Biochemistry and genetics of abamectin resistance in the house fly

Abstract

We investigated the biochemical basis and genetic inheritance of high level abamectin resistance (>;60,000-fold) in the AVER strain of house fly. Resistance was associated with a 2.4-fold decreased rate of cuticular penetration and altered abamectin binding. There was no apparent difference between resistant and susceptible strains in the affinity ( K D ) of abamectin binding to its receptor. However, the AVER strain had significantly less (1.5-fold) receptors/mg protein compared to the susceptible strain as judged by B max values. No difference in the in vivo metabolism of abamectin was found between the resistant and susceptible strains. The resistance was inherited as a strongly recessive trait that was not sex linked nor due to cytoplasmic influences based on crosses of the susceptible aabys strain with the AVER strain. The AVER strain was cross-resistant to two abamectin analogues: MK-243 and abamectin oxide.