Inheritance of mefenoxam resistance in selfed populations of the homothallic oomycetePhytophthora erythroseptica (Pethybr.), cause of pink rot of potato

Abstract

The inheritance of mefenoxam resistance in the oomycetePhytophthora 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 inP. erythroseptica is controlled by a single gene exhibiting incomplete dominance. Alternative hypotheses are proposed such as the genetics of mefenoxam resistance inP. erythroseptica is probably under the control of more than one major gene and perhaps some minor genes of additive effect.

Resumen

La herencia de la resistencia del oomycetePhytophthora erythroseptica causante de la pudrición rosada de la papa al mefenoxam fue investigada en dos generaciones autofecundadas sucesivas de aislamientos provenientes de una sola oospora. Catorce aislamientos de tres fenotipos sensibles al mefenoxam (sensible, intermedio-resistente y resistente) fueron utilizados para producir los aislamientos progenle S1 y S2, autofecundando cada aislamiento y produciendo aislamientos provenientes de una sola oospora. Se probaron los aislamientos de las dos generaciones para sensibilidad al mefenoxam, utilizando la prueba de inhibición de crecimiento radial y calculando los valores EC₅₀. Se probaron 2,400 aislamientos de las generaciones S1 y S2 para determinar su sensibilidad al mefenoxam. Los resultados demostraron la falta de segregación para sensibilidad a la acción del mefenoxam entre los aislamientos de las progenies S1 y S2 provenientes de progenitores resistentes y sensibles. La mayoría de los aislamientos de la progenie S1 provenientes de progenitores con resistencia intermedia también tuvieron resistencia intermedia, pero demostraron un cambio cuantitativo sustancial en respuesta al mefenoxam, con más frecuencia hacia una mayor insensibilidad. Unos pocos aislamientos de la progenie S1 mostraron sensibilidad al mefenoxam y un aislamiento mostró resistencia. De la misma manera, la mayoria de los aislamientos de la progenie S2 con progenitores de resistencia intermedia, tuvieron también resistencia intermedia con algunos cambios cuantitativos en sensibilidad, similares a aquellos observados en la progenie S1 e igualmente linos pocos aislamientos fueron sensibles. Estos resultados no apoyan la hipótesis de que la resistencia delP. erythroseptica al mefenoxam es controlada por un solo gen de dominancia incompleta. Se propone la hipótesis alternativa de que la resistencia genética delP. erythroseptica al mefenoxam está probablemente bajo el control de más de un gen mayor y tal vez de algunos genes menores de efecto aditivo.