Virulent pathogen uses a genetic decoy to foil host’s immune defenses

CORVALLIS, Ore. – A virulent plant-disease agent called Phytophthora sojae knocks out resistance in its soybean host by sending out a “decoy” protein to confuse the plant’s immune system, according to a study published today in the journal Science.

The newly uncovered mechanism may explain why the group of plant pathogens known as Phytophthora are so devastating to crops and natural ecosystems worldwide, said Brett Tyler, director of Oregon State University’s Center for Genome Research and Biocomputing and a plant pathologist in the College of Agricultural Sciences.

“This discovery could open new approaches to controlling a wide diversity of destructive plant pathogens, including fungi and bacteria,” said Tyler, professor in the botany and plant pathology department and co-leader of the 17-member team of Chinese and American scientists.

The study builds on 13 years of collaboration between the Chinese and American research teams to combat Phytophthora pathogens, which cause billions of dollars in agricultural losses each year.

Phytophthora, a genus with more than 160 species, are members of a group of fungus-like microorganisms called oomycetes. They are serious pests in many vegetable and tree crops worldwide. The Irish potato famine in the mid-19th century was caused by a Phytophthora pathogen, P. infestans. Phytophthora also wreak havoc on trees and shrubs in native ecosystems; P. ramorum is causing the ongoing outbreak of sudden oak death in Oregon and California.

The study provides a vivid glimpse into the evolutionary arms race between Phytophthora species and their hosts. The researchers focused on P. sojae, which attacks soybeans, and particularly on a critical protein called a xyloendoglucanase, or XEG.

The XEG protein initiates infection by attacking the walls of plant cells, weakening the tissue and releasing sugars for the pathogen to feed on during the early hours of infection. In a first line of defense, the soybean’s immune system releases protective proteins that block XEG.

“But now we find that the pathogens strike back by releasing XEG-look-alikes that distract the XEG-blockers,” Tyler said.

The mechanism, he explained, resembles decoy flares released by aircraft to distract heat-seeking missiles. The soybean’s immune system goes after the decoy protein, leaving the real one free to do its damage.

“The decoys are actually the second mechanism we discovered by which Phytophthora protects XEG,” said Yuanchao Wang of Nanjing Agricultural University in China, who co-led the study with Tyler. “Two years ago we discovered that many plants can sense XEG to launch an effective immune response, but the pathogen produces proteins called effectors that block that immune response.”

Most other Phytophthora species contain genes that encode both XEG and a look-alike effector protein, Tyler said. The researchers also discovered a similar decoy mechanism operating in another Phytophthora species, P. parasitica.

To probe the mechanism further, Tyler’s student Yufeng Wang developed CRISPR gene-editing technology to destroy the genes that code for both the XEG and the decoy protein. The altered Phytophthora didn’t infect the soybeans. “That’s how we know that both these proteins are essential to successful infection by Phytophthora,” said Fang.

This one-two punch, Tyler said, may be the key to Phytophthora’s virulence in its many hosts.

“P. sojae goes to extraordinary lengths to protect its XEG from the plant’s immune system,” he said. “If we can find a way to block the pathogen’s XEG, we could protect many crops from destruction by Phyophthora pathogens.”

The work was supported by funding from the Chinese government and by the United States Department of Agriculture’s National Institute of Food and Agriculture.

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Brett Tyler

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