GENETICS AND BIOCHEMICAL-MECHANISMS OF ABAMECTIN RESISTANCE IN 2 ISOGENIC STRAINS OF COLORADO POTATO BEETLE

Abamectin resistance in two isogenic strains of Colorado potato beetle was determined to be autosomal, incompletely recessive, and polygenic. Both resistant strains exhibited high levels of synergism to piperonyl butoxide and moderate levels to S,S,S,-tributyl phosphorotrithioate compared to that of a susceptible strain as judged by synergistic ratio and relative percentage synergism values. Both resistant strains had significantly elevated levels of cytochrome P450 and oxidative metabolites of [3H]abamectin B1a under both in vivo and in vitro conditions compared to those of the susceptible strain. High levels of oxidative synergism, elevated cytochrome P450 levels, and increased amounts of oxidative metabolites of [3H]avermectin B1a substantiate a monooxygenase-based resistance mechanism. Additionally, the polygenetic form of resistance, esteratic synergism, and elevated hydrolytic activity indicate the possibility of a carboxylesterase-based resistance mechanism. The lack of hydrolytic metabolites of [3H]avermectin B1a and low inhibitory action of abamectin on carboxylesterase activity, however, suggest principally a sequestration role for the resistant carboxylesterase. Penetration and excretion factors play no significant role in resistance nor does there appear to be a significant glutathione-S-transferase component in the abamectin-resistant strains. © 1992.