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.
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| 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.
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| 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.
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| 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.
