An international research team has decoded the genome of the notorious blight that caused the Irish potato famine in the 1840s.
That same organism now threatens tomato and potato crops across the U.S. — even attacking genetically resistant potatoes that have been bred to fend off infection.
The study, published in Nature, reveals that the organism’s unusually large genome size — more than twice that of closely related species — and “extraordinary genome structure” enable the rapid evolution of genes.
That ability helps the pathogen to outsmart its plant hosts. Now discovered, it may clue researchers into unlocking 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 Genome Sequencing and Analysis Program at the Broad Institute of MIT and Harvard, in a statement. “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.”
The team’s findings suggest that different parts of the genome are evolving at different rates. As the team sequences additional strains and close relatives of the pathogen, they’ll be able to develop a more comprehensive understanding of the blight’s adaptation.
The potato famine that gripped Europe, especially Ireland, in the mid-19th century was long thought to be a fungus. The blight, Phytophthora infestans, is now considered a “water mold,” more closely related to the malaria parasite. It thrives in cool, wet weather and can infect potatoes, tomatoes and related plants, causing a “late blight” disease that can destroy entire crops in days.
The researchers, led by scientists at the Broad Institute and the Sainsbury Laboratory, first decoded the P. infestans genome and compared its sequence to the genomes of two relatives: P. sojae, which infects soybeans, and P. ramorum, which causes a condition known as sudden oak death.
The researchers found a large amount of repetitive DNA in the massive genome.
The findings reveal the pathogen’s unusual strategy to support the rapid evolution of critical genes, known as “effector” genes, that can disrupt plants’ normal physiology, enabling it to establish a foothold.
On the other hand, some “effector” genes can also trigger plants’ immune responses — making them prime targets for combating P. infestans infection.
Co-lead author Brian Haas of the Broad Institute explains:
“The repeat-rich regions change rapidly over time, acting as a kind of incubator to enable the rapid birth and death of genes that are key to plant infection. As a result, these critical genes may be gained and lost so rapidly that the hosts simply can’t keep up.”
Further study should yield a deeper understanding of plant infection and help identify potential targets for fighting back.
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