The legacy of the American chestnut (Castanea dentata) is inextricably linked to its losing battle against a fungal pathogen, chestnut blight (Cryphonectria parasitica). But, a virus and some genetic engineering may help us return this tree to the upper canopy of our forests.

In the Audubon Guide to North American Trees, the American chestnut has 3 descriptions. The first is a memory of this tree’s historical stature, which was once so common and useful that it would make both cribs and caskets. The second, more practical, entry describes how these trees look to the modern observer: small and enfeebled by the unrelenting chestnut blight fungus that prevents these trees from reaching their full potential. The third entry describes the etiology of chestnut blight, which killed an estimated 4 billion American chestnuts in the 50 years following its introduction to New York in the early 1900’s.

The loss of the American chestnut is often framed as a loss for American industry, but Native Americans in the Eastern United States have valued this tree for centuries. The tree’s abundant and edible nuts were easily storable provisions that could be stewed into porridge. This dish introduced chestnuts into Iroquois mythology, where a boy named Hodadenon foolishly uses up the remaining stored chestnuts and must brave great danger to collect more. This story ultimately places chestnuts as key to survival during hard times, and its moral is that chestnuts (and food generally) must be shared and planted widely. In this context, the damages done by chestnut blight are not just financial, but ecological and cultural.

How Chestnut Blight Kills American Chestnuts

Today, American chestnuts bear the scars of chestnut blight cankers. After C. parasitica enters the tree through breaks in the bark of chestnuts, it grows in the living layer beneath it called the cambium. As the fungus stretches its hyphae around this layer, the tree responds with thick growth to try to contain the pathogen. These outward symptoms of the struggle are called cankers. These become more obvious when bark is sloughed off where cambium has been killed by the fungus, revealing the wood underneath. The fungus kills the cambium by producing oxalic acid and enzymatically digesting this layer in order to grow. Throughout this battle, the fungus produces little orange, spore-bearing structures (perithecia) on the canker. These spores are spread by wind, water or other organisms to the next chestnut. Eventually, the hyphal threads of chestnut blight encircle the entire stem of the tree, strangling it in a process called girdling. Ultimately, these trees that used to live for centuries are now lucky to live a couple of decades.

Since the fungus does not grow in the soil, buried roots are spared. If large enough, they will send up sprouts around the stump of old trees. These clones are susceptible to chestnut blight, just as the original tree was, so their fungal fate is spelled out before they even produce their first leaf. The lucky ones live long enough to produce some chestnuts, and may grow enough roots to support another generation of sprouts. This cycle is nearly ubiquitous, despite over a century of efforts to control the spread of chestnut blight since its initial sighting at the Bronx Zoo in New York. Even with humans as allies, chestnut trees have withered and the fungus has thus far prevailed.

The Virus of the American Chestnut’s Enemy Is Our Friend

There is one battle that C. parasitica is losing: its standoff with a naturally infecting hypovirus. Discovered in chestnut blight cankers in Italy by Antonio Biraghi in 1953, this virus lives in the fungal cytoplasm. When infected with the hypovirus, C. parasitica is weakened, preventing it from producing the devastating cankers that are a blight on American chestnuts. However, because these hypoviruses are limited to the cytoplasm, they are only passed on during the exchange of cytoplasm that takes place during anastomosis: when hyphae of 2 fungi join to form a single hyphal network. Fungi, perhaps to protect against the transmission of such viruses, have genes, called vegetative incompatibility genes (vic), that make this fusion incompatible in most cases.

To be 'compatible' for anastomosis, 2 fungi must have matching sets of vic genes. C. parasitica has 5 vic gene loci, each with 2 possible versions, or alleles. That means, for any given C. parasitica fungus, only 1 in 32 other C. parasitica strains will be compatible. This natural hurdle makes it difficult to introduce hypovirus to natural C. parasitica strains through hyphal fusion. When vic genes don't match,the hyphal cells that attempt anastomosis die, thus preventing the virus from being transmitted from one fungus to another.

Genetic Engineering Aids Virus Transmission