Skip to main content Skip to navigation

Why Aren’t Plants Sick More than They Are?

New Research Offers Insight on Molecular Signaling of Non-host Resistance Mechanism

PULLMAN, Wash. — Why are plants immune to most of the diseases surrounding them in the environment? That’s a question Lee Hadwiger, Washington State University professor of plant pathology, has been wrestling with most of his career.

Lee Hadwiger with peas in greenhouse. Photo by Brian Charles Clark. Click image to download high resolution version.
Lee Hadwiger with peas in greenhouse. Photo by Brian Charles Clark. Click image to download high resolution version.

Called non-host resistance (NHR), the mysterious trait gives plants their most robust and durable immunity to the myriad pathogens challenging them. If NHR weren’t a commonplace in nature, plants would be constantly attacked by fungi, bacteria and other pathogens swarming in air, soil and bodies. But, for the most part, plants are immune to those challenges.

In a paper published in the January issue of the peer-reviewed journal Phytopathology, Hadwiger and his colleague, USDA Agricultural Research Service plant pathologist James Polashock, offer new insight into the mechanism triggering the NHR response in plants.

“Innate immunity has to be triggered by something,” Hadwiger said, “but we are only now gaining some insight on how signaling occurs at the molecular level.”

Hadwiger and Polashock show that fungal DNase enzymes trigger the NHR response in a variety of plant species. They further theorize that these fungal DNase genes appear to provide an unlimited source of components for developing transgenic resistance in all transformable plants.

DNase is generic term for a wide variety of enzymes that catalyze changes in DNA molecules. Hadwiger explained that DNases from fungal mitochondria have a small peptide molecule that enables them to move through plant cell membranes and thus induce expression of NHR in the plant. Hadwiger and Polashock demonstrated that when a plant encounters a fungal DNase purified in the lab, the NHR response is triggered.

Hadwiger and Polashock used baker’s yeast, a relatively innocuous fungus not known to cause disease, to trigger the NHR response in pea. Hadwiger and students in his laboratory had previously induced this defense response by transferring a fungal DNase gene to tobacco. The tobacco plants then expressed the NHR response to a known tobacco pathogen.

“The potential positive impact of this for agriculture would be a reduction in the use of fungicides,” Hadwiger said. Currently, disease resistance genes are typically introduced in commercially important plants through conventional breeding techniques. But, Hadwiger said, conventional breeding targets races of specific diseases and the introduced immunity may last only about seven years before the fungus evolves and overcomes the plant’s resistance.

“The natural NHR resistance would be preferable,” Hadwiger said. Towards that end, Hadwiger said he will remain vigilant about how best to transfer this natural process to plants that succumb to their specific diseases. He is optimistic that non-genetic engineering techniques may be devised to enhance the activity of the DNases transferred in the fungal-plant interactions.

-30-

Media Contacts

Lee Hadwiger, WSU professor of plant pathology, 509-335-3751