Methomyl resistance in Musca domestica: mechanisms and inheritance

Methomyl resistance is a documented problem in Musca domestica field strains worldwide, including Pakistan, where the insecticide is commonly used. To address this, a methomyl-resistant near-isogenic line (Meth-R) was created specifically to determine its resistance inheritance mode and cross-resistance profile. Analysis of reciprocal F₁ and F_1' crosses demonstrated autosomal inheritance of methomyl resistance in the Meth-R strain, as evidenced by similar median lethal dose (LD₅₀) values and the absence of sex linkage or maternal effects. Resistance expression was incompletely dominant, with dominance values of 0.7 (F₁) and 0.6 (F_1'). Significant deviations between observed and expected mortality in self-bred (F₂ and F_2') and backcross (BC₁-BC₄) progenies (chi-square analyses) indicate resistance is likely controlled by multiple genes. The Meth-R strain showed no cross-resistance to alpha-cypermethrin, fluralaner, pirimiphos-methyl, or clothianidin. Additionally, observing significant synergism of methomyl with both piperonyl butoxide (PBO; oxidase inhibitor) and S,S,S-tributyl phosphorotrithioate (DEF; esterase inhibitor) implicates metabolic detoxification as a key mechanism of methomyl resistance. The Meth-R strain exhibits methomyl resistance inherited as an autosomal, incompletely dominant trait under polygenic control. Although there was cross-resistance in the Meth-SEL strain to alpha-cypermethrin, fluralaner, pirimiphos-methyl, and clothianidin versus the lab susceptible strain, selection with methomyl did not increase the level of cross-resistance. These results offer a foundation for combating methomyl resistance.