Cultivated tepary bean (Phaseolus acutifolius A. Gray var. latifolius Freeman) has potential for production during the hot, dry seasons in the tropics. Bean golden mosaic virus (BGMV), however, seriously limits production of Phaseolus spp. in such environments. Twelve select tepary beans were evaluated for reaction to BGMV across four field nurseries near Isabela, Puerto Rico. Disease reaction was principally determined by measurement of seed yield (kg·ha–1) and weight (g 100/seeds). All tepary beans possessed some tolerance to BGMV, as they produced comparatively moderate seed yield despite expression of severe foliar yellow mosaic symptoms. On average, tepary bean yielded 133% of the BGMV-resistant dry bean (Phaseolus vulgaris L.) control `Dorado'. Four teparies, Neb-T-6-s, GN-610-s, Neb-T-8a-s, and PI 321637-s, expressed superior tolerance to BGMV as they yielded above the trial mean in at least three of four trials. Harvested seed quality was uniformly poor across all lines, averaging 18% less weight than in the non-BGMV trials. The combination of the observed tolerance with escape mechanisms and cultural disease control practices may enable production of tepary bean in regions and seasons that experience moderate to severe BGMV epidemics.
Phillip N. Miklas and Jose Santiago
Phillip N. Miklas and J. Rennie Stavely
Foliar diseases are a major constraint to cultivated tepary bean (Phaseolus acutifolius A. Gray var. latifolius Freeman) production in some environments. The reactions of 12 cultivated teparies to eight individual races (41, 47, 49, 51, 53, 58, 67, and 73) of the bean rust fungus Uromyces appendiculatus (Pers.) Unger var. appendiculatus maintained at Beltsville, Md., were examined under greenhouse conditions. These diverse races, used together, overcome all of the major rust-resistance genes present within the 19 host differential cultivars of common bean (Phaseolus vulgaris L.). Seven lines (GN-605-s, GN-610-s, PI 321638-s, PI 502217-s, Neb-T-6-s, Neb-T-8a-s, and Neb-T-15-s) exhibited similarly high levels of resistance (immunity or necrotic spots without sporulation) to all eight races. Inheritance of resistance was examined across five susceptible × resistant (S × R) and three resistant × resistant (R × R) populations. The rust reactions in the F1, F2, and F3 generations derived from S × R crosses revealed that the immune or necrotic resistance response was conditioned by a single locus exhibiting incomplete dominance. The rust resistance of four lines tested for allelism in R × R crosses was found to be derived from the same gene. This apparent lack of variability for rust resistance suggests that a single introgression event may realize the full potential for cultivated tepary bean to contribute rust resistance to common bean through interspecific hybridization. In addition, the limited variability for resistance to the highly variable rust pathogen in cultivated tepary bean supports the occurrence of a “bottleneck effect” during domestication of this species, as observed in germplasm diversity studies.
Mark J. Bassett and Phillip N. Miklas
The inheritance of blue pattern flower (BPF) expression was investigated in common bean (Phaseolus vulgaris L.). The BPF trait was derived from accession line G07262, and the flowers express blue banner petal and white wings with blue veins. Crosses between a BPF stock and three other parents, t p mic long micropyle stripe BC3 5–593, t z Fib arcus BC4 5–593, and t Z bip ana Fib marginata BC3 5–593, all segregated in F2 for BPF or white flowers in a 9:7 ratio, respectively. Progeny tests in F3 from two of the crosses supported the hypothesis that two complementary dominant genes control BPF expression and permitted a genetic linkage estimate of cM = 32.4 ± 7.91 map units between p mic and one of the two genes for BPF. A cross between t z fib virgarcus BC3 5–593 and T Prp i-2 V BC2 5–593 demonstrated that t Prp i-2 did not express BPF. Two crosses, T Prp i-2 V BC2 5–593 t p mic BC3 5–593 and 5–593 × a BPF stock, segregated in F2 for plants expressing BPF in a 3/16 frequency. The combined data demonstrated that a new gene, t bp (bp = blue pattern), interacts with Prp i-2 to express BPF and that P is linked with Prp i-2 by 32 map units. The dominance order at the T locus is T > t bp > t. The pedigree source of the t bp gene and the heterogeneity of PI 632736 (t p mic long micropyle stripe BC3 5–593) are discussed.
Mark J. Bassett and Phillip N. Miklas
‘Painted Lady’ (Phaseolus coccineus L.) has bicolor flowers with vermilion banner petal and white wing petals. This flower color pattern is not known in common bean (P. vulgaris L.). The bicolor trait was backcrossed into common bean and its inheritance investigated, including allelism tests with other genes in common bean (T, P, and V) for flower color or pattern and brown seed coat. A pure line (line 33) with bicolor flower and dark olive brown seed coat was crossed to line 5-593 (no flower pattern and black seed coat). Data from the F2 and F3 progenies from that cross demonstrated that a single recessive gene controlled both the bicolor flower and dark olive brown seed coat by pleiotropic gene action. Allelism tests between the bicolor trait (line 179c) and standard genetic tester stocks involving the T, P, V, and Wb (white banner) genes for flower color or seed coat color demonstrated independence of bicolor from those genes and further supported the hypothesis of pleiotropic action on flower and seed coat. Also, the Wb gene was demonstrated to be independent of T and P. The gene symbol bic is proposed for the bicolor gene.
Mark J. Bassett and Phillip N. Miklas
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.
Phillip N. Miklas, Richard Delorme, and Ron Riley
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.
Phillip N. Miklas, Kenneth F. Grafton, and Phillip E. McClean
We investigated the partial physiological resistance (PPR) of common beans (Phaseolus vulgaris L.) to white mold disease caused by Sclerotinia sclerotiorum (Lib.) deBary. The activity of phenylalanine ammonia-lyase (PAL) was measured in detached stems inoculated with a growing mycelium of the pathogen. Noninoculated detached stems and whole plants were included as controls. Five bean cultivars-Upland, Bunsi, Sierra, UI-114, and Montcalm-and one breeding line-NY 5394-were tested; all varied in PPR to white mold disease. Greater PAL activity in the resistant NY 5394 than in the susceptible `Upland' suggests that PAL activity may be involved in the PPR of common beans to S. sclerotiorum.
An N. Hang, Matt J. Silbernagel, and Phillip N. Miklas
Carlos A. Urrea, Phillip N. Miklas, and James S. Beaver
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.
Phillip N. Miklas, Valerie Stone, Carlos A. Urrea, and James S. Beaver
A genetic linkage map of 170 RAPD markers mapped across 79 recombinant inbred lines (Dorado and XAN-176) reveal genomic regions that condition multiple disease resistance to fungal (Ashy Stem Blight—Macrophomina phaseolina), viral (bean golden mosaic virus—BGMV), and bacterial (common bacterial blight—Xanthomonas campestris pv. phaseoli) pathogens of common bean (Phaseolus vulgaris). A genomic site on linkage group US-1 had a major effect, explaining 18%, 34%, and 40% of the variation in phenotypic reaction to ashy stem blight, BGMV, and common bacterial blight disease, respectively. Adjacent to this region was a QTL conditioning 23% of the variation in reaction to another fungal pathogen, web blight (Thanatephorus cucumeris). A second genomic site on linkage group US-1 had minor affect on multiple resistance expression to the same fungal (15%), viral (15%), and bacterial (10%) pathogens. It is unknown whether these specific genomic regions represent a series of linked QTL affecting resistance to each disease separately or an individual locus with pleiotropic effect against all three pathogens.