The molecular and population genetics of cyclodiene insecticide resistance

Cyclodiene resistance has accounted for over 60% of reported cases of insecticide resistance. Understanding of this resistance can therefore help us answer questions relating to the mechanism and origin of representative resistance-associated mutations, questions fundamental to the molecular and populations genetics of pesticide resistance. The cyclodiene resistance gene Rdl (resistance to dieldrin) was cloned from a mutant of the model insect Drosophila resistant to cyclodienes and picrotoxinin. Rdl codes for a subunit of a novel class of GABA gated chloride ion channels and resistance is correlated with replacement of the same amino acid residue in a wide range of species from different insect orders. This single amino acid replacement Ala302 > Ser, within the proposed lining of the chloride ion channel, also confers insensitivity to the blocking action of cyclodienes and picrotoxinin on GABA gated chloride ion channels expressed in Xenopus oocytes. The resistance mechanism involves both changes in cyclodiene binding site affinity and also a change in the rate of receptor desensitization which destabilizes the cyclodiene-favored conformation. Documentation of the resistance associated mutation has allowed for the design of a PCR based molecular monitoring technique. This technique gives more accurate estimates of resistance gene frequency from smaller sample sizes and has shown the frequency of resistance in apparently unselected populations of Drosophila to be as high as 1%. We are still uncertain as to why resistance persists in the apparent absence of selection pressure and any severe reduction in the fitness of resistant strains, besides a paralytic phenotype at high temperature, remains undocumented.