Common bean (Phaseolus vulgaris L.) exhibits a wide variety of seed coat patterns and colors. From a historical perspective, extensive genetic analyses have identified specific genes that control seed coat pattern (T, Z, L, J, Bip, and Ana) and color (P, C, R, J, D, G, B, V, and Rk). Many of these genes exhibit epistatic interactions with other genes, interactions that define the many seed coat patterns and colors observed within the species. To better understand these complex interactions, we began a molecular marker discovery program that previously identified random amplified polymorphic DNA (RAPD) markers linked to many of these genes. We report here the discovery of RAPD markers linked to three additional genes-C, G, and V. These markers, and five RAPD markers we previously discovered linked to other seed coat pattern and color genes, were converted into easily scorable sequence tagged site (STS) markers. We next placed these markers onto a common molecular map shared by the Phaseolus research community and demonstrated a generally wide distribution of the genes throughout the common bean genome. A few previously unrecognized linkages were discovered. The probable existence of multiple genes controlling growth habit in common bean is discussed. Our approach demonstrates the usefulness and feasibility of marker discovery in one population followed by accurate mapping of that marker onto a core, community-wide map.

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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.

Randomly amplified polymorphic DNA (RAPD) molecular markers were used to construct a partial genetic linkage map in a recombinant inbred population derived from the common bean (Phaseolus vulgaris L.) cross PC-50 × XAN-159 for studying the genetics of bacterial disease resistance in common bean. The linkage map spanned 426 cM and included 168 RAPD markers and 2 classical markers with 11 unassigned markers. The seventy recombinant inbred lines were evaluated for resistance to two strains of common bacterial blight [Xanthomonas campestris pv. phaseoli (Smith) Dye] (Xcp). Common bacterial blight (CBB) resistance was evaluated for Xcp strain EK-11 in later-developed trifoliolate leaves and for Xcp strains, DR-7 and EK-11, in first trifoliolate leaves, seeds, and pods. One to four quantitative trait loci (QTLs) accounted for 18% to 53% of the phenotypic variation for traits. Most significant effects for CBB resistance were associated with one chromosomal region on linkage group 5 and with two regions on linkage group 1, of the partial linkage map. The chromosomal region (a 13-cM interval) in linkage group 5 was significantly associated with resistance to Xcp strains DR-7 and EK-11 in leaves, pods, and seeds. The regions in linkage group 1 were also significantly associated with resistance to both Xcp strains in more than one plant organ. In addition, a seedcoat pattern gene (C) and a flower color gene (vlae) were mapped in linkage groups 1 and 5, respectively, of the partial linkage map. The V locus was found to be linked to a QTL with a major effect on CBB resistance.

Diseases of beans (Phaseolus vulgaris L.) are primary constraints affecting bean production. Information on tagging and mapping of genes for disease resistance is expected to be useful to breeders. The objectives of this study were to develop a random amplified polymorphic DNA (RAPD) marker linkage map using 78 F9 recombinant inbred (RI) lines derived from a Middle-American common bean cross Great Northern Belneb RR-1 [resistant to common bacterial blight (CBB) and halo blight (HB)] × black A 55 [dominant I gene resistance to bean common mosaic potyvirus] and to map genes or QTL (quantitative trait loci) for resistance to CBB, HB, BCMV (bean common mosaic virus), and BCMNV (bean common mosaic necrosis virus) diseases. The RI lines were evaluated for resistance to leaf and pod reactions to Xanthomonas campestris pv. phaseoli (Xcp) (Smith Dye) strain EK-11, leaf reactions to two Pseudomonas syringae pv. phaseolicola (Psp) (Burkholder) Young et al. (1978) strains HB16 and 83-Sc2A, and BCMV strain US-5 and BCMNV strain NL-3. The linkage map spanned 755 cM, including 90 markers consisting of 87 RAPD markers, one sequence characterized amplified region (SCAR), the I gene, and a gene for hypersensitive resistance to HB 83-Sc2A. These were grouped into 11 linkage groups (LG) corresponding to the 11 linkage groups in the common bean integrated genetic map. A major gene and QTL for leaf resistance to HB were mapped for the first time. Three QTL for leaf reactions to HB16 were found on linkage groups 3, 5, and 10. Four regions on linkage groups 2, 4, 5, and 9, were significantly associated with leaf reactions to HB strain 83-Sc2A. The gene controlling the hypersensitive reaction to HB 83-Sc2A mapped to the same region as the QTL on LG 4. The I locus for resistance to BCMV and BCMNV was mapped to LG 2 at about 1.4 cM from RAPD marker A10.1750. Five and four markers were significantly associated with QTL for resistance to CBB in leaves and pods, respectively, with four of them associated with resistance in both plant organs. A marker locus was discovered on LG 10, W10.550, which could account for 44% and 41% of the phenotypic variation for CBB resistance in leaves and pods, respectively. QTL for resistance in pod to CBB, leaf resistance to HB, and the I gene were linked on LG 2.

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The inheritance of resistance to bean golden mosaic virus (BGMV) in common bean (Phaseolus vulgaris L.) was studied in crosses between susceptible bean variety XAN176 and resistant breeding lines 9236-6 (T446/A429) and 9245-94 (DOR303/T968). Disease response data were taken on plants from four generations derived from each cross (parents, F1, F2, and backcrosses (BCs) of F1 to both parents) at 25 days after plants were inoculated with BGMV, using whiteflies (Bemisia argentifolii Bellows & Perring) as vectors. The segregation ratios obtained from F2 and BC generations were consistent with the hypothesis that resistance in 9236-6, which prevents a chlorotic response, is conferred by a single recessive gene. The disease response in 9245-94 was controlled by two genes—a dominant gene controlling a dwarfing reaction and a recessive resistance gene preventing a chlorotic response to BGMV infection. An allelism test demonstrated that the gene controlling resistance in 9236-6 is nonallelic with the recessive gene controlling resistance in 9245-94. The gene symbol bgm is proposed for the recessive resistance gene (originally from A429) in 9236-6. The gene symbol bgm-2 is proposed for the recessive resistance gene (originally from DOR303) in 9245-94.