Tough Potatoes

What's the potato equivalent of a sneeze?

For Steve Pechous, a graduate student in plant physiology, it's not a nonsense question. "One of the main things I've learned," he says, "is that at the molecular level, plants and animals are much more similar than they are different. The way they respond to disease looks different, but actually both respond hypersensitively. Animals cough or sneeze. Plants produce defensive chemicals."

potato chops
Gerald Lang and Jennifer Tucker, Penn State Digital Photography Studio

Cheap chips? Not if the potato late blight fungus attacks. To help fight this pest (cause of the 1840s Irish potato famine), Steve Pechous is studying the plant equivalent of an immune response.

In animals, it's called a hypersensitive response when certain cells recognize a pathogen and intensify the signal, triggering an immune response. "It happens in plants too," says Pechous, "but the way it happens is almost completely unknown."

With plant pathologist Eva Pell and veterinary scientist Channa Reddy, Pechous is studying how potatoes fend off the late blight fungus, cause of the Irish Potato Famine in the 1840s. According to the International Potato Center (CIP) in Peru, "This fungus, Phytophthora infestans, remains among the world's most devastating crop diseases. It can destroy a crop in a few days."

It releases spores by the millions. These spores travel miles on the wind to hide in the soil. "When they come into contact with a potato tuber," Pechous explains, "they grow what's known as hyphae—like little tendrils—into the tuber. If the potato is very susceptible, these hyphae will grow throughout the potato, destroying it, basically extracting its nutrients." After the potato is harvested and put into cold storage, the fungus continues to grow. In the spring, when the farmers cut their seed potatoes into pieces to plant a new crop, they perpetuate the fungal lifecycle. From each potato "eye" a new plant will form, one green shoot that will release millions of fungal spores to reinfect the field.

Under a heavy fungal load, a potato tuber turns to black, gooey mush. "In a bad year, farmers might not even bother to harvest—or they might leave cull piles on the sides of their fields. That's a primary place where the fungus lives and thrives," Pechous says. "In the spring, the culls sprout and the farmers may go out to remove them—but then it may already be too late. The spores may be wind borne."

And new, more dangerous strains are arising all the time. Until recently, for example, the fungus was only known to reproduce asexually, "which means that one strain can only give rise to the exact same strain, like a clone," Pechous explains. "Then, a decade ago, a new genotype was found in Mexico, one that could reproduce sexually. That means you can get genetic recombination. You can get a lot more different strains in one season than you ever could before. A few of these will out-compete the rest. They could be very strong, very resistant to fungicides, and potentially very virulent."

If unchecked, such a fungus could spell the end of the cheap potato chip.

So far, resistant potato cultivars and fungicides have been enough. "But even if you have a very resistant tuber, you can get some hyphal growth," Pechous notes, and the fungus can continue to reproduce and evolve. "People are screening potato varieties like crazy," he adds, "but there are tradeoffs. Some varieties may not grow as well, or the chip quality is poor."

Rather than selecting specifically for resistance to P. infestans, a better strategy might be to select potato varieties that have a strong general resistance to disease—a good immune system, as it were. One component of that system is the hypersensitive response. "With the hypersensitive response, the potato cell dies as soon as a fungal hyphae touches it," says Pechous. "The fungus only kills one layer of cells—out of a million layers. But the fungus cannot grow through those dead cells."

What turns on this response?

The fungus secretes a chemical called arachidonic acid. "It's an integral component of the fungal membranes," Pechous explains, "but nobody knows why the fungus is releasing so much of it." Potatoes don't naturally contain arachidonic acid, but when it's present, a potato enzyme called lipoxygenase seems to latch onto it. "The potato enzyme takes the arachidonic acid and from it forms an oxygenated fatty acid. After that, we have no idea what happens. Nobody's done the research yet."

What he and his advisers suspect, however, is that the arachidonic acid is transformed into a signaling molecule—a molecule that, when present in the potato, turns on its disease resistance genes.

"We're looking for the basic mechanism behind how lipoxygenase turns this fatty acid from the fungus into a signaling molecule, which in turn regulates the defense response. You might want to screen varieties for lipoxygenase, for example: the generation of more fatty acid signals might mean that genes involved in general disease resistance are turned on faster."

In animals, lipoxygenase activity produces leukotrienes, fatty-acid derivatives which lead to bronchial constriction and inflammation.

"It's entirely possible that potatoes with too much of these fatty-acid derivatives could have the plant equivalent of aches and pains," Pechous laughs. "The pathways are so similar. Those are the sorts of things we want to find out."

Steve Pechous is a doctoral student in the Intercollege Graduate Degree Program in Plant Physiology, 218 Fenske Lab, University Park, PA 16802; 814-863-4234; swp108@psu.edu. His work is supported by a National Science Foundation Research Training Grant. His advisers are Eva J. Pell, Ph.D., Steimer Professor of Agricultural Sciences, 321 Buckhout Lab; 865-0323; ejp@psu.edu; and C. Channa Reddy, Ph.D., distinguished professor of veterinary sciences in the College of Agricultural Sciences, 226B Fenske Lab; 863-1625; ccr1@psu.edu.

Last Updated January 01, 2000