Figure 1.

Mechanisms of overcoming fitness costs associated with insecticide resistance.

(a) Differential methylation of amplified copies of esterase-4 (E4) in the aphid Myzus persicae. Gene amplification of E4 in highly resistant R₃ clones (only five tandemly duplicated copies are shown here for simplicity) results in an increase in both the E4 transcript and E4 protein which can sequester and hydrolyse a range of organophosphorus and carbamate insecticides. However in the absence of insecticide, ‘revertant’ clones exhibit loss of both E4 expression and insecticide resistance. This loss of E4 expression is associated with loss of CpG sites within the amplified genes, resulting in gene silencing via demethylation. (b) Diazinon resistance evolution in the Rop-1 locus encoding esterase-3 on chromosome IV of the Australian sheep blowfly Lucilia cuprina is followed by evolution of a fitness modifier Scalloped wings (Scl) on chromosome III. This fits the classical model for the evolution of a fitness modifier (see text for discussion). (c) Gene duplication leads to a compound heterozygote in which both a susceptible (ace-1^S) and a resistant (ace-1^R) copy of the ace-1 gene are then found on the same chromosome. In this configuration any fitness costs associated with the ace-1^R allele will be offset by the permanent presence of the susceptible allele along side it in permanent heterozygosis.