Inheritance and stability of resistance to fusarium tuber rot in tetraploid potatoes

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, particularlyFusarium 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 withFusarium sambucinum in the laboratory. Three tubers from each progeny were inoculated at approximately monthly intervals six times in each of 2 years. The depth and diameter of the lesion were measured 40 days after inoculation. Estimates of broadsense 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. The differences in lesion depth for the female parents were significant the second year, but not the first year. The differences in lesion diameter for the female and male parents were significant both years. The female x male interactions were not significant for either lesion depth or lesion diameter. There were significant differences between 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 sometimes may be a genetic component to instability per se. These results indicate that resistance to Fusarium dry rot has a large genetic component. They also indicate that lesion diameter is more informative than lesion depth for evaluating resistance.