Author
BURKHART, CHRISTOPHER - PENN STATE | |
CHRIST, BARBARA - PENN STATE | |
Haynes, Kathleen |
Submitted to: American Journal of Potato Research
Publication Type: Peer Reviewed Journal Publication Acceptance Date: 8/29/2006 Publication Date: 5/1/2007 Citation: Burkhart, C.R., Christ, B.J., Haynes, K.G. 2007. Heritability of resistance to fusarium dry rot in a diploid hybrid potato population. American Journal of Potato Research. 84:199-204. Interpretive Summary: Fusarium dry rot is a major storage disease of potatoes for which there is no fungicidal control. The purpose of this study was to determine if genetic resistance to Fusarium dry rot exists in potatoes and if it can be utilized in breeding improved Fusarium resistant potato cultivars. Although we found that there was genetic resistance for Fusarium dry rot in these potatoes it was not of a form which could be improved by conventional breeding methods. Different breeding strategies will have to be devised if genetic resistance from these parental materials is ever going to be utilized. This information will be useful to potato breeders and pathologists trying to improve disease resistance in cultivated potatoes. Technical Abstract: Fusarium dry rot, caused by several Fusarium species, is a major storage disease of potatoes for which there is no fungicidal control. Levels of resistance in commercial potato germplasm are inadequate. The purpose of this study was to determine the inheritance of resistance to Fusarium dry rot in a diploid hybrid Solanum phureja - S. stenotomum population. Three tubers from each of four half-sibs from each of 38 diploid families were inoculated with a mixture of two isolates of F. sambucinum and one isolate of F. solani four times in both 2003-2004 and 2004-2005. Then, tubers were incubated for 40 days at 15°C and 90% relative humidity. The surface diameter and depth of infected tissue were measured in two directions, at right angles to each other. Depth of infected tissue was determined by cutting the tuber in half through the inoculation point. Mean depth and diameter of infected tissue were analyzed. There were significant differences among clones. The experiment x clone interaction was also significant. Broad-sense heritabilities and their 95% confidence intervals for resistance to Fusarium dry rot in this population were estimated as 0.63 (0.50, 0.71) and 0.81 (0.76, 0.86) in 2003-2004 and 2004-2005, respectively, for mean diameter; and 0.68 (0.57, 0.75) and 0.81 (0.75, 0.86) in 2003-2004 and 2004-2005, respectively, for mean depth. Narrow-sense heritabilities for mean diameter and depth were not significantly different from zero either year. Although there is genetic variation for resistance to Fusarium dry rot in this population, these results indicate that additive genetic variance is lacking or minimal, and therefore, little or no genetic gain in resistance will be realized. A few highly resistant clones could, via 4x-2x crosses, theoretically transfer much of the dominance and epistatic variance governing resistance in this population to the tetraploid level. |