Abstract
Spinosad is a new and highly promising insecticide, derived from the bacteria Saccharopolyspora spinosa, with efficacy against a wide range of insects. The mechanism of action of spinosad appears to be unique, with a primary site of attack being the nicotinic acetylcholine receptor (nAChR) and a secondary site of attack being γ-aminobutyric acid (GABA) receptors. Neural nAChRs are composed of five subunits, with a minimum of 2 αs. Each subunit possesses a large N-terminal extracellular domain that includes the acetylcholine (ACh) binding site and four transmembrane domains (M1-4) with M2 contributing most of the amino acids that line the ion channel. Spinosad resistance has been selected for and characterized in several insect species. Generally, resistance is monofactorial, recessive and cannot be overcome by insecticide synergists. Spinosad resistance in the house fly maps to chromosome 1 and three nAChR subunit genes (α5, α6, and β3) are predicted to exist on chromosome 1 based on Drosophila/Musca homology maps. However, cloning and sequencing of Mdα5, Mdα6, and Mdβ3 from susceptible and spinosad resistant strains of house fly found no differences that could be associated with resistance. Unraveling the mystery of spinosad resistance in house flies will require further study.
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