (I am a member) supports both approaches.

Many environmentalists hope that the forests can be restored without genetic modification of the trees. Some may feel that this would be hubris, that it is a step too far. I cannot see a reason to stop experimenting with these genetically modified trees. We eat that wheat enzyme oxalic acid oxidase in every sandwich.  Humans caused this blight by importing the fungus. Human made methods may be needed to surmount it.


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