By analyzing the genetic makeup of ancient potato leaves, researchers at North Carolina State University shed light on the dynamic evolutionary struggle that occurs between potato plants and Phytophthora infestans.

Through the use of cutting-edge DNA sequencing technology, researchers have discovered new avenues for agricultural strategy in the future by revealing how some disease strains could defeat resistance genes before these were even employed in breeding.

For the first time, the study concurrently examined the pathogen’s effector genes, or genes that aid in host infection, and the plant’s resistance genes using a targeted enrichment sequencing method.

“We use small pieces of historic leaves with the pathogen and other bacteria on them; the DNA is fragmented more than a normal tissue sample. We use small 80 base-pair chunks like a magnet to fish out similar pieces in this soup of DNA. These magnets are used to find resistance genes from the host and effector genes from the pathogen,” Allison Coomber, an NC State graduate student researcher and lead author of the paper, mentioned.

Jean Ristaino, William Neal Reynolds Professor of Plant Pathology at North Carolina State University and corresponding author of a paper published in Nature Communications that describes the study added that this is a first for looking at both potato and pathogen changes at the same time.

“Usually researchers look at one or the other. […] The dual enrichment strategy employed here allowed us to capture targeted regions of genomes of both sides of the host-pathogen relationship, even when the host and pathogen were present in unequal amounts. We couldn’t have done this work 15 years ago because the genomes weren’t sequenced,” Ristaino declared.

A Skillful Enemy

The pathogen – Phytophthora infestans – is highly skilled at fending off potato late blight disease resistance, according to the study’s findings. For instance, the research demonstrates that even before plant breeders introduced the R1 resistance gene into potatoes, the pathogen’s FAM-1 strain was able to overcome the resistance offered by the plant.

“The pathogen would have been able to resist this R1 resistance gene even if it had been deployed years earlier, probably because it was exposed to a potato with that resistance gene in the wild,” Coomber said.

The study also reveals that many of the pathogen’s effector genes have stayed stable despite various mutations that have increased the pathogen’s ability to infect plants as plant breeders have tried to create resistance, particularly after more organized potato breeding programs were started in the US and other countries in 1937.

Additionally, the research demonstrates that throughout 1845–1954, the time frame during which the study’s plant samples were gathered, the virus acquired a pair of chromosomes.

“We show in this work that after 100 years of human intervention, there are some genes that haven’t changed much in the pathogen. They are very stable potentially because they haven’t been selected on, or because they are really important to the pathogen. Targeting those genes would make it hard for the pathogen to evolve an opposing response,” Coomber also mentioned.

According to Ristaino, it’s hard to do effective plant breeding when there isn’t very much to know enough about the pathogen.

“Now that we know what effectors have changed over time, breeders may be able to use more stable resistance genes or pyramid multiple resistance genes from different wild hosts. That’s where I see the future for this type of study – applying it to slow changes in pathogen virulence or other traits such as fungicide resistance,” he concluded.