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Halo blight is one of the most important bacterial diseases of common beans (Phaseolus vulgaris L.). It is serious under moderate temperature and high humidity conditions. The disease is caused by a seed-borne bacterium, Pseudomonas syringae pv. phaseolicola (Burkh.) Dowson (Psp). The inheritance of leaf reactions to Psp, flower, and stem color was studied using greenhouse-grown 109 F₉ recombinant inbred lines (RI) from the P. vulgaris cross BelNeb 1 [resistant (R)] (USDA/NE) × A 55 [susceptible (S)] (CIAT). Two Psp strains, HB16 (NE) and 83-Sc2A (NE), were inoculated using the water-soaking method. A segregation ratio of 1 R:1 S RI lines were observed for disease reactions in leaves for both strains indicating major gene control. The presence of recombinants for SR, RS to the strains indicated that different genes were involved. Stem (SC) and flower (FC) color traits were each determined by two major genes. Linkages were found for reactions to the two Psp strains and also between FC and SC. No linkages were observed from FC and also SC with reactions to Psp strains.

Halo blight (HB), brown spot (BS), and rust incited by the bacterial pathogens Pseudomonas syringae pv. phaseolicola (Psp), Pseudomonas syringae pv. syringae (Pss) and the fungal pathogen Uromyces appendiculatus, respectively, are important diseases of common beans. The objectives were to construct a RAPD linkage map, and to locate HB and BS resistance genes and genes for some other traits. One-hundred-seventy RAPD markers were mapped in 78 RI lines of the cross BelNeb 1 and A 55. Eleven main and nine minor linkage groups were identified. MAPMAKER/QTL, interval mapping, was used to identify genomic regions involved in the genetic control of the traits. One region was found to control HB leaf reactions to strain HB16 while three regions controlled reactions to strain HB 83. These regions accounted for 22% and 18%, 17%, and 17% of phenotypic variation of resistance, respectively. Four putative QTLs were identified for resistance to BS, and accounted for 37%, 26%, 23%, and 19% of the phenotypic variation. Rust resistance was determined by a single major gene to both rust strains US85NP 5-1 and D82vc74fh. However, linked markers were not identified. The V gene controlling flower and stem color was tightly linked with the Operon marker O10.620.

Breeding for resistance is a major method to control the common bacterial blight disease caused by Xanthomonas campestris pv phaseoli (Xcp) in common bean (Phaseolus vulgaris L.). It is necessary to determine if prior inoculation of the first trifoliolate leaf with Xcp will influence the subsequent reaction in other plant parts through induced resistance. It is difficult to get an accurate estimate of heritability (H) of disease reaction in pods since environment (E) greatly affects the H estimate if flowering occurs over extended time periods. Thus the disease reaction in attached pods vs detached pods was also observed. Four common bean lines were used in a split plot design with two replications. Two bacterial strains were used for inoculations. Two growth chambers were used as replicates. The first trifoliolate leaves, later developed leaves and attached pods and detached pods were inoculated. No effect of prior inoculation on the disease reactions of subsequently inoculated leaves and pods were observed indicating that the different plant parts can be inoculated at different times. Detached and attached pods showed similar disease symptoms. The former may be used to reduce E variance and improve H estimates.

Breeding for resistance is an important strategy to manage common bacterial blight disease caused by Xanthomonas campestris pv. phaseoli (E. Smith) Dye (Xep) in common bean (Phaseolus vulgaris L.). It is necessary to determine if prior inoculation of the first trifoliolate leaf with Xcp influences subsequent reactions in other plant organs by increasing or decreasing resistance to Xcp. It is difficult to get an accurate estimate of heritability of disease reaction in pods since environment greatly affects the heritability estimate if flowering occurs over extended time periods. Thus, the disease reaction in attached pods versus detached pods was compared. A split-split plot design with two replications (growth chambers as blocks) was used, with bean lines as the whole-plot factors, Xcp strains as subplot factors, and bacterial inoculation treatments for leaf reactions or pod treatments as split-split plot factors. The first trifoliolate leaves, later developed leaves, and attached and detached pods were inoculated. No effects of prior inoculation on the disease reactions of subsequently inoculated leaves and pods were observed, indicating that the different plant organs can be inoculated at different times. The fact that detached and attached pods showed similar disease symptoms would suggest use of the former to reduce environment variance and improve heritability estimates of resistance.

The inheritance and heritability (H) of leaf and pods reactions and seed infection of common beans (Phaseolus vulgaris L.) to Xanthomonas campestris pv. phaseoli (Smith) Dye (Xcp) were studied in three crosses along with flower and stem color, and the association of reactions to Xcp in the plant organs. Recombinant inbred lines from the crosses `PC 50' × XAN 159, BAC 6 × HT 7719, and BelNeb 1 × A 55 were used. Quantitative inheritance patterns were observed for disease reactions in leaves, pods, and seeds. Stem and flower color were inherited qualitatively. Low to intermediate and intermediate H estimates were found for pod reactions when inoculated on the same time, allowing the infection to occur in a uniform environment. Intermediate to high H estimates were found for leaf and seed reactions to Xcp, respectively. Significant positive intermediate to moderately high correlations were found between the reactions to Xcp of the first trifoliolate with later-developed leaves and pods in all three populations. The moderately high genetic correlations between leaves and pods suggested that some common genes may control the reactions to Xcp in these plant organs. No association was detected between flower or stem color and reactions to Xcp.

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 (v^lae ) 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.

Common blight, web blight, and rust, incited by the bacterial pathogen Xanthomonas campestris pv. phaseoli (Smith) Dye (Xcp) and the fungal pathogens Thanatephorus cucumeris (Frank) Donk (Tc) and Uromyces appendiculatus (Pers.:Pers) Unger, respectively, are important diseases of common beans (Phaseolus vulgaris L.). The objectives of were to construct a linkage map, and to locate CBB, rust, and WB resistances and plant architecture traits using RAPDs. Ten linkage groups were identified. Eighty-nine RAPD markers and rust resistance were mapped in 128 RI lines of the cross BAC-6 and HT-7719. Regression analysis and interval mapping using MAPMAKER/QTL were used to identify genomic regions involved in the genetic control of the traits. One, two, two, and three putative QTLs were identified for leaf, seed, and pod reactions to Xcp, and foliar reaction to Tc. These regions accounted for 11%, 9%, 32%, and 30% of the phenotypic variation in the resistances. Two, two, and three regions were identified for plant uprightness, branch density, and pod distribution. These regions accounted for 27%, 13%, and 16% of the phenotypic variation. Unassigned marker G17d influenced some of the phenotypic variation in all three traits. A rust resistance gene controlling pustule size on primary leaves was located in linkage group 1.

Our objective was to identify quantitative trait loci (QTL) for seed weight, length, and height segregating in a recombinant inbred line population derived from the common bean (Phaseolus vulgaris L.) cross `PC-50' × XAN-159. The parents and progeny were grown in two separate greenhouse experiments in Nebraska, and in field plots in the Dominican Republic and Wisconsin. Data analysis was done for individual environments separately and on the mean over all environments. A simple linear regression analysis of all data indicated that most QTL appeared to be detected in the mean environment. Based on these results, composite interval mapping (CIM) analysis was applied to the means over environments. For seed weight, strong evidence was indicated for five QTL on common bean linkage groups (LGs) 3, 4, 6, 7, and 8. Multiple regression analysis (MRA) indicated that these QTL explained 44% of the phenotypic variation for the trait. Weaker evidence was found for three additional candidate QTL on bean LGs 4, 5, and 8. All eight markers associated with these QTL were significant in a MRA where the full model explained 63% of the variation among seed weight means. For seed length, CIM results indicated strong evidence for three QTL on LG 8 and one on LG 2. Three additional putative QTL were detected on LGs 3, 4, and 11. The markers associated with the three seed length QTL on LG 8, and the QTL on LGs 2 and 11 were significant in a MRA with the full model explaining 48% of the variation among seed length means. For seed height, three QTL on LGs 4, 6, and 11 explained 36% of the phenotypic variation for trait means. Four of the seven QTL for seed length and two of three QTL for seed height also appeared to correspond to QTL for seed weight. Four QTL for common bacterial blight resistance [Xanthomonas campestris pv. phaseoli (Smith Dye)] and for smaller seed size were associated on LGs 6, 7, and 8. The implications of these findings for breeders is discussed.

Random amplified polymorphic DNA (RAPD) markers were used to construct a partial linkage map in a recombinant inbred population derived from the common bean (Phaseolus vulgaris L.) cross BAC 6 × HT 7719 for studying the genetics of disease resistance in common bean. The linkage map spanned 545 cM and included 75 of 84 markers used in this study. The population of 128 recombinant inbred lines was evaluated for resistance to common bacterial blight, foliar resistance to web blight [WB; Thanatephorus cucumeris (Frank) Donk], and resistance to rust [Uromyces appendiculatus var. appendiculatus (Pers.:Pers) Unger]. Common bacterial blight [CBB; Xanthomonas campestris pv. phaseoli (Smith) Dye] resistance was evaluated for CBB strain Epif-IV in later-developed trifoliolate leaves and for CBB strain EK-11 in seeds, first trifoliolate leaves, later-developed trifoliolate leaves, and pods. In addition, lines were rated for plant uprightness and branch density. Two to six markers accounted for 14% to 34% of the phenotypic variation for each trait. Significant marker locustrait associations were found for 14 mapped loci and 7 of the 9 unmapped markers. The distribution of detected QTL appeared to be nonrandom with most significant markers associated with more than one trait or closely linked to markers significantly associated with variation for a different trait. One marker, BC409₁₂₅₀, was significantly associated with WB resistance, resistance for CBB strain Epif-IV in later-developed trifoliolate leaves, and resistance for CBB strain EK-11 in first trifoliolate leaves, later-developed trifoliolate leaves, and pods. A rust resistance gene was mapped in an interval 14.6 cM from RAPD marker H19₁₀₅₀ and 12.5 cM from marker AJ16₂₅₀.