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Sclerotinia stem rot [caused by Sclerotinia sclerotiorum (Lib.) de Bary] is considered the second most important cause of yield loss in soybean [Glycine max (L.) Merr]. Soybean cultivars show variability in susceptibility, but no complete resistance to the disease has been reported and little information on the genetics of resistance is available. The objective of this study was to identify putative quantitative trait loci (QTLs) associated with Sclerotinia stem rot resistance in soybean. Recombinant inbred lines (RILs) from five populations were developed by crossing Williams 82, a susceptible cultivar, with five cultivars exhibiting partial resistance: Corsoy 79, Dassel, DSR173, S19‐90, and Vinton 81. The F2 to F5 generations were advanced by single seed descent. Parental polymorphism was tested with 507 simple sequence repeat (SSR) primers from the integrated linkage map of soybean, and primers were selected for progeny screening in the five populations on the basis of polymorphism and distribution in the genome. Five hundred RILs, consisting of 100 F5:6 lines from each population, were evaluated for resistance to Sclerotinia sclerotiorum isolate 143 by a detached leaf method in the laboratory to measure lesion area on leaves inoculated with mycelium plugs. Single degree‐of‐freedom contrasts in PROC MIXED and interval analysis were used to detect putative QTLs. Twenty‐eight putative QTLs for resistance to Sclerotinia stem rot of soybeans were identified on 15 different linkage groups in five RIL populations by single degree‐of‐freedom contrasts. Alleles involved in reduction of lesion size came from both the resistant and susceptible parents, and transgressive segregates were identified in two populations. The amount of phenotypic variation explained by individual QTLs ranged from 4 to 10%. Seven QTLs on seven different linkage groups were identified in multiple populations with some QTL regions corresponding with mapped resistance genes and resistance gene analogs. The results suggest that several genes control resistance to Sclerotinia stem rot and that markers could facilitate an initial screen of segregating breeding populations.

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White mold (WM), incited by Sclerotinia sclerotiorum (Lib.) de Bary, is a serious disease of common bean (Phaseolus vulgaris L.). However, plant breeders have had very limited success in developing resistant (R) cultivars. Molecular markers linked to genes for R to WM may improve selection for R. The objective was to identify random amplified polymorphic DNA (RAPD) markers linked to quantitative trait loci (QTL) for partial physiological resistance (PPR), partial field resistance (PFR), porosity over the furrow (POF), and plant height (PH) in a linkage map by means of recombinant inbred lines (RILs) from the cross ‘PC‐50’ (R) × XAN‐159 (susceptible). The parents and RILs were inoculated in two separate greenhouse experiments for each isolate and were also infected naturally in the field. Significant correlations (0.39, 0.47) were found for the WM reactions in the greenhouse and field. Nine candidate QTL were found affecting PPR isolate 152 (comparison‐wise P < 0.05) with strong evidence (genome‐wise P < 0.01) for three QTL on linkage groups (LGs) 4, 7, and 8, based on composite interval mapping analysis. Candidate QTL affecting PPR to isolate 279 were found on LGs 2, 3, 4, 7, and 8 with very strong evidence (genome‐wise P < 0.001) for a QTL linked to the C locus for seedcoat pattern. Seven candidate QTL for PFR were observed on LGs 4, 7, 8, and 11. Six of the seven candidate QTL for PFR were found in the same locations as QTL for PPR. However, two of the seven genomic regions were associated with PFR and POF that may contribute to disease avoidance.

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.