Reduction of dADAR activity affects the sensitivity of Drosophila melanogaster to spinosad and imidacloprid

The insecticides spinosad and imidacloprid cause toxicity by acting at the nicotinic acetylcholine receptor (nAChR), but at distinct sites on the receptor. Mutations or deletions of specific nAChR subunits cause resistance to these compounds. Transcripts of nAChR subunits are subject to A-to-I RNA editing by adenine deaminase acting on RNA (ADAR), which may result in altered receptor physiology. However, reports on the influence of A-to-I RNA editing on insecticide sensitivity have been very limited. We used the Gal4–UAS system in Drosophila melanogaster to reduce the expression of dAdar in specific tissues and evaluated the toxicity of spinosad and imidacloprid. Ubiquitous reduction of dAdar increased spinosad sensitivity, while dAdar reduction in cholinergic neurons and muscle reduced spinosad sensitivity. Imidacloprid sensitivity was reduced by decreased dAdar expression in cholinergic neurons, muscle and glia. While reduction in editing of nAChR subunits may explain some of these changes in insecticide toxicity, it is likely that editing of genes other than nAChRs can affect toxicity of these insecticides.

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► Silencing of dADAR resulted in decreases in A-to-I RNA editing.
► Ubiquitous reduction in RNA editing increased spinosad sensitivity up to 5.9-fold.
► Tissue specific reduction of RNA editing decreased spinosad sensitivity.
► Tissue specific reduction of RNA editing decreased imidacloprid sensitivity.