Monitoring for MACE resistance in the tobacco-adapted form of the green peach aphid, Myzus persicae (Sulzer) (Hemiptera: Aphididae) in the eastern United States

Organophosphate and carbamate insecticides exert their neurotoxic effects by inhibiting acetylcholinesterase (AChE), thereby, prolonging the action of acetylcholine at cholinergic synapses, resulting in neuronal hyperexcitation. Mutations at the AChE target site confer modified acetylcholinesterase (MACE) phenotypes. Target-site insensitivity of AChE was characterized in field-collected, tobacco-adapted forms of the green peach aphid, Myzus persicae (Sulzer), from nine different states in the eastern United States from 2004 to 2007. The specific activity of the AChE among the 65 aphid colonies screened by Ellman's assay ranged from 0.017–0.259 U/min/mg protein. Eight colonies, with a wide range of specific activities were chosen to study the inhibition of AChE in the presence of two carbamate insecticides, methomyl and pirimicarb. IC₅₀ values for methomyl ranged from 0.35 to 2.4 μM, while six out of eight colonies had lower values that ranged from 0.16 to 0.30 μM for pirimicarb. Two colonies that were inhibited by methomyl had very high IC₅₀ values for pirimicarb, 40.4 and 98.6 μM respectively. The target-site insensitivity in these two colonies that are resistant to pirimicarb could be due to an ace2 gene mutation. This is the first instance where MACE phenotypes in M. persicae from the United States were studied and confirmed. The results indicate that the possible insensitivity due to MACE resistance in some colonies may render selected carbamate insecticides ineffective. Concerns of MACE resistance in managing the tobacco-adapted form of the green peach aphid on tobacco in the United States are discussed.