Biochemistry and genetics of abamectin resistance in the house fly

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 (KD) 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 Bmax 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.