Abstract
The primary target of pyrethroids is the sodium channel in neuronal membranes. We have used mutations in Drosophila melanogaster to define two different types of target site alterations which affect pyrethroid sensitivity. The first alteration is illustrated by the para ts locus on the X chromosome. Gene cloning experiments by the laboratory of B. Ganetzky suggest that this locus is the structural gene for a protein homologous to the α-subunit of vertebrate sodium channels. We demonstrate that mutations at the para locus show changes in pyrethroid sensitivity when assayed by either a knockdown assay or a lethality assay. Some alleles show increased resistance and some show decreased resistance to fenvalerate. These changes are probably due to changes in the primary structure of one class of sodium channels in Drosophila. Such mutational changes can be used to define specific amino acid residues in the sodium channel which affect pyrethroid binding.
A second type of target site alteration is exemplified by the nap ts mutation which maps to the second chromosome and which has recently been shown by Kernan, Kreber and Ganetzky to be an allele of the maleless (mle) locus. This locus is involved in the regulation of genes on the X chromosome. The nap mutation shows resistance to all pyrethroids tested (fenvalerate, permethrin, and Pay-Off). Although there is no evidence for structural changes in nap sodium channels, the density of saxitoxinbinding sites is reduced. In this mutant strain the nap mutation appears to down regulate the class of sodium channels coded for by the X-linked para locus. This reduction in target site density causes increased resistance to pyrethroids.
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© 1989 Plenum Press, New York
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Hall, L.M., Kasbekar, D.P. (1989). Drosophila Sodium Channel Mutations Affect Pyrethroid Sensitivity. In: Narahashi, T., Chambers, J.E. (eds) Insecticide Action. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-1324-3_6
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DOI: https://doi.org/10.1007/978-1-4684-1324-3_6
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