Molecular mapping of qualitative and quantitative loci for resistance to Leptosphaeria maculans causing blackleg disease in canola (Brassica napus L.)
2012
Raman, R. | Taylor, B. | Marcroft, S. | Stiller, J. | Eckermann, P. | Coombes, N. | Rehman, A. | Lindbeck, K. | Luckett, D. | Wratten, N. | Batley, J. | Edwards, D. | Wang, X. | Raman, H.
Blackleg, caused by Leptosphaeria maculans, is one of the most important diseases of oilseed and vegetable crucifiers worldwide. The present study describes (1) the construction of a genetic linkage map, comprising 255 markers, based upon simple sequence repeats (SSR), sequence-related amplified polymorphism, sequence tagged sites, and EST-SSRs and (2) the localization of qualitative (race-specific) and quantitative (race non-specific) trait loci controlling blackleg resistance in a doubled-haploid population derived from the Australian canola (Brassica napus L.) cultivars Skipton and Ag-Spectrum using the whole-genome average interval mapping approach. Marker regression analyses revealed that at least 14 genomic regions with LOD ≥ 2.0 were associated with qualitative and quantitative blackleg resistance, explaining 4.6–88.9 % of genotypic variation. A major qualitative locus, designated RlmSkipton (Rlm4), was mapped on chromosome A7, within 0.8 cM of the SSR marker Xbrms075. Alignment of the molecular markers underlying this QTL region with the genome sequence data of B. rapa L. suggests that RlmSkipton is located approximately 80 kb from the Xbrms075 locus. Molecular marker-RlmSkipton linkage was further validated in an F2 population from Skipton/Ag-Spectrum. Our results show that SSR markers linked to consistent genomic regions are suitable for enrichment of favourable alleles for blackleg resistance in canola breeding programs.
Показать больше [+] Меньше [-]Rosy Raman, Belinda Taylor, Steve Marcroft, Jiri Stiller, Paul Eckermann, Neil Coombes, Ata Rehman, Kurt Lindbeck, David Luckett, Neil Wratten, Jacqueline Batley, David Edwards, Xiaowu Wang, Harsh Raman
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Эту запись предоставил University of Adelaide