Non-additive genetic variance governs resistance to Fusarium dry rot in a diploid hybrid potato population

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-Solanum 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 Fusarium sambucinum and one isolate of Fusarium solani four times in both 2003-2004 and 2004-2005. Tubers were then 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 as 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.