Lethal genes behind the nineteenth-century Irish famine pinned down.
Researchers have traced the key genetic changes that enabled the plant pathogen responsible for the 1845 Irish potato famine (Phytophthora infestans) to jump from wild plant hosts to cultivated potatoes. These genetic clues could aid the development of fungicides and disease-resistant varieties of potato that the pathogen will find much more difficult to adapt to and overcome.
"We looked at how this pathogen evolved and found which genes we should focus on to tackle it," says study author Sophien Kamoun, a plant pathologist and head of the Sainsbury Laboratory, a not-for-profit plant science company in Norwich, UK. The blight — an oomycete, or fungus-like microorganism, that destroys both the tuber and its leaves — continues to be a major problem for farmers. Epidemics are currently raging in the United Kingdom and United States, and the oomycete annually destroys more than US$6 billion worth of crops worldwide.
The researchers identified the key genes by comparing the genetic make-up of the potato blight pathogen and several of its sister species. To do so, they sequenced the genomes of four of the potato blight's sister species, including Phytophthera phaseoli, which infects lima beans (Phaseolus lunatus). They computationally analysed and compared these genomes with the genome of the previously sequenced P. infestans.
They discovered that the pathogens shared many 'housekeeping' genes, including that for spore generation, but that they also had numerous regions made up of non-coding repeated DNA sequences. Genes were sparser in these regions, but most were associated with pathogenicity, having roles such as suppressing host immunity and destroying host cell walls. These genes varied between the species, either in their sequence or in the number of copies present.
In their report, published in Science today1, the researchers say that the function of these genes and the variation between the sister species suggests that these regions are involved in the evolution and adaption of the pathogen to new hosts. "It seems that the genes for host adaptation are in the DNA-repeat-rich regions," Kamoun says.
Targeting control methods, including fungicides, towards the genetically similar regions, where evolution is slower, will make it more difficult for the pathogen to evolve resistance to the controls. "The genetically conserved part of the genome could be the potato blight pathogen's Achilles heel," adds Kamoun.
The study's findings are bolstered by similar discoveries reported in a second paper in Science2, which describes the genetic make-up of an unrelated powdery mildew (Blumeria graminis) that affects barley.
Pietro Spanu, a molecular plant pathologist at Imperial College London, UK, and his team found that B. graminis genes responsible for infection and pathogenicity are also located in areas of the genome that are enriched with non-coding DNA repeats.
"Evolution seems to be going on in these islands," he says. Commenting on the potato blight paper, he says: "They, like us, suggest that these regions are highly plastic and enable the pathogens to run faster in an arms race."
As a result of climate change and the loss of habitats from where important crops originated, "there is a big risk that we will run out of options for natural genetic resistance", says Spanu. Developing a better grip on the molecular make-up and evolution of plant pathogens, current control methods can be better targeted slowing the chances that they evolve resistance, he adds.
Raffaele, S. et al. Science 330, 1540-1543 (2010).
Spanu, D. et al. Science 330, 1543-1546 (2010).
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Gilbert, N. Evolution of potato blight pathogen traced. Nature (2010). https://doi.org/10.1038/news.2010.664