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.
Carlos A. Urrea, Phillip N. Miklas, James S. Beaver and Ronald H. Riley
Geunhwa Jung, Dermot P. Coyne, Paul W. Skroch, James Nienhuis, E. Arnaud-Santana, James Bokosi, H.M. Ariyarathne, James R. Steadman, James S. Beaver and Shawn M. Kaeppler
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.
Geunhwa Jung, Dermot P. Coyne, Paul W. Skroch, James Nienhuis, E. Arnaud-Santana, James Bokosi, H.M. Ariyarathne, James Steadman and James S. Beaver
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.
Phillip N. Miklas, Richard Delorme, Valerie Stone, Mark J. Daly, J. Rennie Stavely, James R. Steadman, Mark J. Bassett and James S. Beaver
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.
Juan M. Osorno, Carlos G. Muñoz, James S. Beaver, Feiko H. Ferwerda, Mark J. Bassett, Phil N. Miklas, Teresa Olczyk and Bill Bussey
Bean golden yellow mosaic virus (BGYMV), incited by a whitefly (Bemisia tabaci Gennadius) transmitted geminivirus, is an important disease that can limit common bean (Phaseolus vulgaris L.) production in Central America, the Caribbean, and southern Florida. Only a few genes are currently deployed in BGYMV-resistant common bean cultivars. The identification of novel sources of resistance would help bean breeders broaden the genetic base of resistance to this important virus. Phaseolus coccineus L. germplasm accession G35172 was found by International Center for Tropical Agriculture scientists to be resistant to BGYMV. Populations derived from an interspecific cross between P. vulgaris and P. coccineus were evaluated to study the inheritance of resistance to BGYMV. Segregation ratios of F2 plants and other populations suggest that BGYMV resistance from P. coccineus is controlled by two genes. A recessive gene, with the proposed symbol bgm-3, confers resistance to leaf chlorosis and a dominant gene, with the proposed name Bgp-2, prevents pod deformation in the presence of BGYMV. Results from allelism tests with previously reported BGYMV resistance genes (bgm, bgm-2, and Bgp) and the absence of the SR-2 sequence-characterized amplified region marker for bgm support the hypothesis that bgm-3 and Bgp-2 are different genes for BGYMV resistance.