By SHELLY STRAUTZ-SPRINGBORN
Michigan Correspondent

KNOXVILLE, Tenn. — A group of researchers has decoded the genome of the notorious pathogen late blight. That organism, Phytophthora infestans, triggered the Irish potato famine in the 1840s and threatens this season’s potato and tomato crops across much of the United States.

Dr. Kurt Lamour, an associate professor in the University of Tennessee Department of Entomology and Plant Pathology and a core faculty member in the Genome Science and Technology graduate program, said the study findings mean scientists are one step closer to unraveling the secrets of a disease that has been able to mutate over time to avoid control measures.

“Hopefully this is a step that helps us have a better understanding of some more reasonable ways to control this disease,” Lamour said. “Having this piece of information opens a lot of doors to understanding the biology of the disease.”

He said although domestic growers apply fungicides to help control the disease, producers in other countries do not have the resources to do so. “We need other ways to combat it,” he said.

Late blight is one of the most devastating diseases of potatoes and tomatoes worldwide. Since 1990, late blight has caused widespread damage throughout the U.S. and Canada. If left unmanaged, it can result in complete destruction of potato or tomato crops.

Published in the Sept. 9 issue of the journal Nature, the study reveals that the P. infestans organism boasts an unusually large genome size and an unusual genome structure. Together these characteristics appear to enable the rapid evolution of genes, particularly those involved in plant infection. These data expose an unusual mechanism that enables the pathogen to outsmart its plant hosts and may help researchers unlock new ways to control it.
“This pathogen has an exquisite ability to adapt and change, and that’s what makes it so dangerous,” said senior author Chad Nusbaum, co-director of the Sequencing and Analysis Program at the Broad Institute of MIT and Harvard. “We now have a comprehensive view of its genome, revealing the unusual properties that drive its remarkable adaptability. Hopefully, this knowledge can foster novel approaches to diagnose and respond to outbreaks.”

Co-lead author Sophien Kamoun, a research leader at the Sainsbury Laboratory in Norwich, United Kingdom, said the research indicates “a ‘two-speed’ genome, meaning that different parts of the genome are evolving at different rates. Future sequencing of additional strains and close relatives of this pathogen will help test this hypothesis and could transform our understanding of how it adapts to immune plants.”

Lamour, along with his then-graduate student Alon Savidor and Dr. W. Hayes McDonald at Oak Ridge National Laboratory, assisted in the research by analyzing the organism’s proteins. Their experiments validated or refined many of the genes predicted in the genome.

To understand the genetic basis for the pathogen’s success, researchers decoded the P. infestans genome. They produced a high-quality genome sequence and compared it to the genomes of two relatives. A striking finding of the effort is the size of the P. infestans genetic blueprint. It is 2.5 to four times the size of its relatives’ genomes. The source of the genome’s large size is a massive amount of repetitive DNA.

As part of his Ph.D. studies, Savidor, with input and mentoring from Lamour and McDonald, refined a protocol to measure a large number of proteins in the genome and helped check the quality of the predicted genes. Lamour said the effort generated useful proteomic data that supported the overall genome sequencing effort.

The overall findings suggest that P. infestans utilizes an unusual genomic strategy to support the rapid evolution of the “effector” genes that disrupt the host plant’s normal physiology.

“We think this could be a tactic that enables P. infestans to rapidly adapt to host plants,” said co-lead author Brian Haas, manager of genome annotation, outreach, bioinformatics and analysis at the Broad Institute.

Lamour said the complex nature of late blight is the reason the disease has been a problem for more than 150 years. “Even with all the time and effort that has been spent breeding different varieties, it doesn’t take long before the Phytophthora has overcome a resistance,” he said.