First author: Department of Plant Pathology, University of Wisconsin, Madison 53706; second author: Departments of Botany and Statistics, University of Wisconsin, Madison 53706; and third and fourth authors: Department of Plant Pathology, Washington State University, Pullman 99164
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Accepted for publication 19 February 2004.
Sclerotinia sclerotiorum, the causal agent of potato stem rot, is prevalent and poorly managed on potatoes in the Columbia Basin of Washington. Because of the ubiquitous nature of the fungus and high crop diversity within the Columbia Basin, understanding the population structure and the potential for outcrossing of the pathogen would be helpful in developing disease management strategies. The population structure of S. sclerotiorum in the Columbia Basin from potato was examined using microsatellite markers and mycelial compatibility. Analysis of molecular variance revealed that 92% of the variability among 167 isolates was found within subpopulations, with limited, yet statistically significant impact of the collection date, but not the year or location of collection. Linkage disequilibrium and index of association analyses noted a potential for outcrossing in two locations, which was substantiated by the discovery of recombinant ascospores in three field-generated apothecia from the 12 apothecia examined. Microsatellite haplotypes were not correlated with mycelial compatibility groups. This high haplotypic diversity did not seem to impact pathologically important phenotypes. Greenhouse inoculations of potato plants exhibited no significant differences in aggressiveness on potato stems. Moreover, in vitro studies of response to fungicides and temperature stimuli yielded no significant differences among studied isolates. These findings illustrate the potential for outcrossing in warm temperate regions of North America, where a diversity of crops are planted simultaneously and in neighboring fields. This study also indicates that the unsatisfactory management of potato stem rot is likely not directly attributable to genetic factors, but to gaps in agricultural practices.
© 2004 The American Phytopathological Society