The American chestnut (Castanea dentata) and related Allegheny and Ozark chinquapins (Castanea pumila & Castanea ozarkensis) were once important components of upland forests in eastern North America.
Chestnut blight (causal agent Cryphonectria parasitica) was first reported in 1904, when cankers were observed on trees in the New York Zoological Garden in the Bronx. Over the next decades, the blight killed more than three billion American chestnuts throughout the species’ natural range. By the 1950s, virtually all chestnut and chinquapins had been reduced to short-lived stump sprouts and disease-ridden shrubs (Burnham et al. 1986).
American chestnut’s range extended from Maine to Mississippi, including nearly every state east of the Mississippi River, plus southern Ontario. Billions of trees occupied this areas constituting about 200 million acres. American chestnut was adapted to a broad range of environmental and climatic conditions, although it preferred well-drained, sandy, and slightly acidic soil, often on slopes and ridges. It grew at every elevation from sea level to higher than 5000 feet. In many areas, especially on Appalachian slopes, chestnut was dominant. In other places it grew in association with oak, hickory, basswood, tulip poplar, and beech, with an ericacious shrub understory. While established seedlings and stump sprouts can persist for years in low light conditions, when released by light penetrating the canopy the sapling can grow more quickly than other species. Consequently, its abundance was probably increased by human clearing and burning.
American chestnut provided a consistent nut crop that was consumed by numerous mammals, birds, and insects. As a large tree growing to heights of 70 to 100 feet, and diameters up to 5 feet, with hollow centers (USDA 2022), American chestnut provided habitat for numerous birds, mammals, and herps that depend on cavities for nesting or sheltering sites. Chestnut wood is very slow to rot. The leaf litter influenced both terrestrial and aquatic ecosystem structure and function in areas where it was a dominant tree.
Humans used the chestnut by harvesting the nuts for themselves and as fodder for their livestock; they used the wood for construction lumber, shingles, fence posts and rails, telephone and telegraph poles, paneling, trim, furniture, coffins, interior decoration and firewood (USDA EIS 2022). Chestnut bark was a primary source of tannin for the leather industry.
In the late 19th century prior to the introduction of chestnut blight, the range of American chestnut was already contracting in the south, apparently as a result of Phytophthora root rot/ink disease (caused by Phytophthora cinnamomi). This pathogen was introduced to the southern United States probably before 1824. Additionally, the Asiatic oak weevil and chestnut gall wasp negatively affect surviving American chestnuts.
Also at the turn of the prior century, American chestnut was increasingly found to the north and northwest of its historical range, e.g., lower peninsula of Michigan, southwest Wisconsin, Illinois, Iowa, probably hastened by deliberate planting. The original historical range overlapped with the ranges of Ozark and Allegheny chinquapins; these are shrubs and subcanopy trees that produce one nut per bur. Ozark chinquapin was a prominent overstory tree in parts of its relatively small range in the Ozark plateau, where it provided ecosystem services similar to those of the American chestnut farther east.
Early attempts to control spread of Cryphonectria parasitica included quarantine and destruction of diseased trees. These efforts were ineffective because the fungus produces prolific spores that are spread by animals and the wind. Also, Cryphonectria parasitica persists and reproduces on dead or living American chestnuts, chinquapins, and on numerous other tree species, including multiple oak species, maple, hickory, American beech, and tulip poplar. As a result, the fungus (and resulting chestnut blight) remains prevalent in North America.
No wild-type American chestnut tree has been documented to contain full blight resistance, although anecdotally, there appears to be a range of susceptibility (i.e. differences in damage to stems and survival times). Over the past century there has been considerable research on various strategies, e.g., chemical controls, biocontrol (hypovirulence), and radiation treatment of seeds. None has proved effective in controlling blight on a landscape scale in North America.
Breeding for resistance – through crossing American and Asian species – began in the 1920s under the auspices of the U.S. Department of Agriculture’s Office of Forest Pathology. This program was abandoned in 1960. At the same time, Arthur Graves began efforts to develop hypovirulence, a biocontrol method that uses a fungal virus to help attenuate the pathogen, which was later continued by the Connecticut Agricultural Experiment Station. Again, none of these early programs succeeded in producing a fast growing, timber-type (tall and straight) tree with good blight resistance; every candidate fell short in at least one respect.
The American Chestnut Foundation (TACF) began a systematic program of backcrossing hybrid American – Chinese trees with pure American chestnut trees, selecting for blight resistance and American phenotype at each step. This program has resulted in trees with resistance to blight at levels intermediate between susceptible American and resistant Chinese chestnut. However, this approach now appears unlikely to produce a highly blight-resistant chestnut with a genome that is predominantly American. TACF now plans to incorporate the use of transgenic techniques to enhance resistance to the blight fungus (Gustafson et al. 2022).
None of the previous breeding and modification efforts, including TACF back-cross breeding, has succeeded in producing American chestnuts sufficiently able to tolerate chestnut blight to be restored to the eastern forest ecosystem. In 1997, the State University of New York (SUNY) College of Environmental Science and Forestry (ESF) established the American Chestnut Research and Restoration Project. a non-profit initiative with the support and close collaboration of TACF. The project has applied biotechnology to insert a gene conveying tolerance of the blight pathogen into the chestnut’s genome. The Project’s goal is to facilitate introgression of the blight tolerance trait into surviving American chestnut population and so ultimately to produce a viable and diverse population to restore the tree as a functioning part of the ecosystem. Because offspring of the transgenic “Darling 58” trees will include both transgenic and non-transgenic individuals, the original wild-type American chestnut will be conserved far into the future.
The project is attempting to restore ecological relationships missing from eastern North America for more than 100 years.
The ESF projected inserted a gene taken from wheat into the “Darling 58” chestnut. The added gene promotes the tree to produce an enzyme called oxalate oxidase (OxO). This enzyme doesn’t kill the blight fungus. Instead, it detoxifies the oxalic acid (oxalate) produced by the fungus. It is this acid that kills the tree’s tissues. In the presence of OxO, the damage caused by the oxalate is significantly restricted, resulting in superficial cankers with which the tree can coexist with the fungus. For details on how the gene was inserted and the chemical processes involved, see the SUNY ESF petition or APHIS PRA or DEIS – sources cited at end of profile.
Ozark Chinquapin Foundation (ozarkchinquapinmembership.org) is currently using traditional breeding and selection processes in an effort to develop blight-resistant chinquapins. The Foundation has informed SUNY that they support the concept of exploring development of transgenic Ozark chinquapin- but the development of a blight resistant Ozark chinquapin using OxO would be many years away.
In 2020, ESF petitioned the USDA Animal and Plant Health Inspection Service (APHIS) to determine that the “Darling 58” American chestnut tree differs in no other substantive ways from wild chestnuts and traditionally bred hybrids and therefore should be exempted from further regulation.
Two other agencies also must evaluate the potential risks and approve de-regulation of transgenic chestnuts: the Food and Drug Administration (FDA) has jurisdiction over the safety of chestnuts as food for both people and livestock; and the Environmental Protection Agency (EPA) has jurisdiction over whether the OxO gene is a pesticide.
ESF also expects to seek approval of the Canadian Food Inspection Agency (CFIA) so that transgenic trees might be planted in Canada. Gustafson et al. 2022 suggest that planting in Canada will probably be necessary to minimize exposure to the Phytophthora root disease.
These regulatory requirements mean that it will be at best several years before transgenic American chestnuts will be available for planting as part of a restoration effort.
SOURCES
Gustafson, E.J., B.R. Miranda, T.J. Dreaden, C.C. Pinchot, D.F. Jacobs. 2022. Beyond blight: Phytophthora root rot under climate change limits populations of reintroduced American chestnut Ecosphere. 2022;13:e3917.
Powell, W.A., A. Newhouse, V. Coffey, L. McGuigan, A. Oakes, K. Breda, D. Mathews, J. Drake, J. Dougherty, J. French, M. Braverman, C. Maynard. Petition under 7 CFR 340.6 to request that the Administrator make a determination that the article should not be regulated under 7 CFR 340.6. Petition 19-309-01p
United States Department of Agriculture. 2022. State University of New York College of Environmental Science and Forestry Petition (19-309-01p) for Determination of Nonregulated Status for Blight-Tolerant Darling 58 c’nut (Castanea dentata) Draft Environmental Impact Statement July 2022
United States Department of Agriculture. 2022. State University of New York College of Environmental Sciences and Forestry for Determination of Nonregulated Status for Blight-Tolerant Darling 58 American Chestnut Draft Plant Pest Risk Assessment. June 2022