The devastating Irish potato famine triggered an "arms race" between plants and pathogens, reveals new research.
A ground-breaking examination of the genetic material found in historic potato leaves by American scientists has uncovered "tit-for-tat" evolutionary changes in both potato plants and the diseases that caused the deadly blight in Ireland in the 1840s.
Known as the Great Famine, or the Great Hunger , around one million people died in Ireland between 1845 and 1852, while more than a million more fled the country, causing the population to fall by up to 25%.
The new study, published in the journal Nature Communications , used a targeted enrichment sequencing approach to simultaneously examine both the potato plant’s resistance genes and the pathogen’s effector genes – genes that help it infect hosts – in the first analysis of its kind.
Lead author Allison Coomber said: “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.”
Corresponding author Dr. Jean Ristaino , of North Carolina State University, said: “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 host and pathogen were present in unequal amounts.
"We couldn’t have done this work 15 years ago because the genomes weren’t sequenced.”
The findings study’s results show that the pathogen, Phytophthora infestans, is very adept at fighting off potato late blight disease resistance. For example, the study shows that the FAM-1 strain of the pathogen had the ability to defeat the resistance provided by the plant’s R1 resistance gene – even before plant breeders deployed it in potatoes.
Coomber a graduate student researcher, said: “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."
The research also shows that many of the pathogen’s effector genes have remained stable, although different mutations have happened to increase its infection prowess as plant breeders attempted to breed resistance – specifically after 1937 when more structured potato breeding programs commenced in the United States and elsewhere.
The research team also found that the pathogen added a set of chromosomes between 1845 and 1954, the period in which the study’s plant samples were collected.
Coomber said: “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 really hard for the pathogen to evolve an opposing response.”
Dr. Ristaino said: “It’s hard to do effective plant breeding when we don’t know enough about the pathogen.
"Now that we know what effectors have changed over time, breeders may be able use resistance genes that are more stable or pyramid multiple resistance genes from different wild hosts."
She added: “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.”
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