|Grafton, Kenneth - NDSU, FARGO, ND|
Submitted to: Proceedings of the International Sclerotinia Workshop
Publication Type: Proceedings
Publication Acceptance Date: December 1, 2002
Publication Date: January 1, 2003
Citation: GRAFTON, K.F., MIKLAS, P.N. INHERITANCE OF FIELD RESISTANCE TO WHITE MOLD IN AN ND88-106-04 (NAVY) X AZTEC (PINTO) DRY BEAN MAPPING POPULATION. PROCEEDINGS OF THE INTERNATIONAL SCLEROTINIA WORKSHOP, Vol. 1, p. 4. 2003. Technical Abstract: Pinto bean (Phaseolus vulgaris L.) is extremely susceptible to white mold disease caused by Sclerotinia sclerotiorum (Lib.) de Bary, and breeding resistance into them is difficult, due in part to the paucity of resistance sources in a related Middle American background. `Bunsi¿ navy bean, a well known source of resistance to white mold from the Middle American gene pool, could be useful for improving resistance of pinto bean. The objective of this project was to determine the inheritance of Bunsi-derived resistance in a pinto bean background. Field research was conducted in North Dakota and Washington in 2001 and 2002 to characterize white mold reaction of an F5:8 population of 85 recombinant inbred lines (RIL) from the cross `Aztec'/ND88-106-04. Aztec pinto bean is susceptible to white mold and ND88-106-04 is a navy bean with resistance to white mold derived from Bunsi. The lines were rated for disease severity (scored from 1 = no disease to 9 = completely susceptible) and yield. Traits associated with disease avoidance such as canopy porosity, plant height, lodging, and maturity were also measured. Average disease severity of Aztec and ND88-106-04 across environments was 6.9 and 2.5, respectively, compared to 4.6 for Bunsi and 7.6 for the susceptible pinto cultivar Montrose. Moderately high heritability (Hns = 59%) and normal distribution of disease score among the RILs were observed, indicating that resistance was influenced by environment and likely conditioned by more than one gene. The green-stem trait, present in Bunsi and ND88-106-04, was expressed among the RILs and was correlated with less disease severity (-30%). Molecular marker analysis of the disease reaction data collected for this mapping population should enable identification of quantitative trait loci (QTL) that specifically condition disease avoidance or physiological resistance, and lead to marker-assisted selection of the QTL with consistent expression across environments.