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Scientists decode potato-blight genome

An international team of scientists has sequenced the genome of potato blight, the pathogen that caused the Irish potato famine and still costs farmers USD 6.7 billion (EUR 4.6 billion) every year in potato-crop losses. The findings, published in the journal Nature, help to ex...

An international team of scientists has sequenced the genome of potato blight, the pathogen that caused the Irish potato famine and still costs farmers USD 6.7 billion (EUR 4.6 billion) every year in potato-crop losses. The findings, published in the journal Nature, help to explain how potato blight adapts so quickly to attempts to eliminate it, and could lead to the development of new strategies to control the pathogen. Potato blight is caused by an organism called Phytophthora infestans that thrives in cool, wet weather. Potatoes are the fourth largest food crop in the world, and P. infestans is the potato grower's biggest enemy., and once infected, plants die within a week. Farmers spend vast amounts of money spraying crops with fungicides in an attempt to keep the blight at bay. Scientists have even created strains of potato that are resistant to potato blight, yet the pathogen quickly adapts to these new strains. How P. infestans does this is a long-standing puzzle. In this latest study, the researchers sequenced the genome of P. infestans and compared it to the genomes of two related water moulds: P. sojae, which causes root rot in soybeans, and P. ramorum, which causes sudden oak death. The results were surprising. Firstly, at 240 million base pairs, the genome of P. infestans is much larger than those of its close relatives, P. sojae (95 million base pairs) and P. ramorum (65 million base pairs). The P. infestans genome also has an unusual structure. Most of the pathogen's 18,000 genes are tightly packed into gene-dense regions that together account for around a quarter of the genome. Most of these genes are 'housekeeping' genes that have changed little over the course of evolution and are responsible for the day-to-day maintenance and reproduction of the pathogen. In contrast, the remaining three quarters of the genome consist largely of long stretches of multiple copies of DNA segments, The few genes found in these 'repeat-rich' regions are key to P. infestans' ability to infect potatoes and other plants. 'Our findings suggest a 'two-speed' genome, meaning that different parts of the genome are evolving at different rates,' explained one of the lead authors of the study, Professor Sophien Kamoun of the Sainsbury Laboratory in the UK. 'This two-speed genome structure might enable P. infestans to rapidly adapt to host plants while the core set of genes for the basic biology of the organism remains conserved.' 'In contrast to the well-conserved regions where most genes are found, 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,' added Co-lead author Brian Haas of the Broad Institute in the US. Once thought to be a fungus, P. infestans is now known to be a 'water mould', and as such is more closely related to the malaria parasite than to fungi. The pathogen is best known for causing the Irish potato famine in the middle of the 19th century, which left over a million people dead and triggered a massive wave of immigration to the US. However, even today it is a major problem for farmers and poses a serious threat to global food security. Farmers in Ireland report that this year has been the worst for blight in living memory, while their colleagues in the UK say they have been forced to increase spraying by up to 30% in recent years. The Dutch potato crop is treated with more fungicide than any other crop. On the other side of the Atlantic, American potato and tomato farmers are also experiencing a serious, costly blight problem. 'This pathogen has an exquisite ability to adapt and change, and that's what makes it so dangerous,' commented Dr Chad Nusbaum of the Broad Institute. '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.'