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United States Department of Agriculture

Agricultural Research Service

Title: Genetic Change Within Populations of Phytophthora Infestans in the United States and Canada During 1994 to 1996: Role of Migration and Recombination

Authors
item Goodwin, Stephen
item Smart, Christine - CORNELL UNIVERSITY
item Sandrock, Robert - CORNELL UNIVERSITY
item Deahl, Kenneth
item Punja, Zamir - SIMON FRASER UNIVERSITY
item Fry, William - CORNELL UNIVERSITY

Submitted to: Phytopathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 28, 1998
Publication Date: N/A

Interpretive Summary: Late blight, caused by the fungus-like Oomycete Phytophthora infestans, is one of the most damaging diseases of potato and tomato worldwide. For many decades late blight was effectively managed in the United States and Canada by frequent fungicide application. However, a resurgence of the disease began during 1992; losses to United States potato and tomato growers were estimated at more than $230 million during 1994-1995 alone. Previous studies showed that the 1992-1993 epidemics were caused primarily by a new strain, US-7, that was probably imported from northwestern Mexico. This strain was a mating type, previously rare in the United States, and was resistant to the fungicide metalaxyl. The purpose of the present study was to determine the cause of the 1994-1996 epidemics, to test the hypothesis that they were caused by the new strain, US-7. Analysis of 556 isolates of P. infestans from the United States and Canada revealed a striking change. Instead of US-7, a different strain, US-8, predominated during 1994-1996. This strain is a mating type, resistant to metalaxyl, and highly pathogenic to potato. It was rare during 1992 and 1993 but spread rapidly during 1994, probably in infected seed potatoes. The US-7 strain effectively disappeared, and by 1996 a new fungicide-resistant strain, US- 17, appeared on tomato. A few other strains appeared which probably represent the first instances of sexual reproduction of P. infestans in the United States. This is bad news for United States potato and tomato growers: sexual reproduction could mean that epidemics will now occur earlier in the season and be much more difficult to control. This information will be very important to plant pathologists as they design future strategies for managing this destructive disease.

Technical Abstract: Dramatic changes occurred within populations of Phytophthora infestans in the United States and Canada from 1994 through 1996. The previously rare US-8 genotype increased rapidly and predominated during 1994 through 1996. US-7, which infected both potato and tomato and made up almost 50% of the sample during 1993, was detected only rarely among 330 isolates analyzed during 1994. It was not detected at all in more limited samples from 1996 Ability to infect both potato and tomato apparently did not increase the fitness of this genotype relative to US-8. The previously dominant US-1 genotype made up 8% or less of the samples analyzed during 1994 through 1996. A few additional genotypes were detected that could indicate the beginnings of sexual reproduction of P. infestans within the United States and Canada. However, clonal reproduction still predominated; opportunities for sexual reproduction probably were limited because the A1 and A2 mating types usually were separated geographically. The previous correlation between metalaxyl sensitivity and genotype was confirmed and extended: all US-1 isolates tested were sensitive; all isolates of the US-7, -8 and -17 genotypes tested to date have been resistant. Isolates of P. capsici and P. erythroseptica, two other species often found on tomato or potato, could be distinguished easily from each other and from P. infestans using a rapid allozyme assay. This technique could be useful for identification of species, in addition to genotype of P. infestans. It generally was not possible to predict which genotypes would be present in a location from one year to the next. Long-distance movement of US-8 in seed tubers was documented and was probably the primary means for the rapid spread of this genotype from 1993 through 1996.

Last Modified: 8/29/2014
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