Wednesday, November 15, 2006 - 2:10 PM
219-4
RAPD Markers Associated with Resistance to Blackleg Disease in Brassica Species.
Blackleg, caused by Leptosphaeria maculans, is a serious disease of Brassica species. This disease is controlled most effectively and economically by the use of resistant cultivars. In an effort to identify molecular markers associated to resistance to blackleg disease, 15 accessions from the USDA Brassica germplasm collections, representing diploid (A) and tetraploid (AC) genomes respectively; and 9 cultivated cultivars from the National Winter Canola Variety Trials (NWCVT) all carrying the AC genomes were screened with RAPD and SSR primers. All 24 genotypes were screened for resistance to blackleg disease at the cotyledon stage. The results indicated that 45.84% of the cultivars were resistant, among which 45% were diploids genotypes with the A genome. RAPD primers, previously reported to be associated with resistance to blackleg disease in the B genome of B. nigra were used to determine if similar markers can be identified in the A and AC genomes. Correlation and regression analysis indicated that five amplified fragments from three of the primers: OPE03-4000bp, OPI01-280bp, OPE16-1100bp, OPE16-1300bp, and OPE16-1900bp were significantly associated with blackleg resistance rating at the cotyledon growth stage. The SSR primers used in this study, however, did not result in any association with resistance to blackleg disease rating. The amplified fragments from the RAPD primers analyzed were also used to measure the degree of relatedness among and within the Brassica species in this study. The resulting phylogenetic tree showed that the genotypes in this study are closely grouped within species. The results from this study demonstrated that, RAPD primers could potentially be used to identify DNA markers that are associated with the blackleg disease resistance within and across the diverse genomes of Brassica species, and that resistance to L. maculans may also exist in the A and/or C genomes similar to previous findings on the B genome.
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