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Sandra L. Anagnostakis, The Connecticut Agricultural Experiment Station, Box 1106, New Haven, CT 06504, phone 203-974-8498, fax 203-974-8502



Connecticut's Early Forests

Connecticut was heavily forested in 1600, but by the early 1800's forest covered only about 20% of the state. Now trees have grown up on land no longer farmed, and we are back to about 60% tree cover. In 1910 when chestnut blight started killing our trees, half of the standing timber was chestnut. Chestnut was the only wood used for telephone poles, and most of the railroad ties were chestnut. The trees were tall and straight, and after clear-cutting they easily out-competed the other hardwoods to dominate the forests, making pure stands. Castanea dentata is native from southern Maine to northern Georgia, all along the Appalachian mountain range. Ink Disease, caused by Phytophthora cinnamomi, killed trees in the southern coastal part of the range in the early 1800's, and can still be a problem in places with clay soil (5). The chestnut blight fungus (now called Cryphonectria parasitica (Murr.) Barr) came into the U.S. on Japanese chestnuts, first imported in 1876, and was spread around by mail order (Japanese trees were available from many catalogs) and by everything walking across the cankers (5). This disease reduced the American chestnuts to understory shrubs, which die, sprout from the base, die and sprout again.

Experiment Station History

The Connecticut Agricultural Experiment Station was founded in 1875. Offices and laboratories are in the city of New Haven on the former estate of Eli Whitney, the inventor. We have a 50 acre field station in the central Connecticut valley and a 75 acre farm in Hamden where annual and perennial plantings can be made for experimentation. Our first plant pathologist, George Clinton, studied the progress of chestnut blight, through our native chestnuts. The pathogen was described, and the species named (Endothia parasitica, Anderson and Anderson), by another of our scientists, Paul J. Anderson.

Chestnut breeding work was begun early in the U.S., but the only program that has continued without interruption is that at The Connecticut Agricultural Experiment Station. In 1930, Arthur Graves made his first crosses of American and Japanese chestnut, and began a long collaboration with geneticist Donald Jones. Graves gave us about 9 acres of his land in Hamden, CT with plantings of species and hybrids, to insure the continuation of Connecticut's chestnut breeding program. Graves's students Hans Nienstaedt and Richard Jaynes made many of the hybrids that we still use today.

My early work at The Experiment Station included studying the basic genetics of the blight fungus, and the system of vegetative compatibility that restricts transfer of cytoplasmic elements from one strain to another, and tests of extracellular enzymes produced by this fungus (1, 2, 10, 14).

Chestnut Breeding in Connecticut

Our breeding plan was first based simply on making hybrids of resistant Asian trees with susceptible American trees and testing the hybrids for resistance to chestnut blight (4). When it became clear that at least two genes were responsible for this resistance, we began a back-cross breeding system based on the plan of Charles Burnham (7). Resistant Asian trees are crossed with susceptible American trees, and the partially resistant hybrids are crossed to American trees again. one out of four of the progeny from these crosses have one copy of both resistance genes (giving them partial resistance), and these are crossed again to American. This repeated back-crossing increases the percentage of American genes in the hybrids, and selecting for partial resistance insures passage of the resistance genes. A final cross of two trees with partial resistance should result in one of sixteen trees having two copies of both resistance genes, which will make them fully resistant to the chestnut blight fungus (7). We bag female flowers in June, and use selected pollen on the flowers in July. Many hybrids are male sterile; the catkins form but the flowers never bloom. This is only seen in interspecific hybrid trees, but is a feature valued by nut growers who want to plant orchards of male sterile trees with a few pollinator trees for bigger yields of nuts.

We have what is probably the finest collection of species and hybrids of chestnut in the world for use in this breeding program, with all seven species represented. The breeding work has been greatly helped by a genetic map prepared by Thomas Kubisiak (12). He has RAPD markers for the chromosomal regions ("genes") associated with resistance to chestnut blight, which will make selection much easier. Trees of two kinds are being chosen: for timber and for nut production, both with resistance to chestnut blight.

Biological Control of Chestnut Blight

In the late 1950’s, a recovery phenomenon was discovered and studied by Jean Grente in France. He called the system "hypovirulence", because the blight fungus that he isolated had less than normal ability to kill chestnut trees, and the "sickness" could spread. We found that this is due to a viral parasite of the blight fungus (9, 5). The genes of three kinds of these (dsRNA) viruses have now been sequenced, and the viruses placed in the genus Hypovirus by Bradley Hillman and his collaborators (11). In Connecticut, hypovirulence can keep trees alive in the forest and orchards, and we have studied the many kinds of creatures that move both killing and curing strains of the fungus from tree to tree (3, 5). There has not been a general recovery of forest chestnuts, as seen in Italy, and our new efforts to improve hypovirulence for biological control of chestnut blight include use of genetically engineered strains with the genes of the Hypovirus added to the genome of the fungus. This was done by Donald Nuss at the University of Maryland, using Connecticut strains (8). We obtained permission from USDA/Plant Quarantine to test these strains in the forest in 1994. We first made a single release, using plug inoculations and by painting conidia onto the surface of cankers, and we can now say that transgenic strains survive, make sexual spores, transfer virus to new cankers, and initiate cankers (6). new vegetative compatibility groups are formed by strain recombination as the sexual spores develop after mating, and these may carry the genes for Hypovirus. the virus gene packet segregates as a single gene on the fungal chromosome.

Now we are trying a population replacement experiment with transgenic strains. We have a clear-cut in a State Forest with abundant chestnut where we are spraying chestnut sprouts at least twice a year with conidia from three transgenic strains, and spraying chestnuts in the control plot with water. We will continue to cut competing trees to allow the chestnuts to have the best chance to grow, and continue treating until we see that we have effected a stable biological control. Then we can monitor the spread of these strains through the forest in all directions, to see whether we can make American chestnuts useful as timber trees again.

At the very least, we will be able to maintain American trees as fruiting populations. Then if we plant our new resistant hybrids out into these plots, they will cross with native trees, incorporating the enormous genetic diversity that still exists in the forest. The first generation offspring will be intermediate in resistance, but in subsequent generations trees with full resistance will be produced. These will be well adapted to all the regions of the country where such plantings have been made, and should compete well with the additional help of biological control by hypovirulence.

The Next Problem

Of course, no project is ever quite "finished." The oriental Chestnut Gall Wasp, Dryocosmus kuriphilus, was introduced into the U.S. in 1974 by a grower who evaded plant quarantine (13). The insect lays its eggs in leaf and flower buds, resulting in defoliated trees with no flowers. Entomologist Jerry Payne chronicled the devastation of orchards of Chinese chestnut trees planted in the state of Georgia. We have reports of infestations throughout Alabama, North Carolina, and into Tennessee. Unfortunately, the insect has now reached the part of Tennessee where most of the mail-order companies get their chestnut trees for retail sale. I expect that gall wasp will be inadvertently shipped all over the United States, just as chestnut blight was. Our breeding work must now include selection for resistance to gall wasp. Jerry Payne has observed that American and Chinese chinquapins, Castanea pumila and C. henryi, resist infestation, and some cultivars of C. crenata are resistant. Once again our collection of species and hybrids is being used to make new progeny for testing in Georgia and North Carolina where the insect is now endemic. We hope to understand how resistance is inherited, and will incorporate this resistance into our trees as quickly as possible.

Since we now live in a world where travel and transport of pests and pathogens is all too easy, global communication and cooperation is our hope for the future.


  1. Anagnostakis, S. L. 1977. Vegetative incompatibility in Endothia parasitica. Experimental Mycology 1:306-316.
  2. Anagnostakis, S. L. 1988. Cryphonectria parasitica, cause of chestnut blight. p123-136 IN: Advances in Plant Pathology, vol. 6, Genetics of Plant Pathogenic Fungi, G. S. Sidhu, D. S. Ingram, and P. H. Williams, eds., Academic Press, New York
  3. Anagnostakis, S. L. 1990. Improved chestnut tree condition maintained in two Connecticut plots after treatments with hypovirulent strains of the chestnut blight fungus. Forest Science 36. 113-124.
  4. Anagnostakis, S. L. 1992. Measuring resistance of chestnut trees to chestnut blight. Canadian Journal of Forest Research 22:568-571.
  5. Anagnostakis, S. L. 1995. The Pathogens and Pests of Chestnuts. p125-145 IN: Advances in Botanical Research, vol. 21, J. H. Andrews and I Tommerup, eds., Academic Press, New York.
  6. Anagnostakis, S. L., Chen, B., Geletka, L. M., and Nuss, D. L. 1998. Hypovirus transmission to ascospore progeny by field-released transgenic hypovirulent strains of Cryphonectria parasitica. Phytopathology 88:598-604.
  7. Burnham, C. R. 1988. The restoration of the American chestnut. American Scientist 76:478-487.
  8. Choi, G. H. and Nuss, D. L. 1992. Hypovirulence of chestnut blight fungus conferred by an infectious viral cDNA. Science 257:800-803.
  9. Grente, J. 1965. Les formes Hypovirulentes d'Endothia parasitica et les espoirs de lutte contre le chancre du châtaignier. Académie d’Agriculture de France, Extrait du Proces-verbal de la Séance. 51:1033-1037.
  10. Hankin, L. and Anagnostakis, S. L. 1975. The use of solid media for detection of enzyme production by fungi. Mycologia 67:597-607.
  11. Hillman, B. I., Fulbright, D. W., Nuss, D. L., Van Alfen, N. K. 1994. Hypoviridae. In. "Virus Taxonomy: Sixth Report of the International Committeefor the Taxonomy of Viruses" (F. A. Murphy, C. M. Fauquet, D. H. L. Bishop, S. A. Ghabrial, A. W. Jarvis, G. P. Martelli, M. P. Mayo, and M. D. Summers, eds.). Springer-Verlag, Wein, New York, 580 pp.
  12. Kubisiak, T. L., F. V. Hebard, C. D. Nelson, J. Zhang, R. Bernatzky, H. Huang, S. L. Anagnostakis, and R. L. Doudrick. 1997. Mapping resistance to blight in an interspecific cross in the genus Castanea using morphological, isozyme, RFLP, and RAPD markers. Phytopathology 87:751-759.
  13. Payne, J. A., Green, R. A., and Lester, D. D. 1976. New nut pest: an oriental chestnut gall wasp in North America. Annual Report of the Northern Nut Growers Association 67:83-86.
  14. Puhalla, J. E. and Anagnostakis, S. L. 1971. Genetics and nutritional requirements of Endothia parasitica. Phytopathology 61:169-173.