Researchers are shedding light on the evolutionary dance between potato plants and the pathogen responsible for the devastating Irish potato famine of the 1840s.
A recent study by North Carolina State University researchers has uncovered fascinating details about the mutual evolutionary adaptations happening in both potato plants and the pathogen linked to the infamous 1840s Irish potato famine.
The research utilized a specialized sequencing method to analyze both the resistance genes from the potato plants and the effector genes of the pathogen, which are crucial for infection. This innovative approach marks the first time such an analysis has been conducted.
“We worked with tiny samples of historic leaves that contained both the pathogen and other bacteria; these samples had more fragmented DNA than typical tissue samples,” explained Allison Coomber, a former graduate student at NC State and the lead author of the study. “We used small pieces of 80 base pairs as a sort of magnet to extract similar fragments from a complex DNA mixture. These magnets helped us locate both the plant’s resistance genes and the pathogen’s effector genes.”
“This research uniquely investigates the changes in both potatoes and their pathogens during the same timeframe; typically, studies focus on one or the other,” said Jean Ristaino, a leading professor in Plant Pathology at North Carolina State University and the study’s corresponding author. “Our dual enrichment technique enabled us to pinpoint specific sections of the genomes from both the host and the pathogen, even when they were present in varying quantities. We wouldn’t have been able to conduct this study 15 years ago due to the lack of sequenced genomes.”
The findings indicate that the pathogen, Phytophthora infestans, has effectively adapted to overcome the late blight resistance of potato plants. For instance, the research reveals that the FAM-1 strain of this pathogen was capable of evading the protection offered by the R1 resistance gene in the plants, and this ability existed even before plant breeders had introduced the gene into potato crops.
“The pathogen could counter the R1 resistance gene even if it had been used sooner, likely because it had already interacted with wild potatoes containing that gene,” Coomber shared.
The study also indicates that while many of the pathogen’s effector genes have remained consistent, various mutations emerged to enhance its infection capabilities as plant breeders sought to breed for resistance—especially after 1937 when more organized potato breeding initiatives began globally.
The research highlights that between 1845 and 1954, a key timeframe reflected in the plant samples collected, the pathogen incorporated additional chromosomes.
“Our findings demonstrate that despite a century of human interventions, certain pathogen genes have shown little change,” Coomber noted. “These stable genes might be crucial for the pathogen’s survival, meaning targeting them could hinder the pathogen’s ability to evolve counter-responses.”
“Understanding the pathogen better is essential for effective plant breeding,” Ristaino mentioned. “Now that we’ve identified how effector genes have altered over time, breeders can potentially select more stable resistance genes or combine multiple resistance genes from various wild relatives.”
“I envision the future of this research focusing on gradual changes in pathogen virulence or other important traits such as resistance to fungicides,” Ristaino added.
