Department of Plant Pathology, North Dakota State University, Fargo, ND 58105 USA

Background and objectives
Phytophthora infestans, the cause of potato late blight, is known to be a highly variable plant pathogen. The existence of physiological races within this fungus, corresponding to race-specific resistance genes in the host, has been known for some time. Recent migrations of new' genotypes of P. infestans has affected the population of this potato pathogen worldwide. Many of the 'new' genotypes of P. infestans displaced the existing 'old' population. This led to the hypothesis that the 'new' genotypes were more pathogenic or virulent than the P. infestans population that had previously existed in a specific location.

The current nomenclature used to discuss genotypes of P. infestans in the USA is based on mating type, two allozymes (Gpi/Pep), DNA fingerprint using the RG57 probe [1] and occasionally, sensitivity to metalaxyl [2]. This system, however, provides no indication of the structure of physiological races that exist within a genotype among the many solanaceous hosts of P. infestans. Furthermore, very little work has been done to determine the extent of physiological races of P. infestans within the US population [1,2]. The purpose of this study was to perform a comparative analysis of the race structure of old' and 'new' populations of P. infestans collected from potato, tomato and hairy nightshade throughout the USA

Materials and methods
R-gene differentials were obtained from the Scottish Crop Research Institute, Dundee, Scotland, and the USDA Potato Introduction Station, Sturgeon Bay, WI, USA. Leaves were detached, dipped in Murashige and Skoog salt base, and incubated at 15C with 16 h of light for 24 hours prior to inoculation. Abaxial surfaces of the youngest fully developed leaves were inoculated with 30 l droplets containing 103 zoospores/ml of P. infestans. Our culture collection contains isolates from Alabama, Colorado, Florida, Idaho, Illinois, Kansas, Minnesota, Nebraska, New Mexico, North Dakota, South Dakota, Texas, and Washington, including US-1, US-7, US-8, and US-11 genotypes. All isolates were grown on Rye B agar for approximately 15 days at 15C in the dark. Sporangia were collected from the agar using sterile distilled water and placed in the dark at 5-7C for 2 h to allow for zoospore production. Symptoms of late blight infection were read on a daily basis for four consecutive days beginning on the fourth day after inoculation. Race determinations were made based on compatible host-pathogen reactions after 7 days.

Results and conclusions
Physiological races were found to be quite diverse among the genotypes tested. The 'new' genotypes, US-7 and US-8, both A2 mating types, were generally more complex than 'older' genotypes, notably US-1 (A1). A notable exception exists with isolates of the 'new' genotype US-11 (A1) in which virulence gene complexity is substantially lower than that observed in US-7 and US-8. Interestingly, isolates of US-8 collected prior to 1997 were frequently deficient in the virulence gene corresponding to the race-resistance gene R8. Some isolates of US-8 collected in 1997 from the USA contained all virulence genes corresponding to the race-specific resistance genes in potato (R1-R11). Although US-7 has shown a host preference for tomato, isolates of this genotype recovered from potato are as virulence gene diverse as US-8, which has a host preference for potato. This is not surprising considering that very little race-specific resistance, other than R0, exists in the potato cultivars currently grown in the USA. Virulence complexity did not appear to be associated with the potato production area where the P. infestans isolate originated or the potato cultivar from which it was recovered. These results are important for potato breeding programmes involved in screening and incorporating germplasm with durable resistance. The variability noted among genotypes and within isolates of certain genotypes makes it imperative that breeding programmes use P. infestans isolates of known virulence gene composition to avoid the selection of race-specific resistance.

1.Goodwin SB, Sujkowski LS, Fry WS, 1995. Phytopathology 85, 669-76.
2.Deahl KL, Inglis DA, DeMuth SP, 1993. American Potato Journal 70, 779-95.