Inheritance and stability of sodium channel mutations associated with permethrin knockdown resistance in Aedes aegypti

Abstract

Our earlier study has found that V1023G and D1794Y amino acid substitutions in the voltage-gated sodium channel were associated with knockdown resistance to permethrin in Aedes aegypti. By crossing the resistant Per-R strain with the susceptible NS strain, the inheritance and stability of this resistance were analyzed phenotypically and genotypically. KT50 values and degrees of dominance in the reciprocal cross progeny suggest that the knockdown resistance to permethrin in this mosquito was an autosomal and incompletely recessive trait governed by a single gene. Frequency of both V1023G and D1794Y mutations in F1 and F2 progeny also suggest that the inheritance of this resistance was monofactorial. With the relaxation of selection pressure, the knockdown resistance to permethrin and frequencies of resistance alleles declined concomitantly in Per-Rx strain; and after 15 generations, the permethrin susceptibility and mutation frequency regressed nearly to those of the susceptible strain. These results are expected to provide important information for the prediction and management of pyrethroid resistance in field populations of Ae. aegypti.