See more from this Session: Breeding for Resistance to Biotic Stress
Monday, November 1, 2010
Long Beach Convention Center, Exhibit Hall BC, Lower Level
Fusarium head blight (FHB) is a fungal disease caused by Fusarium graminearum. The disease causes losses in both yield and quality due to shriveled kernels and accumulation of mycotoxins in the kernels of wheat and other cereal crops. ‘Frontana’, a spring wheat cultivar originating from Brazil, is a source of resistance genes to FHB, and it is believed to express resistance to both incidence and spread of FHB (Type I and II resistance, respectively). Reciprocal backcross monosomic (RBCM) lines were developed from crosses involving Frontana and ‘Chris’, a susceptible spring wheat cultivar with variant lines monosomic for chromosomes 3A, 6A, and 4D. The RBCM lines developed from these parents were evaluated to determine which of these critical chromosomes expresses Type I and II resistance to FHB in Frontana. Spray and single floret inoculation techniques were employed to assess both types of resistance in four greenhouse experiments. Inoculations were done when 50% of the plants per experimental unit reached anthesis (Feekes Growth Stage). Data for FHB incidence, spread, and severity, as well as deoxynivalinol (DON) content and Fusarium damaged kernels (FDK) were analyzed based on observations at 21 d after inoculation. In general, RBCM lines with Frontana chromosomes generated low FHB incidence, spread, and severity scores. The RBCM lines with chromosome 3A from Frontana had the lowest FHB severity and spread scores following spray and single floret inoculation, respectively. Similarly, Frontana 3A RBCM lines exhibited the lowest FHB incidence scores after spray inoculation. These results imply the presence of a major resistance gene or QTL on chromosome 3A governing resistance to FHB incidence and spread. However, 3A most likely interact with other chromosomes to confer resistance to FHB incidence and spread considering that Frontana, the cultivar, typically expressed higher levels of resistance to FHB incidence and spread. Chromosome 4D seem to be important for both resistance to incidence and spread whereas chromosome 6A plays a role in restricting spread of FHB within the spike.