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  • Author or Editor: Phillip N. Miklas x
  • Journal of the American Society for Horticultural Science x
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Among light red and dark red kidney common bean (Phaseolus vulgaris L.) varieties, pink seedcoat color (light red kidney) is dominant to dark red, but when Red Mexican varieties (with dark red seedcoats) are crossed with dark red kidney varieties, dark red seedcoat is dominant to the pink segregants observed in an F2 population. A genetic investigation of this reversal of dominance was performed by making crosses in all combinations among standard varieties of the four recessive-red market classes—Light Red Kidney `California Early Light Red Kidney', Pink `Sutter Pink', Red Mexican `NW 63', and Dark Red Kidney `Montcalm'—and observing segregation for seedcoat colors in F2 and F3 progenies. The data were consistent with the hypothesis that `NW 63' carries a new allele at Rk, viz., rk cd, where cd stands for convertible dark red kidney. Thus, C rk cd expresses dark red kidney seedcoats and c u rk cd expresses pink seedcoats. Also, C B rk cd expresses garnet brown seedcoats, whereas C B rk d expresses liver brown seedcoat color. Thus, we propose the gene symbol rk cd for the Rk locus gene in `NW 63'. The rk gene from Light Red Kidney `Redkloud' and `Sutter Pink' was backcrossed (with c u b v) into the recurrent parent 5-593, a Florida dry bean breeding line with seedcoat genotype P [C r] J G B V Rk. In the F2 progenies of BC2 to 5-593, the c u b v rk segregants from `Redkloud' gave true pink seedcoats, whereas those derived from `Sutter Pink' gave consistently very weak pink color under humid Florida growing conditions. We propose the gene symbol rk p, where p stands for pale pink, for the distinctive rk allele in `Sutter Pink'. The more general implications of the above findings were discussed.

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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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High levels of resistance to common bacterial blight caused by Xanthomonas campestris pv. phaseoli (Smith) Dye (Xcp) have been observed for tepary bean (Phaseolus acutifolius A. Gray var. latifolius Freeman). However, the inheritance of resistance from this source is unknown for many lines. The inheritance of common bacterial blight resistance was studied in four tepary bean lines crossed with the susceptible tepary bean MEX-114. Progenies were inoculated with a single Xcp strain 484a. Segregation ratios in the F2 generation suggested that resistance in Neb-T-6-s and PI 321637-s was governed by one dominant gene, and Neb T-8a-s had two dominant genes with complementary effects. These hypotheses for inheritance of resistance were supported by various combinations of F1, F3, BC1Pn segregation data in all lines except PI 321637-s where an additional minor-effect gene with recessive inheritance was indicated. Generation means analyses corroborated that multiple resistance genes were present in PI 321638-s. Lack of segregation for susceptibility among testcrosses for allelism between Neb-T-6-s/PI 321637-s, Neb-T-6-s/Neb-T-8a-s, PI 321637-s/Neb-T-8a-s, and PI 321637-s/PI 321638-s, suggested that one or more loci conditioning resistance to common bacterial blight were in common across the four tepary lines.

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The objective of this study was to evaluate the degree of RAPD marker variability between and within commercially productive market classes representative of the Andean and Middle American gene pools of common bean (Phaseolus vulgaris L.). Six sets of near-isogenic lines were screened with oligonucleotide primers in the polymerase chain reaction-based RAPD assay. Simultaneous analyses with at least three sets of lines enabled us to score RAPD markers between the two major gene pools, races within the same gene pool, and different genotypes of the same race (within race). A “three-tiered” pattern of polymorphism was observed: between gene pools> between races> within races. The overall level of polymorphism between the Andean and Middle American gene pools was 83.4%. The overall level of polymorphism between races within the same gene pool was similar for Andean races (60.4%) and Middle American races (61.7%). The level of polymorphism between related commercial navy bean lines was 39.2% and between related commercial snap bean lines was 53.6 %. The inherent simplicity and efficiency of RAPD analyses, coupled with the number of polymorphisms detectable between related commercial genotypes, should facilitate the construction of RAPD-based genetic linkage maps in the context of populations representative of most bean breeding programs.

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Bean golden mosaic virus (BGMV) is a devastating disease of common bean (Phaseolus vulgaris L.) in tropical America. The disease is effectively controlled by combinations of genetic resistances. The most widely deployed source of resistance to BGMV is a recessive gene (bgm-1) derived from the dry bean landrace cultivar Garrapato (Mexico) that conditions a nonmosaic partial resistance response to the pathogen. To expedite introgression of partial resistance into snap bean for southern Florida and other susceptible dry bean market classes for the Caribbean and Central American regions, a RAPD marker tightly linked to bgm-1 has been identified. Two contrasting DNA bulks, one consisting of five BGMV-resistant and the other five susceptible F6 recombinant inbred lines, were used to screen for polymorphic fragments amplified by 300 decamer primers in the polymerase chain reaction. RAPDs generated between the bulks were analyzed across F2 populations segregating for the marker and the gene. One codominant RAPD marker (R2570/530) tightly linked to the recessive resistance gene bgm-1 was found. The 530-base pair (bp) fragment was linked in repulsion with bgm-1 and the other 570-bp fragment was linked in coupling. No recombinants between R2570/530 and bgm-1 were observed among 91 F2 progeny from one dry bean population, and there were two recombinants (4.2 cM) observed among 48 F2 progeny combined across four snap bean populations. Assays of R2570/530 across susceptible germplasm and lines likely to have the `Garrapato'-derived partial resistance to BGMV have revealed that the codominant marker is gene-pool nonspecific and maintains its original linkage orientation with the recessive bgm-1 gene through numerous meioses. The codominant marker is useful for rapidly introgressing partial resistance to BGMV into susceptible germplasm.

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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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