Insecticide resistance resulting from an absence of target-site gene product.
Genetic changes in insects that lead to insecticide resistance include point mutations and up-regulation/amplification of detoxification genes. Here, we report a third mechanism, resistance caused by an absence of gene product. Mutations of the Methoprene-tolerant (Met) gene of Drosophila melanogaster result in resistance to both methoprene, a juvenile hormone ( JH) agonist insecticide, and JH. Previous results have demonstrated a mechanism of resistance involving an intracellular JH binding protein that has reduced ligand affinity in Met flies. We show that a gamma-ray induced allele, Met27, completely lacks Met transcript during the insecticide-sensitive period in development. Although Met27 homozygotes have reduced oogenesis, they are viable, demonstrating that Met is not a vital gene. Most target-site resistance genes encode vital proteins and thus have few mutational changes that permit both resistance and viability. In contrast, resistance genes such as Met that encode nonvital insecticide target proteins can have a variety of mutational changes that result in an absence of functional gene product and thus should show higher rates of resistance evolution.[1]References
- Insecticide resistance resulting from an absence of target-site gene product. Wilson, T.G., Ashok, M. Proc. Natl. Acad. Sci. U.S.A. (1998) [Pubmed]
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