Agriculture Reference
In-Depth Information
17.2.1 Origin and early migrations
Migration has had a dramatically important role in the population biology of
P. infestans . The first records of the disease in temperate potato production occurred
in the mid 19 th century. The disease was noticed as a severe problem in northeastern
United States in the early 1840s (Stevens, 1933). It was clearly widespread
throughout Europe by the end of the growing season in 1845 (Bourke, 1964). Prior
to the mid 19 th century, late blight had been unknown in North America, Europe,
Africa and Asia. After the mid 19 th century, the disease became problematic
throughout the rest of the world, usually shortly after potato production was
established (Cox and Large, 1960).
Evidence has accumulated that most worldwide populations of P. infestans had
been dominated by single clonal lineage of P. infestans prior to the 1980s (Goodwin
et al ., 1994a). These populations were obviously asexual. A likely explanation for
this population genetics structure was that a single clonal lineage had 'colonized'
most continents. This could have happened if the pathogen escaped a centre of
origin of greater diversity, going through a severe bottleneck such that only one or
very few clonal lineages escaped. Through subsequent bottlenecks, a single clonal
lineage could have survived and then been distributed throughout much of the world
in subsequent migrations. A feasible alternative explanation is difficult to identify.
The current centre of diversity of P. infestans and the location from which the
primary migrations originated seem to be in the highlands of Central Mexico. It was
in this location that isolates with the A2 mating type were first discovered. Other
populations throughout the world were asexual and comprised of a single mating
type of the organism (Goodwin et al ., 1994a). Not only were both mating types
found, but they occurred in equal frequencies (Gallegly and Galindo, 1958; Tooley
et al ., 1985; Niederhauser, 1991). Populations in these highlands are sexual (Tooley
et al ., 1985; Fernández-Pavía et al ., 2004) and remarkably diverse for all neutral
markers and for pathotype (Tooley et al ., 1986; Rivera-Peña, 1990; Goodwin et al .,
1992). No other location has the genetic diversity reported for Central Mexico.
It seems highly likely that migrations led to the occurrences of late blight in the
United States and Europe in the mid 19 th century. At this point, the mechanism by
which P. infestans was removed from Mexico and introduced to the United States
and Europe is uncertain and the subject of renewed debate (Andrivon, 1996; Abad
and Abad, 1997; May and Ristaino, 2004). Three possible theories are proposed:
1. the pathogen migrated from Central Mexico into the USA and then into Europe
(Fry et al ., 1993); 2. the pathogen was introduced into the USA and Europe from the
Andean region (Tooley et al ., 1989); and 3. P . infestans migrated from Mexico to
Peru and then to the USA and Europe (Andrivon, 1996). The chronology of late
blight detection suggests that the first migration might have been into the United
States/Canada, because the disease was detected first in eastern USA and then in
Europe (Fry et al., 2002). Migration from the north eastern United States to Europe
could have occurred via transport of infected tubers. Migrations out of Mexico were
very limited, because potatoes ( Solanum tuberosum ) were not a common crop in
Mexico and certainly were not an export crop until the late 20 th century. Movement
on infected potato seed tubers is probably the most efficient mechanism for transport
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