Return of the Potato Blight


Irish infestationGlobal blightA resistant spud?The poor farmers' stake

Potato photos, this page: Courtesy John Helgeson, Department of Plant Pathology, University of Wisconsin-Madison.

The individual cells made from protoplast fusion are starting to develop into tiny potato plants. These plants will be tested for resistance to late blight.













Round cells contain a smattering of round, green bodies.
These plant cells have lost their rigid walls and are about to fuse. Protoplast fusion allows the mixing of genes between plants that don't naturally cross. Those bitty greenies are chloroplasts, the tiny organs where sunlight powers the decomposition of carbon dioxide.

Tiny plants show roots, stems and leaves (in a tube)Chemicals may slow late blight, but wouldn't it be nice to find a spud that just ignored -- resisted -- p. infestans? While some potato varieties are less susceptible to late blight than others, nothing on the market -- so far -- is immune. After years of breeding, fungicides are still needed to get a good crop in damp seasons, even for varieties with limited resistance to late blight.

Resistance, conferred by the plant's genes, involves dimly understood defense mechanisms that still play a critical part in our ability to feed ourselves. Over the millennia since agriculture was invented, selection came mainly by default: Farmers and breeders raised the plants that survived any diseases or insects that were present. In fact, agriculture arose from simple evolution, artificially controlled.

Plants may look passive, but they have some tricks up their stalks. What can happen when a disease reaches a plant?

The affected cell may die and prevent the disease from spreading. This so-called "hypersensitive response" occurs in some fungus-resistant plants, says John Helgeson, a professor of plant pathology at University of Wisconsin-Madison. If a fungal spore lands on a leaf, he explains, the cell dies, trapping the fungus.

The plant may make chemicals that toughens its tissue, making it impervious or less appetizing to the disease.

The plant may make gooey chemicals -- like pine pitch -- and direct it to the injury site.

The plant may make chemicals that inactivate or digest key chemicals from the pathogen.

Indeed, the plant may take several protective measures simultaneously after receiving the initial alarm of attack.

None of this jibes with our image of plants as passive victims of whatever nature throws at them, but it's critical to the problem of survival -- for plants and all the animals that eat them.

Healthy breeding
These days, disease resistance is a key concern of crop breeders. To overcome the rusts, blasts, wilts, blights and spots caused by Oomycetes, viruses, fungi, bacteria, protozoans and other pathogens, breeders evaluate many crop strains. The desired resistance often appears in an unpromising variety grown in a global backwater -- often where the disease is worst. These plants, after all, evolved along with the pathogen.

The task then becomes moving that trait into a strain with other desired traits -- say heavy yield, strong stalk and resistance to other diseases. The process takes years at best, but it's a key reason why agriculture can feed a booming population.

Needed: Sturdy genes
The whole system wilts, however, if good resistance does not appear in a variety of the crop. The next step is to scan the crop's wild relatives (this is a key economic reason for conserving wild areas and the relatives that live there). Grasses related to wheat and corn, for example, have supplied defensive genes against deadly viruses.

But related species don't always cross. And that was the problem facing Helgeson in 1994, when late blight struck a field of spuds he was testing for resistance to another disease. By the middle of August, he says, the field "was essentially dead stubble, with the exception of a few plants carrying genes from a wild potato relative from Mexico."

A healthy, happy potato flourishes, with pale purple flowers on top.This plant couldn't care less about late blight -- it's equipped with a resistance gene derived from a wild relative of potato.

By no coincidence, the wild relative (Solanum bulbocastanum) came from an area west of Mexico City, in the shadow of the Volcano Toluca, that's considered the home of late blight -- Phytophthora infestans. "There are a tremendous variety of fungal isolates there," says Helgeson.

Because the two plants would not cross-breed, Helgeson turned to protoplast fusion. Here's how this "shotgun wedding" between related plants is done:

With chemicals, you strip away the hard wall found around all plant cells, leaving squishy, rounded cells called protoplasts.

More chemicals weaken the remaining cell membrane, allowing the two cells to fuse. You're left with one cell with a double copy of all the organelles inside.

Eventually, the nuclei also fuse, the cells begin dividing, and form a gob of undifferentiated cells called a callus.

Using tissue culture, you grow some of these cells into full-size plants.

You use standard plant-breeding techniques to grow marketable potatoes that are also fungus-resistant. Essentially, you "back-cross" the resistant plants with good varieties and select only the plants that still resist blight.

Eventually, after five to 20 or more plant generations, you may move the resistance gene -- without genetic engineering -- from the wild relative into a resistant crop. And that is exactly what Helgeson has done, as you can see from the photo above. The gene in question, he says, "Slows down the infection on the plant. It just doesn't allow the fungus to grow very fast, so it does not take over the plant and reduce it to nothing."

A better way?
Plants may look passive, but they have some tricks up their stalks.But Rebecca Nelson, head of the late blight program at the International Potato Center in Peru, warns that "strong resistance" may not be the best way to combat late blight. In "lots of cases of strong, complete resistance, the breeding record says this does not last long. You can have beautiful plants one year and complete destruction the next." The single gene "is an easy target" that can be outfoxed by the fungi's ability to adapt, evolve and survive.

A better approach, she suggests, might involve "quantitative resistance," which depends on many genes rather than one. "If you have quantitative resistance, in many genes, each changes expression with changes in the environment." The advantage, she says, is that this type of resistance "can erode gradually, not go kaboom" like strong resistance from a single gene.

For his part, Helgeson says the new variety has survived fierce field tests. "We were very concerned, that was the reason to test them in Mexico," he says, where many strains of late blight are active. "Our idea initially was that what's resistant here in Wisconsin might not be resistant in a year or two. However, since the plant eventually becomes infected, these genes may not be as readily overcome as the 'strong ones' mentioned by Nelson," he says.

The potatoes, he says, have grown in Toluca, where the fungus is so virulent that farmers spray susceptible potatoes with fungicides 25 times a season. "The pressure is very intense," says Helgeson. "Day after day you get reinoculation [reinfection]. So far, it's looking very good."

Helgeson's variety hasn't reached the market, and may never help poor, third-world farmers. Can they fight blight?




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