Kansas State University researchers Andres Salcedo (right) and Eduard Akhunov look over gene sequencing data from a recent study that identified a key mechanism that causes the devastating stem rust disease in wheat. | Download this photo.
K-State researchers make key discovery in fight against wheat stem rust
Study is published in Dec. 22 issue of Science Magazine
December 21, 2017
MANHATTAN, Kan. — Kansas State University researchers have characterized the mechanism used by wheat to defend against the devastating stem rust disease, a finding they think can help them stay ahead of future disease outbreaks.
Their work, which is published in the Dec. 22 issue of Science Magazine, characterizes the relationship between a gene in the fungus that causes stem rust, and the gene in wheat that provides resistance to the disease.
“This is one of the first wheat rust avirulence genes characterized where we know the fungal protein and corresponding wheat resistance gene that is interacting with this protein to trigger the resistance response,” said Eduard Akhunov, professor of plant pathology.
Wheat stem rust is a devastating disease caused by the fungus, Puccinia graminis f. sp. tritici. The disease made headlines in 1999 when a particularly virulent strain, Ug99, was discovered in Uganda and quickly spread to the surrounding regions. That outbreak caused yield losses of 70 percent or more.
At the time of the Ug99 discovery, the United Nations’ Food and Agricultural Organization estimated that 80 to 90 percent of global wheat cultivars were susceptible to this particular fungal strain.
The K-State scientists found that a specific protein encoded by a fungal gene – also called an avirulence factor (Avr) – ultimately can lead to the death of the fungus when it interacts with a resistant gene in the wheat crop.
The scientists dubbed the fungal gene AvrSr35, because it makes the fungus susceptible to resistance gene Sr35, a gene identified by Akhunov and his team in 2013 that is known to provide resistance to Ug99 stem rust.
“This protein (AvrSr35) is secreted by the fungus early in the infection stage, and once Sr35 senses the presence of this protein, it triggers the immune response,” Akhunov said.
During this response, Sr35 is able to prompt a cell death pathway in the wheat, essentially cutting off nutrients to the fungus until it dies.
“The plant sacrifices some groups of cells instead of compromising the entire tissue,” said Andres Salcedo, a graduate student who was instrumental in the discovery and is the lead author for the article appearing in Science.
But fungi are hardy characters and eventually they find a way to overcome the resistant genes, leading to new strains of the disease. Sometimes this happens because the fungus no longer contains a trigger gene, such as AvrSr35, which means the resistant gene – Sr35 – no longer senses the presence of the fungus.
“You have this cycle where you have breeders developing new varieties with resistant genes, and over time fungi learn how to overcome these resistant genes,” Akhunov said.
This ongoing tit-for-tat battle means that scientists and wheat breeders are constantly on guard against developing strains of the disease.
But Akhunov says that the identification of AvrSr35 by K-State’s researchers and AvrSr50 by a team of researchers from Australia (published in the same issue of Science magazine), “gives wheat geneticists an opportunity to develop new avenues of resistance.”
“These discoveries provide valuable tools for pathogen surveillance and early detection of virulent strains, and can guide the selection of complementary resistance genes in future varieties of wheat to maximize the durability of the deployed resistance gene cassettes.”
He added that knowing pairs of avirulence and resistance genes is “one of the first steps to detailed understanding of the disease resistance mechanisms and a deeper understanding toward devising new strategies to developing disease resistant crops and protecting yield.”
“All of these secreted fungal proteins, including AvrSr35, have targets inside the plant cells that they bind to and somehow interact with,” Akhunov said. “This interaction is important for the fungus to grow and feed on the plant.”
According to Akhunov, once scientists know which target in the plant cells that the fungus is trying to change, they can implement new strategies to develop disease resistant plants in the future.
“For example, we can modify this target in wheat using biotechnology or CRISPR/Cas9 gene editing, so that this target is not recognizable by the fungus,” he said.
Salcedo, a native of Colombia, has been with the project since the beginning. He will complete a doctoral degree from Kansas State University next year.
William Rutter, a former postdoctoral research associate in Akhunov’s lab who currently works at the U.S. Department of Agriculture-Agricultural Research Service Vegetable Laboratory in Charleston, South Carolina, was another lead author in the study. K-State researchers worked closely with scientists from the USDA’s Cereal Disease Lab in St. Paul, Minnesota and the Hard Winter Wheat Genetics Research Unit in Manhattan, Kansas.
Akhunov also credited a team of K-State and University of California-Davis scientists who have worked on the project, including experts in bioinformatics, protein chemistry, next generation sequencing, and confocal microscopy. The project began in 2011.
The National Institute of Food and Agriculture, an agency of the USDA, and the Bill & Melinda Gates Foundation, one of the key partners of the Borlaug Global Rust Initiative, provided funding for this research.
