Most potato growers in the United States have certainly heard of the late blight disease and the pathogen (Phytophthora infestans) that causes it. The disease has been the scourge of potato production throughout the world, beginning in the U.S. and Europe in the mid-19th century. Until the latter part of the 20th century, there was only one mating type (A1) worldwide (except for the highlands of central Mexico, where the other mating type -A2- also existed).
Mating type controls sexual reproduction in P. infestans, such that if there is only one mating type there is no sexual reproduction. However, there is huge diversity among individuals of either mating type (just as there is huge diversity among breeding individuals of any species). For example, the strains (clonal lineages) of P. infestans predominating in the U.S. in the 21st century illustrate diverse A1 and A2 individuals.
Why does it matter if there is sexual reproduction in P. infestans? There are two very important reasons, both involving the product of sexual reproduction, the oospore.
First, these tiny structures can survive for years in soil, on equipment or just about anywhere. They survive freezing and drying. However, they do not survive high temperatures—oospores held for 30 minutes in a water bath at temperatures above 110 degrees Fahrenheit were killed. Thus, if oospores are formed in infected plants and these materials are returned to the soil, the soil can be a source of P. infestans. The oospores survive long after the plant materials have decomposed. If there are many such oospores in production fields, they produce what is known as a residential oospore population. Fortunately, such populations have so far been documented only in central Mexico and portions of northwestern Europe. In those parts of northwestern Europe with residential sexual populations, late blight control is more difficult. Late blight epidemics typically start two to four weeks earlier there than before a residential oospore population became established. Growers now have to make more fungicide applications to achieve adequate disease suppression than was previously the case.
Second, sexual reproduction leads to new combinations of genes in the progeny, and these combinations can produce individuals that have new combinations of traits that can be problematic in terms of disease management. An example concerns the US-11 clonal lineage. US-11 was first detected in the western part of the U.S., but has subsequently been detected throughout the country. It is a very aggressive strain on both potatoes and tomatoes. It was probably generated by a sexual recombination event that was detected in the early 1990s in the Pacific Northwest.
Where sexual reproduction does not occur (where only one mating type is present) oospores are not produced and the soil is not a source of the pathogen.
The next question is: How common is sexual recombination in the U.S.? The answer now is that it is not at all common. There are only two documented recombination events detected in the U.S.—one in the early 1990s in the Pacific Northwest, and one in 2010 in the Northeast. In neither case have we been able to detect a residential oospore population. In contrast, most populations of P. infestans in the U.S. are composed of single lineages of P. infestans—populations which contain only one mating type, and in which sexual reproduction does not occur. However, given that there are both A1 and A2 lineages established in the U.S., it seems likely that eventually there will be sufficient sexual recombination to lead to some residential oospore populations.
Unfortunately, as most readers are aware, even without sexual reproduction, P. infestans is still capable of causing rapid, devastating epidemics. Asexual reproduction can be dramatically rapid. The structures involved are sporangia, and these sporangia most commonly germinate to produce zoospores. Each zoospore can initiate an infection that produces a lesion. Large lesions can result within five days after inoculation. Under appropriate environmental conditions (60 to 75 degrees with eight to 10 hours of leaf wetness), each lesion can produce hundreds of thousands of sporangia—and hundreds of thousands the next day and the day after that.
Fortunately, in the absence of sexual reproduction, P. infestans is essentially an obligate parasite—it requires a living host for survival. Sporangia can survive for weeks in the soil, but they do not survive drying. Sporangia are killed within minutes by bright sunlight.
My prediction and hope is that it will be years before production fields have residential oospore populations.