Strides Made in Defense of Farm Crops : Science: Discovery by Salk Institute researchers could lead to designer crops that can ward off invasion by fungus and bacteria.

A research team at San Diego’s Salk Institute has brought science one step closer to understanding when and how plants respond to invading microbes--work that could lead to designer crops that protect themselves from fungal and bacterial onslaughts and require less pesticide.

Results of the work appeared today in the scientific journal Cell.

Bean plants in Dr. Christopher Lamb’s lab responded to a piece of harmful fungus by erecting little walls of linked proteins to protect their cells from invasion. The hardening of the cell walls is completed in less than 30 minutes, the fastest plant defense scientists have ever witnessed, Lamb said.

“We’ve discovered a very rapid response to the plant’s perception of attack,” Lamb said.

When the plant senses trouble it emits a burst of hydrogen peroxide, which in turn causes two proteins to link together, reinforcing the cells’ protective wall, the research found.

“These cross-linked molecules act as a barrier, much as a self-sealing tire seals itself after a puncture,” said Joseph Varner, a scientist at Washington University in St. Louis, Mo., who is familiar with the work.

Although scientists have long observed the way plants react after they’ve been attacked, the early moments, when the plant first puts its defense strategy into motion, have remained a mystery, said Roger Beachy, a plant biologist at Scripps Research Institute, also familiar with Lamb’s work.

“Lab groups have been attempting to identify the very early stages, where the pathogen first begins to probe the surface of the leaf,” Beachy said. “How the plant responds, and the rate at which it responds, determine whether (the pathogen) will invade. Anything we can do to look at those very first steps will help us determine how to enhance resistance.”

The nature of the work is laborious, Beachy added.

“If you apply a fungus to the surface of a leaf, it can penetrate any one of several hundred cells. The question is how do you identify the cell it’s penetrating? It’s a numbers game. If you have 10 out of a thousand cells, how do you find those 10?”

Earlier research has shown that it takes plant cells several hours to start cranking out antibiotics, hours the attacking pathogen can use to grow and develop, Beachy said.

By pinpointing what appears to be the plants’ first line of defense, the Salk research provides a “completely new approach” to the genetic engineering of crops, Lamb said.

Eventually, researchers may engineer crop cells to produce even more of the proteins when attacked, increasing the plants’ chances of survival, he said. His team also understands the structure of the linked molecule, and may work to perfect it, creating an even stronger protective barrier for plant cells, Lamb added.

The quest to tap crops’ natural defenses against pests has been spurred in part by the need to move away from chemical-dependent farming. California farmers used more than 160 million pounds of pesticides in 1990 alone, according to the state Department of Pesticide Regulation. The agricultural industry is racing to find alternatives to the most harmful chemicals before they are banned. On Wednesday, the U.S. 9th Circuit Court of Appeals ruled that four widely used, cancer-causing agricultural chemicals can no longer be used on crops that are processed into food.

Although the Salk team worked only on soybeans and regular beans, Lamb believes that most higher plants will show a similar response. He conducted the research with Dr. Desmond Bradley, now in England, and Dr. Per Kjellbom, now in Sweden.

The discovery came as a surprise. Four years ago, the team was studying the cell walls of bean plants, applying fragments of a harmful fungus and looking for clues to the plants’ early defense system. Suddenly, two proteins the scientists were tracking seemed to disappear.

They later discovered that the proteins had linked to form a rigid barrier to resist invasion.

The same type of protein cross-linking occurs during normal plant development in places where the plant needs structural support, like junctions where stems meet leaves. But that reaction is much slower than the one the Salk team pinpointed, Lamb said.

A big piece of the puzzle, however, remains unsolved: what gives the plant the signal to spew out hydrogen peroxide.

“Exactly what is causing the reaction is still a black box,” said Vic Knauf, vice president of research for Calgene Inc., a Davis, Calif.-based company that works to genetically engineer crops. “As I understand it, they described much better how the plant responds, but the box is still pretty black. Hydrogen peroxide is not on all the time. Where did it come from? What elicited the hydrogen peroxide?”

That’s the next step, Lamb said.

“We want to work back and see how the plant recognizes it’s being attacked and translates that into a cellular response,” he said.

Nevertheless, Knauf said, the research has exciting implications.

“The big payoff for disease resistance, applicable in the field, is how to trigger the (cell hardening) mechanism. Now that you understand the mechanism, you may learn how to turn it on at will,” Knauf said. “An agrichemical company might like to find the chemical that would turn on that reaction and sell it to a farmer, who could spray it on his crops at certain times to make them resistant to fungus.”

“We’re getting closer to designer chemicals--chemicals designed to perform a specific function in the plant, with minimal impact on the environment,” he said.

Work with fungal diseases has been slow, however, said John Ryals, a research director with Ciba-Geigy Corp., an agrichemical company in North Carolina. His research team has found a tobacco gene that fends off blue mold, but they don’t yet understand how.