Ron Bockenhauer sounds remarkably cheerful for a man living among orphans of one of the country’s most infamous ecological tragedies. He resides in the largest remaining stand of American chestnut trees. The straight-trunked giants once accounted for a third or more of the trees covering the Appalachian chain, and wags claimed that a squirrel could go from Maine to Georgia by jumping from chestnut to chestnut and never touching the ground. In 1904, a killer fungus showed up in New York and swept throughout the range. The chestnut forests vanished.
Devastating as the chestnut blight was, it missed some trees. Bockenhauer’s grandfather lived in Wisconsin, outside the normal range of the American chestnut. Around the beginning of the 20th century, a neighbor planted a grove of American chestnuts. For years, separated from the epidemic’s hot zone, the stand expanded to some 60 acres, moving onto Bockenhauer’s property.
“Basically, they grow like a weed,” Bockenhauer says. Now, the fungus is moving through his patch.
The chestnut’s last stands–far-flung patches like Bockenhauer’s, some two dozen or so sick trees in the traditional range, and many stumps that keep sprouting–have attracted optimists trying to bring back the chestnut forests after 99 years of blight. Make that extraordinary optimists. None of the chestnut varieties bred to resist blight so far has the shoot-the-sun height of the pure American chestnut and its famed scrappiness for competing in a forest canopy. The Department of Agriculture ended its chestnut-breeding program decades ago, so private citizens have largely financed recent decades of work.
What’s more, a major test of biological control for the disease turned in less-than-hoped-for results last year (SN: 8/10/02, p. 94: Available to subscribers at Disease outpacing control in largest chestnut patch left).
Yet the work to restore chestnuts in the United States, both by breeding hardier varieties and controlling the fungus, goes on passionately. Scientists soar to heights of administrative creativity in finding budgetary and schedule cracks in which to squeeze chestnut projects. Champion tree-climber teams donate aerial labor to apply experimental treatments. Volunteers from unwoodsy professions give first aid to individual diseased trees and drive hundreds of miles to care for venerable specimens. These fans’ dedication is surprising given that the great chestnut woods had already disappeared before most of today’s chestnut savers were born.
Bockenhauer, however, did grow up in a chestnut grove and can describe the goal from his personal experience. “They’re the prettiest trees you’ve ever seen,” he says.
Strategies to beat the chestnut blight fall into two main groups: attempts to breed trees that resist it and attempts to enlist one of its biological enemies to quash it. The goal of the foremost efforts to breed a fungus-resistant tree is a chestnut that looks American but fights Chinese-style when it comes to disease.
The blight seems to have originated in Asia, and some trees of the Chinese chestnut species don’t even develop cankers when they encounter the fungus.
Decades ago, the USDA did create blight-resistant hybrids of American and Chinese species, explains Fred Hebard of the American Chestnut Foundation’s breeding farm near Meadowview, Va. These trees, however, achieved only modest height, as the Chinese species does, and dwindled away in the ruthless competition for light that determines the king of the forest canopy.
Some 20 years after the USDA program ended, the late Charles Burnham, a corn geneticist, decided to take up the cause. He founded the American Chestnut Foundation to approach the problem from a different angle. The USDA had started by crossing an American tree with a Chinese species and then crossing each successive generation of their progeny with another Chinese tree. No wonder the final products looked too Chinese, Burnham concluded. He decided to cross each generation of progeny with American trees instead.
Hebard is carrying on with this general plan. The big moment came for him, he says, in the mid-1990s, “when I realized it would work.” Hebard made various crosses of Chinese and American trees and methodically exposed them to blight fungus. By keeping track of how many out of each generation showed resistance to the disease, he determined that only two or three main genes control resistance. Therefore, he predicts that if he starts by crossing a Chinese tree with an American one, crosses their offspring with American chestnuts for three generations, and interbreeds the progeny he should have a 1 in 64 chance of finding high resistance to the disease among the offspring.
He’s also succeeded in tricking the plants into flowering years sooner than they normally would. The original plan assumed 10 years per generation, but by pampering trees, Hebard has squeezed it down to 6 years. He’s finished his third generation of back crosses and hopes to harvest nuts as early as 2008 that will grow into soaring hybrids resistant to chestnut blight.
His research program is a bit ambitious for one lifetime. “I’ll know whether we’ve got blight resistance,” he says, but the full test of his work will take another century. That’s because he’s trying to create a resistant tree that not only looks American, but also can dominate a forest.
Another breeding effort, also funded mostly by private donations, skips the Chinese genes entirely. Gary Griffin of the Virginia Polytechnic Institute and State University in Blacksburg runs breeding programs for the American Chestnut Cooperators’ Foundation. This band of enthusiasts has located a few dozen old survivors, as they call them–trees that are hanging on in the historical range of the American chestnut. Griffin, his wife, Lucille Griffin, and other volunteers graft branches from the old trees onto healthier rootstock to create a reservoir of genetic material for crossing the sturdiest of the old chestnuts with each other to bring out resistance.
Instead of conventional plant breeding, William A. Powell and Charles Maynard of the State University of New York at Syracuse are trying to genetically engineer an American chestnut for homeowner yards. So far, the researchers have constructed several dozen promising bits of genetic material–modeled after genes from wheat, amaranth, and frog–that should bring resistance. The hard part, however, has been getting a lump of chestnut tissue in a laboratory dish to grow into a tree.
Much of the energy for creating new chestnuts comes from volunteers. For example, Carl Mayfield of Springfield, Va., has appointed himself guardian of the largest known old survivor in the blight zone, a chestnut 14 inches in diameter that still stands in a farmer’s field in southwestern Virginia. Mayfield drives more than 200 miles to cut brush around the tree, and when the farmer moved draft horses onto the field, Mayfield built a sturdy fence to protect his charge.
He visits other chestnut trees, too, packing mud on their cankers and clipping flowers for use in breeding programs. He’s working on the next chestnut generation himself and coddles several dozen grafted plants in his basement.
“I quit working for money at [age] 76, and I devote myself to this,” he says. “It’ll work–there’s no doubt.” Then Mayfield mischievously offers an invitation to the celebration he’ll throw when a field of his seedlings matures.
He’ll be 126, he says, but restoring the American chestnut is a job for optimists.
Killer fungus killer
While some scientists have staked their efforts on breeding blight resistance into the giant trees, others are contemplating a biological attack. The largest test of the biocontrol strategy is taking place in the grove owned by Bockenhauer and his neighbors.
Scientists first discovered signs of an interesting enemy of chestnut blight in Italy during the 1950s, says William McDonald of West Virginia University in Morgantown, one of the U.S. leaders in biological blight control. The European species of chestnut catches the disease, too, and early researchers noticed some Italian trees that seemed to have spontaneously recovered their health. In general, European chestnut trees haven’t suffered as devastating an outbreak as their American cousins.
At first, observers wondered whether the Italian trees had acquired resistance to the blight. It turned out, though, that the fungus itself had caught a disease-causing virus.
Since then, MacDonald and other pioneers have been looking for particularly useful strains of the virus and investigating how to deploy them. The basic plan depends on dosing trees with sick, so-called hypovirulent fungus in expectation that its strands will fuse with those of wild blight, something that fungi often do when they encounter their own species. Once the strands unite, the wild blight fungus contracts the disease and its killing power wanes.
The idea may be elegant, but it hasn’t been easy to implement, according to MacDonald. In one of his early experiments, “the particular virus that we chose made the fungus so sick it didn’t reproduce so well.” A wimpier virus turned out to make a better control agent because it left infected fungus with enough vigor to spread.
MacDonald’s system got its big test after a plant pathologist, Jane Cummings Carlson of the Wisconsin Department of Natural Resources, officially diagnosed chestnut blight at the Bockenhauer grove in 1987. She says that she’s not sure how the disease reached the remote patch. The spores might have hitchhiked in on birds or even on some of the many people who visit the grove each year.
At first, Cummings Carlson tried stamping out the infection by taking down the sick trees, but the blight flared up anew each year. Starting in 1992, she, MacDonald, and other concerned workers organized volunteers to test the virus-infected fungus as a biological control. They located chestnut trees with ominous breaks in the bark revealing blobs of orange fungus. As the disease progresses, the fungus clogs a tree’s water-conducting tissues and kills the branches and trunk above the infection.
Punching holes around each canker, Cummings Carlson’s team inoculated the tree with a slurry of hypovirulent fungus. The volunteers treated each sick tree they could find. Cankers often were at inconvenient heights, so a team of climbers who had won championships in Wisconsin’s tree-work competitions donated their services for the high jobs.
The first step of the scheme seemed to work. Fungus that received dollops of hypovirulent fungi would pick up the virus. “We were getting a reasonable level of biocontrol on treated trees,” says MacDonald. However, cankers of uninfected, vigorous fungus burst out on new trees each year.
After 1997, the researchers decided to go for the decisive test of their system. They stopped treating any new cankers. “If it’s going to work, this virus has got to spread on its own,” says MacDonald.
Alas, the biocontrol virus doesn’t seem to be spreading as widely as the healthy blight fungus, MacDonald and Cummings Carlson reported last year at the annual meeting of the American Phytopathological Society in Milwaukee. “The verdict is still out,” MacDonald cautioned at the time, speculating on scenarios that could improve the outcome. Still, he says, “I think we’re going to lose a lot of trees.”
This spring, the researchers will start treating trees again.
“The biology is fascinating, which is why I’ve stuck with it for years,” says another collaborator, Michael Milgroom of Cornell University. He was ruminating about population diversity in fungi during the 1980s when he started studying the blight organism. Like many other fungi, this species displays what biologists call vegetative incompatibility, an apparent mismatch of certain strains of the fungus that for some reason refuse to fuse when they meet. This has implications for biocontrol because when the killer strains of the fungus and its virus-carrying relatives don’t fuse, the desired virus doesn’t spread well.
Milgroom and his colleagues have so far described six genes in the blight fungus for which a clash of two possible forms nixes union. So, the blight fungus can splinter into a least 64 incompatible types, and Milgroom strongly suspects that there are even more.
Other scientists have noted, and Milgroom agrees, that North America bristles with a lot more diversity in blight-incompatibility types than Europe does, creating a tougher challenge for viral biocontrols.
Recent research from his lab fuels speculations about the forces underlying incompatibility. Strands of incompatible fungal types actually do fuse briefly, but then a preset program of cell death breaks the connection. If the program ends that connection slowly, more viruses can creep over the bridge to the previously uninfected organism, he and his colleagues said in the Nov. 7, 2002 Proceedings of the Royal Society of London B. This difference might mean that the virus has evolved to slow the programmed cell death and enhance its own spread.
Mix and match
Other scientists see value in a combination of breeding and biocontrol. Sandra Anagnostakis at the Connecticut Agricultural Experiment Station in New Haven says that inoculating trees with the strains doesn’t cure them of chestnut blight or save their value as timber. However, “it keeps trees alive, preserving valuable germ plasm,” says Anagnostakis.
For example, 17 years ago, she and her colleagues planted 75 small trees raised from nuts collected in the blight zone. Within 2 years, blight struck, and during the next 4 years, the researchers treated every canker they could find with a mix of hypovirulent fungus strains. Many of the trees died back to stumps, which continue to send up sprouts. Still, about a third of the trees have their original trunks, even though some have cankers from ground level to about 30 feet.
“I am amused that the feeling folks got from the [American Phytopathological Society] meeting was that hypovirulence ‘wasn’t working,'” she says. “I think it is working very well. The problem is people’s expectations.”
Because her treated trees flower abundantly each year, she has high hopes. “If we can keep populations alive and flowering, we can plant our resistant trees in their midst,” she says. Over the generations, those resistance genes can migrate into the old chestnut lineages.
Even if those genes originate from the disease-resistant Chinese species, the ultimate chestnuts could end up an only slightly altered version of the American classic.
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