Abstract
Barley yellow dwarf (BYD) is one of the most important viral diseases in small grains, including oat (Avena sativa L.). Breeding for BYD tolerance is an effective and efficient means to control the disease. Characterization of major sources of tolerance, and identification of marker and the trait associations, will directly benefit breeding for BYD tolerance. Genomic regions underlying BYD tolerance were mapped and characterized in an oat population consisting of 152 recombinant inbred lines from the cross of 'Ogle' (tolerant)/MAM17-5 (sensitive). Tolerance was evaluated in replicated field trials across 2 years under artificial inoculation with viruliferous aphids harboring BYD virus isolate PAV-IL. Composite interval mapping was used for quantitative trait loci (QTLs) analysis with a framework map consisting of 272 molecular markers. Four QTLs, BYDq1, BYDq2, BYDq3 and BYDq4, for BYD tolerance were identified on linkage groups OM1, 5, 7 and 24, respectively. All but BYDq2 were consistently detected across both years. Significant epistasis was found between some QTLs. The final model including the epistatic effect explained 50.3 to 58.2% of the total phenotypic variation for BYD tolerance. Some QTLs for BYD tolerance were closely linked to QTLs for plant height and days to heading. Potential problems with QTL mapping for BYD tolerance have been discussed. The identified association of markers and tolerance should be useful to pyramid favorable alleles for BYD tolerance into individual oat lines.
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Acknowledgements
The authors thank Nancy McCoppin and Leslie L. Domier, USDA-ARS, for maintaining aphid cultures, and Norman J. Smith for excellent assistance with planting, inoculating and managing field plots. This research was supported by Hatch Grant No. WIS 03920 and a Plant Breeding and Genetics Fellowship from Pioneer Hi-Bred International, Inc.
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Zhu, S., Kolb, F.L. & Kaeppler, H.F. Molecular mapping of genomic regions underlying barley yellow dwarf tolerance in cultivated oat (Avena sativa L.). Theor Appl Genet 106, 1300–1306 (2003). https://doi.org/10.1007/s00122-003-1198-z
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DOI: https://doi.org/10.1007/s00122-003-1198-z