Abstract

Powdery mildew (Erysiphe polygoni DC [synonym E. betae {Vanha} Weltzien]) of sugar beet (Beta vulgaris L.) has been a significant problem in many sugar beet growing areas of the United States since the first serious epidemic in 1974. Disease has been attributed solely to the asexual stage of the pathogen in the United States, except for one report of the perfect stage in a single field in Washington coincidental with the 1974 epidemic (1). In August 2001, ascomata were observed in several fields in Owyhee County in southwestern Idaho near Grand View. The perfect stage was widespread and easily found, and in one field the surfaces of leaves collected from 50 randomly sampled plants were between 10 and 90% covered with ascomata. Subsequently, the ascigerous stage was found in September and October in multiple fields in three additional counties in southwestern and south-central Idaho and two counties in northern Colorado. Ascomata were found on 12 commercial varieties in the two states and six breeding lines in Colorado. Asci contained one to four hyaline or yellow-to-golden pigmented ascospores per ascus. Ascomata observed in Idaho and Colorado are similar to those described from Europe (2). Ascospores appeared intact after leaves were dried and stored at 4 to 7°C more than 4 weeks. However, after leaves with ascomata were dried and stored at 24 to 27°C for 1 week or more, ascomata and asci appeared intact microscopically, but ascospores were no longer delineated and appeared desiccated or degraded. Because the ascigerous stage provides a means of genetic recombination, there is the potential for races of the pathogen to arise with greater frequency. This has serious implications for managing fungicide resistance and breeding for disease resistance to sugar beet powdery mildew.

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