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  • Author or Editor: Richard Delorme x
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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.

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Understanding the genomic associations among disease resistance loci will facilitate breeding of multiple disease resistant cultivars. We constructed a genetic linkage map in common bean (Phaseolus vulgaris L.) containing six genes and nine quantitative trait loci (QTL) comprising resistance to one bacterial, three fungal, and two viral pathogens of bean. The mapping population consisted of 79 F5:7 recombinant inbred lines (RILs) derived from a `Dorado'/XAN 176 hybridization. There were 147 randomly amplified polymorphic DNA (RAPD) markers, two sequence characterized amplified region (SCAR) markers, one intersimple sequence repeat (ISSR) marker, two seedcoat color genes R and V, the Asp gene conditioning seed brilliance, and two rust [Uromyces appendiculatus var. appendiculatus (Pers.:Pers) Unger] resistance genes: one conditioning resistance to Races 53 and 54 and the other conditioning resistance to Race 108. These markers mapped across eleven linkage groups, one linked triad, and seven linked pairs for an overall map length of 930 cM (Kosambi). Genes conditioning resistance to anthracnose (Co-2) [Colletotrichum lindemuthianum (Sacc. and Magnus) Lams.-Scrib.], bean rust (Ur-5), and bean common mosaic virus (I and bc-3) (BCMV) did not segregate in this population, but were mapped by inference using linked RAPD and SCAR markers identified in other populations. Nine previously reported quantitative trait loci (QTL) conditioning resistance to a variety of pathogens including common bacterial blight [Xanthomonas campestris pv. phaseoli (Smith) Dye], ashy stem blight [Macrophomina phaseolina (Tassi) Goid.], and bean golden mosaic virus (BGMV), were located across four linkage groups. Linkage among QTL for resistance to ashy stem blight, BGMV, and common bacterial blight on linkage group B7 and ashy stem blight, BGMV, and rust resistance loci on B4 will complicate breeding for combined resistance to all four pathogens in this population.

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