Submitted to: American Journal of Potato Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: March 11, 2006
Publication Date: July 1, 2006
Citation: Valluru, R., Christ, B.J., Haynes, K.G., Vinyard, B.T. 2006. Inheritance of resistance to fusarium tuber rot in tetraploid potatoes. American Journal of Potato Research. 83:335-341.
Interpretive Summary: Fusarium dry rot is a serious disease that affects potato tubers in storage. Resistance to Fusarium dry rot is generally lacking in potatoes. However, we identified one potato line that had good levels of resistance to Fusarium dry rot and studied the inheritance of resistance in this line. We found that this line passed resistance to Fusarium dry rot onto its offspring. Resistance was fairly consistent across multiple experiments in two years, suggesting that resistance is fairly stable. This research improves our understanding of the inheritance of resistance to Fusarium dry rot in this resistant line. This resistant line can be used for breeding Fusarium dry rot resistant cultivars in the future.
Fusarium tuber rot of potato (Solanum tuberosum L.) is one of the most economically important diseases of stored potatoes. Dry rot is caused by several species of Fusaria, particularly Fusarium sambucinum in North America. The objective of this study was to determine the inheritance of resistance to Fusarium tuber rot. A highly resistant (B0172-22) and a highly susceptible (B0178-34) potato clone were crossed as female parents with two male parents. Tubers from varying numbers of progeny (28-37) from these four crosses were inoculated with Fusarium sambucinum in the laboratory. Three tubers from each progeny were inoculated at approximately monthly intervals six times in each of two years. The depth and diameter of the lesion were measured 40 days after inoculation. Estimates of broad-sense heritability (H) for lesion depth and a 95% confidence interval about these estimates were similar in 2000 and 2001: 0.84 (0.84, 0.91) and 0.77 (0.77, 0.87), respectively, as were the estimates for lesion diameter: 0.83 (0.83, 0.90) and 0.80 (0.80, 0.89), respectively. General combining ability for lesion depth for the female parents was significant the second year, but not the first year. General combining ability for lesion diameter for the female and male parents was significant both years. There was no specific combining ability for either lesion depth or lesion diameter. There were significant differences among clones in each of these four families for both traits both years. In 2000 and 2001, 24% and 38%, respectively, of the clones were unstable for resistance. In only one of the four families did instability increase as susceptibility increased, suggesting that there may sometimes be a genetic component to instability per se. These results indicate that resistance to Fusarium dry rot is a heritable trait with a substantial additive genetic variance component. They also indicate that lesion diameter is more informative than lesion depth for evaluating resistance.