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UNC plant researchers discover proteins interact to form hair-trigger protection against invaders


Experimenting with Arabidopsis, a fast-growing cousin of the humble mustard plant, scientists at the University of North Carolina at Chapel Hill got a big surprise while investigating how plants respond to attacks from disease organisms such as bacteria and viruses.

"Contrary to what we thought we’d find, our experiments showed that at least three different proteins work in concert with one another in tug-of war or teeter totter-fashion to keep plant defenses in a state of constant readiness," said Dr. Jeffrey L. Dangl, John N. Couch professor of biology in UNC’s College of Arts and Sciences.

Previously, he and others believed that the proteins -- RAR1, SGT1 and HSP90 -- were required for what is called signal transduction -- relaying like Paul Revere the message that an enemy had arrived, Dangl said. Instead, they are needed to form an even earlier disease surveillance antenna or hair trigger. When disease invaders pull that trigger, infected plants cells quickly commit suicide, often preventing the invader from destroying the entire plant.

The new discovery appears to be a universal mechanism for defense by all plants against not only bacteria and viruses, but also parasitic fungi, insects and worms, he said.

"This work is important because every year, these organisms cause us to lose some 30 percent of our grain, fruit and vegetable crops after all the human, water and soil energy has already gone into producing them," Dangl said. "The hope is that we might be able to manipulate plants’ immune systems to make them more resistant to pathogens using fewer expensive and polluting chemicals."

A report on the findings appears in this week’s edition (June 24) of Science Express, the online, early-release version of the journal Science. Other authors are postdoctoral fellow Dr. Ben F. Holt III and Ph.D. student Youssef Belkhadir, both in biology.

"Plants use resistance proteins to defend themselves against pathogen attack by initiating a defense response," Holt said. "The proteins RAR1, HSP90 and SGT1 were previously thought to work together to help resistance proteins in this function. To our surprise, we found that SGT1 can actually work against, or antagonize, the other two proteins to disable resistance protein function."

The researchers also showed why they antagonized each other, he said. RAR1 and HSP90 can prevent resistance proteins from disappearing, while SGT1 helps them disappear. The result is that the system remains poised for an immediate response to bacteria and other attackers.

"By controlling disappearance of resisting proteins, RAR1, HSP90 and SGT1 control whether or not the plant is about to recognize that it is under pathogen attack," Holt said. "So the emerging story is that RAR1 and HSP90 keep resistance proteins ready to perceive pathogen signals, and SGT1 probably pulls against these two to send resistance proteins to their destruction."

The National Science Foundation supported the research through its Arabidopsis 20-10 Project, which aims to describe the functions of all 28,000 genes in the model plant.

Scientists study Arabidopsis, also known as thale cress or mouse-eared cress, because it is small and can produce five to six generations a year rather than just one or two like most crop plants. That rapid reproduction allows them to study the plant’s genetics faster than they could with other species.

Understanding Arabidopsis completely will teach scientists an enormous amount about all other flowering plants, which are closely related genetically, Dangl said. The new genomics technology, developed by Patrick Brown and David Botstein at Stanford University, has been applied to yeast, fruit flies and humans but not to plants in a large, systematic way. Arabidopsis was the first plant for which scientists succeeded in mapping its entire genetic composition.

Dangl is also with UNC’s Curriculum in Genetics, Department of Microbiology and Immunology and Carolina Center for Genome Sciences.

David Williamson | EurekAlert!
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