Molecular biology of insecticide resistance.
The widespread use of insecticides has amounted to a large scale 'experiment' in natural selection of insects by chemicals of toxicological importance to humans. Specific examples in which the molecular basis of insecticide resistance has been studied in detail are presented here. The biochemical/physiological mechanisms of resistance can be categorized as target site insensitivity, increased metabolic detoxification and sequestration or lowered availability of the toxicant. These are achieved at the molecular level by: point mutations in the ion channel portion of a GABA receptor subunit (cyclodiene insecticides); point mutations in the vicinity of the acetylcholinesterase (AChE) active site (organophosphorus and carbamate insecticide resistance); amplification of esterase genes (organophosphorus and carbamate insecticides); mutations linked genetically to a sodium channel gene (DDT and pyrethroid insecticides); and yet uncharacterized mutations leading to the up-regulation of detoxification enzymes, such as cytochrome P450 and glutathione S-transferases (many classes of insecticides). In several cases, the selection of a precisely homologous mutation has been observed in different insect species.
Feyereisen
R
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Department of Entomology, University of Arizona, Tucson 85721, USA.
D000818:Animals; D004330:Drosophila / Q000235:genetics; D005784:Gene Amplification; D005786:Gene Expression Regulation; D006801:Humans; D007305:Insecticide Resistance / Q000235:genetics*; D017354:Point Mutation; D015222:Sodium Channels / Q000235:genetics
D015222:Sodium Channels