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Karl J. Sauter, David W. Davis, and James S. Beaver

184 random F2 plants from a high temperature (HT) sensitive X HT tolerant snap bean cross were advanced to the F5 by single seed descent. At anthesis and after HT pre-treatment, all plants in each generation were evaluated in the laboratory for leaf ethylene evolution (EE), % viable pollen (VP), and leaf cell membrane thermostability (CMT). Population means among generations differed significantly for VP and CMT in a paired t-test, while EE means in the F3, F4, and F5 were similar. Correlations among traits were very low (≤.25) with a consistent negative correlation between VP and the others (high VP is a positive trait while low EE and CMT are considered positive). VP and total pollen were highly correlated (r≤.81). To determine if the 3 traits might predict HT tolerance in the field, F5-derived F6 lines were grown at Becker, MN (control), and Isabella, PR (HT environment). Yield component data were collected at both locations. Tolerance may be computed as % yield of the lines in the HT vs. the control environment for any or all of the yield components. Regression analysis showed a very low r2 (≤.16) when EE, VT, and CMT were used to predict tolerance as estimated by pod production. However, as expected, the F5 best predicted F6 performance. Further results from Minnesota field and greenhouse and from Puerto Rico field data will be discussed.

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Jose J. Velez, Mark J. Bassett, James S. Beaver, and Albeiro Molina

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.

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D. P. Coyne, J. R. Steadman, D. T. Lindgren, D.S. Nuland, J. S. Beaver, F. Saladin, and E. Arnaud Santana

Disease of beans, particularly common bacterial blight (CBB) (DR, NE), rust (DR, NE), web blight (WB) (DR) and bean golden mosaic virus (BGMV) (DR) are major constraints to bean yields and seed quality. The objectives were to identify resistant (R) germplasm, to conduct genetic studies, to develop R cultivars (DR, NE), to improve research facilities and capabilities (DR), to train personnel and educate graduate students (DR, NE). The expected impact is (1) the improvement of breeding programs, yields and income to farmers and (2) returning specialists will permit improved research in the DR. The most significant advances in research were as follows: (i) BAC-6 dry bean breeding line was found to be R to CBB seed infection, (ii) The reaction to CBB was inherited quantitatively with low NSH estimates, (iii) Rust race nonspecific R was correlated with abaxial leaf pubescence; the latter trait was inherited qualitatively, (iv) R to BGMV and WB were identified and (v) Improved cultivars and breeding lines were developed (DR, NE).

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E. Arnaud-Santana, D.P. Coyne, J.R. Steadman, A.K. Vidaver, K.M. Eskridge, and J.S. Beaver

Heritabilities (H) of seed transmission and leaf and pod reactions to common bacterial blight (CBB) Xanthomonas campestris pv. phaseoli (Xcp) and to web blight (WB) Thanatephorus cucumeris (Tc) were studied. The reaction to CBB was quantitatively inherited. H values of .36, .46, and .34 for leaf reaction, .14, .12, and .27 for pod reaction, .53, .26, and .36 for seed transmission were estimated based on variation of F6 lines derived from bean crosses 'PC-50' × XAN-159, 'PC-50'× BAC-6, and 'Venezuela 44' × BAC-6 (greenhouse, NE). No significant correlations were detected between leaf and pod reactions or between pod reaction and seed transmission. Quantitative inheritance patterns were observed for leaf reactions to Xcp, Tc, and architecture (AR) in F6lines from the cross BAC-6 × HT 7719 (field, Dominican Republic). H values of .23 (CBB), .14 (WB), and .30 (AR) were obtained. No significant correlations were detected between CBB with WB or AR. A low correlation (+.22) was found between WB and AR.

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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.

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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.