In the 1930s, C. parasitica showed up in Europe. It looked as if European chestnut trees would also be killed off, but in the 1950s researchers started finding chestnut trees that seemed to be recovering from the blight. The fungus isolated from these trees had a unique white color, which was in stark contrast to the bright orange isolates, or samples, recovered from nonhealing trees. Eventually plant pathologists discovered that the blight itself was infected with a unique virus that altered the pigment produced by the fungus and reduced virulence to the host tree, an effect which they called “hypovirulence.”

Numerous “hypoviruses” that infect the blight fungus have been discovered since, and several strains have been used to control chestnut blight fungus in Europe. Managers inoculate chestnut blight cankers with the virus and let it spread through the fungus. Unfortunately, though it once held great promise, using hypoviruses to weaken the effects of blight has not panned out for American chestnuts in forest settings, where the fungus continues to kill new chestnut sprouts unabated.

Kubisiak, geneticist with the SRS Southern Institute of Forest Genetics, and Michael Milgroom at Cornell University are studying the genome of C. parasitica to learn more about the mechanisms that affect the spread of hypoviruses. They’re looking for clues in the system fungi evolved for self-recognition called “vegetative compatibility,” which allows fungi to fuse together to share resources—and to spread hypoviruses.

One clue to the continued virulence of chestnut blight fungus in America may lie in the genetic diversity of American strains. In Europe, one strain of chestnut blight fungus usually dominates in a given area, freely passing along the hypovirus from canker to canker, tree to tree. In American forests, the presence of genetically different but sexually compatible chestnut blight strains ensures that genetic variation in the fungus is high, reducing the chances that any two isolates will be vegetatively compatible—which means they won’t merge and share the virus.

“We wanted to find markers in the blight genome linked to vegetative compatibility so we could clone these genes and begin to study the dynamics of this system in natural populations,” says Kubisiak. “So far, we know of at least seven genes involved in the process, and there is evidence that more are likely to exist, so it won’t be a matter of just changing one gene to turn on or off compatibility. The fungus is quite sexual and keeps producing even more variability that can, in turn, increase incompatibility among strains, making it very difficult to make one alteration that would allow the virus to spread.”

Though the promise of hypovirulence as a biocontrol for chestnut blight in America has waned, Kubisiak is still excited about studying the genes that govern compatibility in chestnut blight. “The ultimate goal is to understand these genes from a fundamental viewpoint—what they do, what their evolutionary purpose is,” says Kubisiak. “Why are they there, and what is the underlying biochemical mechanism? Maybe, at some point, we’ll discover key regulators that could be used as on-off switches to override the entire compatibility system and hence break the barrier that is hampering the spread of the hypoviruses.”—ZH

For more information:
Tom Kubisiak at 228–832–2747, x213 or tkubisiak@fs.fed.us

Recommended reading:
Kubisiak, T.L.; Dutech, C.; Milgroom, M.G. 2006. Fifty-three polymorphic microsatellite loci in the chestnut blight fungus, Cryphonectria parasitica. Molecular Ecology Notes. 7: 428–432.

Kubisiak, T.L.; Milgroom, M.G. 2006. Markers linked to vegetative incompatibility (vic) loci and a region of reduced recombination near the mating type locus (MAT) in Cryphonectria parasitica. Fungal Genetics and Biology. 43: 453–463.