Abstract
Pyrethroid insecticides modify the gating of voltage-gated sodium channels, thus disrupting the function of the nervous system. In Drosophila melanogaster, para encodes a functional sodium channel. Drosophila Sodium Channel 1 (DSC1), although considered as a putative sodium channel gene for decades due to its high sequence similarity with sodium channels, encodes a voltage-gated cation channel with high permeability to Ca2+. Previous study showed that knockout of the DSC1 gene (DSC1-/-) caused Drosophila adults to be more susceptible to pyrethroids and the adult giant fiber (GF) neural circuit were more susceptible to pyrethroids. Considering distinct expression of DSC1 transcripts in adults and larvae, we examined the role of DSC1 channels in regulating pyrethroid susceptibility in Drosophila larvae. We conducted insecticide bioassays and examined the susceptibility of the larval neuromuscular junction (NMJ) to pyrethroids using w1118, an insecticide-susceptible line, DSC1-/-, parats1 (a pyrethroid-resistant line carrying a mutation in para) and a double mutation line parats1; DSC1-/-. We found that, like the adult GF system, the NMJ of DSC1-/- flies is more susceptible to pyrethroids than that of w1118 with the pyrethroid susceptibility ranked as DSC1-/- > w1118 > parats1; DSC1-/- > parats1. However, DSC1-/- larvae were about two-fold more resistant to pyrethroids than w1118 larvae, and the pyrethroid susceptibility of larvae ranked as w1118 > DSC1-/- > parats1; DSC1-/- > parats1. These results reveal common and distinct roles of DSC1 channels in regulating the action of pyrethroids in adults and larvae of D. melanogaster.
