The inheritance of mefenoxam resistance in the oomycete Phytophthora erythroseptica, causal organism of pink rot of potato, was investigated in two successive selfed generations of single oospore isolates. Fourteen parental isolates from three mefenoxam-sensitivity phenotypes (sensitive, intermediately resistant, and resistant) were used to produce S1 and S2 progeny isolates by selfing each isolate and germinating single oospore cultures from each isolate. The two generations of isolates were tested for mefenoxam sensitivity using the radial growth inhibition assay and calculating EC50 values. Twenty-four-hundred isolates from S1 and S2 generations were tested for mefenoxam sensitivity. Results demonstrated the lack of segregation for mefenoxam sensitivity among S1 and S2 progeny isolates from the resistant and sensitive parents. The majority of the S1 progeny isolates from the parents with intermediate resistance also possessed intermediate resistance, but demonstrated substantial quantitative shifts in response to mefenoxam more often toward increased insensitivity. A few isolates from the S1 progeny were sensitive to mefenoxam, and one isolate was mefenoxam-resistant. Similarly, the majority of the S2 progeny isolates from intermediately resistant parents also possessed intermediate resistance with some quantitative shifts in sensitivity to mefenoxam similar to those observed in S1 progeny, as well as a few isolates that were sensitive to mefenoxam. These results do not support the hypothesis that resistance to mefenoxam in P. erythroseptica is controlled by a single gene exhibiting incomplete dominance. Alternative hypotheses are proposed such as the genetics of mefenoxam resistance in P. erythroseptica is probably under the control of more than one major gene and perhaps some minor genes of additive effect.
- Phenylamide fungicides
- Solanum tuberosum