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Widespread Distribution and Probable Origin of Resistance to Metalaxyl in Clonal Genotypes of Phytophthora infestans in the United States and Western Canada. Stephen B. Goodwin, Department of Plant Pathology, 334 Plant Science Building, Cornell University, Ithaca, NY 14853, Current address: USDA-ARS, Crop Production and Pest Control Research Unit, Department of Botany and Plant Pathology, 1155 Lilly Hall, Purdue University, West Lafayette, IN 47907-1155; Ludwik S. Sujkowski(2), and William E. Fry(3). (2)(3)Department of Plant Pathology, 334 Plant Science Building, Cornell University, Ithaca, NY 14853. (2)Current address: Department of Plant Pathology, North Carolina State University, Raleigh, NC 27695-7616. Phytopathology 86:793-800. Accepted for publication 17 April 1996. Copyright 1996 The American Phytopathological Society. DOI: 10.1094/Phyto-86-793.

The sensitivity of 251 isolates of Phytophthora infestans to the phenylamide fungicide metalaxyl was assessed by an in vitro radial growth assay on fungicide-amended agar media. Isolates were collected from many regions of North America from 1987 through 1993, including 15 states in the United States and British Columbia, Canada. A small sample of isolates from Europe and Israel was included for comparison. Isolates that grew less than 40% of the control on media containing 5 g of metalaxyl per ml were considered sensitive; all other isolates were scored as resistant. Field trials and floating leaf-disk assays were used to confirm the accuracy of the amended-agar technique. All isolates collected from 1987 through 1989 were sensitive. Metalaxyl-resistant isolates were detected in 13 of 15 states and in British Columbia during 1992 and 1993. With one exception, sensitivity to metalaxyl was absolutely correlated with clonal lineage as determined by mating type, allozyme genotype, and DNA fingerprint analysis. The US-1 clonal lineage, present in the United States and Canada for many years, was uniformly sensitive. In contrast, all isolates with the recently immigrated US-7 and US-8 clonal genotypes were resistant, even those obtained from fields with no history of metalaxyl application. All US-6 isolates collected since 1990 were resistant, but one sensitive US-6 isolate was collected in California in 1989. The cause of this polymorphism within US-6 could not be determined. Metalaxyl resistance was unimodally distributed within clonal lineages and limited to those that were recently immigrated. This strongly supports the hypothesis that resistance in the United States and Canada originated by migration, rather than by mutation and selection after migration. In contrast, evidence for selection of metalaxyl-resistant mutants within clonal lineages was detected among the limited sample of isolates from Europe and Israel.