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Phillip N. Miklas, Richard Delorme and Ron Riley

Host resistance is an important component of integrated disease management strategies for control of Sclerotinia white mold disease in snap bean (Phaseolus vulgaris L.). Few resistant snap bean cultivars have been bred, however, because genetic resistance to white mold is not well understood. This study was conducted to examine inheritance and identify quantitative trait loci (QTL) for white mold resistance in an F5:7 recombinant inbred line (RIL) population (`Benton'/NY6020-4). `Benton' snap bean is susceptible to white mold. Snap bean germplasm line NY6020-4 has partial resistance. The parents and 77 F5:7 RILs were tested for resistance to white mold across four greenhouse and two field environments. Moderately high heritability estimates were observed for straw test (0.73) and field (0.62) reaction. Selective mapping of 27 random amplified polymorphic DNA (RAPD) markers detected two QTL conditioning resistance to white mold on linkage groups B6 and B8 of the core map. The B6 QTL explained 12% and B8 QTL 38% of the variation for disease reaction in the straw test. The two QTL explained 13% and 26% disease reaction in the field, respectively. Favorable alleles for all the QTL were derived from NY6020-4, except for the B6 QTL conditioning resistance to white mold in the field, which was derived from `Benton'. The B6 QTL was located near the Ur-4 rust resistance gene, and was associated with canopy height and lodging traits that condition disease avoidance. The B8 QTL was associated with increased internode length, an undesirable trait in snap bean, which may hamper use of white mold resistance derived from NY6020-4.