What made the "lumpers" go black during the potato Famine, and where did it come from? Some ingenious plant pathology and forensic DNA techniques at North Carolina State University have been unravelling the mystery, writes Berni Dwan
Up until June 2001, the prime suspect behind the great Famine was believed to be the "Ib" haplotype, or strain, of the late-blight pathogen Phytophthora infestans. This was presumed to have originated in Mexico.
But then plant pathologist Dr Jean Beagle Ristaino put her detective hat on. She and her team analysed DNA extracted from 186 specimens from six different regions of the world, including Irish and British specimens collected between 1845 and 1847 during the height of the Famine.
About 90 per cent of the specimens were found to be infected with P infestans. When the actual strain was studied however, about 86 per cent - including those involved in major epidemics in 1840s Ireland - were shown to be infected with the "Ia" haplotype of P infestans.
The Ib haplotype - the one previously presumed to be the culprit behind the Famine - was present only in more modern samples from Central and South America.
Dr Ristaino is now investigating the origin of the Ia strain, whether Mexico or the Andes. "The Ia strain is in both present-day Mexico and in the Andean region. Our current work with DNA sequences from modern isolates is suggesting an Andean origin," she suggests. "The pathogen probably moved in infected seed potatoes shipped from South America. In 1840s Mexico, Santa Anna was fighting a war, so commercial potatoes were not being grown there. But the Peruvians were shipping potatoes to New Zealand and Australia, and over land and by sea to the US ports of Philadelphia and New York and to Europe.
"Furthermore, bat guano used as a fertiliser was also being shipped out of Peru. Circumstantial evidence from ship records suggests South America. Our gene genealogy work that is now in progress will shed further light on where the pathogen that caused the Famine originated."
And what about its evolution over the past 155 years - has it changed genetically, mutated - and if so, how does this impact on modern potato growing?
"We are still working on this. We know that the old haplotype Ia is still widely distributed worldwide. We are now doing whole mitochondrial genome sequencing at the Institute for Genomic Research (where they did the human genome) and we hope to compare different haplotypes to figure out how they differ genetically."
Dr Ristaino wants to learn how quickly haplotype Ia mutates and responds to certain chemicals. Is fungicide use accelerating the pace of mutations in the pathogen, for example? Knowing what the pathogen looked like 150 years ago compared to what it looks like now enables her to better understand its response to fungicides.
"Modern fungicides keep late blight in check in most places. However, the pathogen has developed resistance to a commonly used fungicide so new chemistries are always under development.
"I am interested in developing less toxic alternatives to fungicides to control the disease. We are particularly interested in medicinal herbs - but have not done the research yet to determine if they will be effective. We also have interests in mechanisms by which the pathogen mutates in response to fungicides in modern-day populations."
Her research could have implications for the way that potato blight is controlled today. Understanding the pathogen's origins could help in the search for more effective treatments.
"My work is of a more basic nature but has implications for control," she says. "Since we have data suggesting a South American origin, that is probably going to be the best location for searching for resistant potato varieties in the wild, since the host and pathogen have evolved the longest in this region."