Identification of QTL Associated with White Mold Resistance in Common Bean

Crop Science ◽  
2005 ◽  
Vol 45 (6) ◽  
pp. 2482-2490 ◽  
Author(s):  
Marcio Ender ◽  
James D. Kelly
2017 ◽  
Vol 11 (3) ◽  
pp. 305-310 ◽  
Author(s):  
Shree P. Singh ◽  
Howard F. Schwartz ◽  
Henry Terán ◽  
Carlos Centeno ◽  
Kristen Otto

Crop Science ◽  
2009 ◽  
Vol 49 (5) ◽  
pp. 1629-1637 ◽  
Author(s):  
Shree P. Singh ◽  
Henry Terán ◽  
Howard F. Schwartz ◽  
Kristen Otto ◽  
Margarita Lema

2016 ◽  
Vol 15 (3) ◽  
Author(s):  
D.A. Souza ◽  
M. Balestre ◽  
A.K.A. Pamplona ◽  
M.E. Leite ◽  
J.A. Dias ◽  
...  

2019 ◽  
Author(s):  
Atena Oladzadabbasabadi ◽  
Sujan Mamidi ◽  
Phillip N. Miklas ◽  
Rian Lee ◽  
Phillip McClean

Abstract Background White mold (WM) is a major disease in common bean ( Phaseolus vulgaris L.), and its complex quantitative genetic control has limited the development of WM resistant cultivars. WM2.2 is one of the nine meta-QTL that has a major effect on WM tolerance. This QTL explains up to 35% of the phenotypic variation and was previously mapped to a large interval on Pv02. Our objective was to narrow the interval of this QTL using QTL-based bulk segregant analysis.Results The phenotypic and genotypic data from two RIL populations (R31 and Z0726-9), which possess different genetic backgrounds for white mold resistance, were used to select resistant and susceptible lines to generate subpopulations for bulk DNA sequencing, and reads were aligned against the sequence of the resistance parent. The QTL physical intervals for each RIL population were mapped by fixed SNPs in 10kb-2kb sliding windows. WM2.2 QTL was split into two regions WM2.2a (3.54-4.56 Mbp; euchromatic) and WM 2.2b (12.19 to 26.41 Mbp; heterochromatic) in populations R31 and Z0726-9, respectively. For each QTL interval, the possible functional contribution of significant non-synonymous and synonymous polymorphisms was investigated. Gene models encoding for pentatricopeptide repeat, gibberellin 2-oxidase, and heat-shock proteins are the likely candidate genes associated with WM2.2a resistance. A TIR-NBS-LRR class of disease resistance protein and a EF-TU receptor are potential candidate genes associated with WM2.2b resistance and most likely trigger a physiological resistance response to WM.Conclusion QTL-based pooled sequencing analysis revealed that the large genomic region associated with WM2.2 meta QTL consists of two major QTL each associated with a different WM resistance function. WM2.2a region is most likely associated with avoidance mechanisms while WM2.2b region triggers physiological resistance.


Crop Science ◽  
2007 ◽  
Vol 47 (6) ◽  
pp. 2285-2294 ◽  
Author(s):  
Judd J. Maxwell ◽  
Mark A. Brick ◽  
Patrick F. Byrne ◽  
Howard F. Schwartz ◽  
Xueyan Shan ◽  
...  

Crop Science ◽  
2011 ◽  
Vol 51 (1) ◽  
pp. 123-139 ◽  
Author(s):  
Marilyn Soule ◽  
Lyndon Porter ◽  
Juliana Medina ◽  
Gloria P. Santana ◽  
Matthew W. Blair ◽  
...  

HortScience ◽  
1999 ◽  
Vol 34 (3) ◽  
pp. 534D-534 ◽  
Author(s):  
Soon O. Park ◽  
Dermot P. Coyne ◽  
James R. Steadman ◽  
Geunhwa Jung

White mold, incited by Sclerotinia sclerotiorum (Ss), is an important disease of common bean (Phaseolus vulgaris). Our objective was to identify RAPD markers and seedcoat pattern associated with QTL affecting resistance to Ss isolates 152 and 279 in a molecular marker-based linkage map previously constructed using a recombinant inbred (RI) population from the common bean cross `PC-50' (resistant to Ss) x XAN-159 (susceptible to Ss). White mold reactions were derived from a greenhouse straw test. Continuous distributions for the reactions to Ss isolates 152 and 279 were observed for RI lines, indicating quantitative inheritance. An intermediate (+0.67) Pearson correlation was observed between the reactions to Ss isolates 152 and 279. Low (0.24 and 0.23) narrow-sense heritabilities were found for the reactions to Ss isolates 152 and 279. Three QTL affecting resistance to Ss isolate 152 explained 33% of the phenotypic variation. Four QTL affecting resistance to Ss isolate 279 explained 54% of the phenotypic variation. The seedcoat pattern marker (C) on linkage group I was most consistently associated with resistance to Ss isolates 152 and 279, and explained 10% and 24% of the phenotypic variation for the traits, respectively. This is the first report on detection of QTL for white mold resistance in common bean. The RAPD markers and seedcoat pattern could be useful in breeding for white mold resistance.


2017 ◽  
pp. 1177-1187
Author(s):  
Monik Evelin Leite ◽  
Izabel Cristina Rodrigues de Figueiredo ◽  
Juliana Andrade Dias ◽  
Filipe Couto Alves ◽  
João Bosco dos Santos

HortScience ◽  
2006 ◽  
Vol 41 (4) ◽  
pp. 973B-973 ◽  
Author(s):  
J. Erron Haggard ◽  
James R. Myers

White mold, caused by Sclerotinia sclerotiorum (Lib.) de Bary, causes major losses in dry and snap bean (Phaseolus vulgaris) production. With little genetic variation for white mold resistance in common bean, other potential sources for resistance must be investigated. Accessions of scarlet runner bean (P. coccineus) have been shown to have partial resistance exceeding any to be found in common bean. Resistance is quantitative with at least six QTL found in a P. coccineus intraspecific resistant × susceptible cross. Our goal is to transfer high levels of resistance from P. coccineus into commercially acceptable common bean lines. We developed interspecific advanced backcross populations for mapping and transfer of resistance QTL. 111 BC2F5 lines from a cross between OR91G and PI255956 have been tested in straw tests and oxalate tests, as well as in a field trial. The data show that the OR91G × PI255956 population carries a high level of resistance, but because of the quantitative nature of resistance, it may be necessary to intercross individuals to achieve higher levels. SSR, RAPD, and AFLP markers are being tested in the population to construct a linkage map for placement of QTL. QTL identified from each type of test (straw, oxalate, and field) may provide additional information about the genetic architecture of white mold resistance. Three other populations are from advanced backcrosses of the recurrent parents G122, OR91G, and MO162, with PI433251B as the donor parent in each. Analyses and advance of these populations will follow, the results of which should confirm QTL identified in the OR91G × PI255956 population, as well as possible additional resistance QTL from PI433251B.


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