Insecticide resistance in the mosquito Culex pipiens: What have we learned about adaptation?

Abstract

Resistance to organophosphate (OP) insecticide in the mosquito Culex pipiens has been studied for ca. 30 years. This example of micro-evolution has been thoroughly investigated as an opportunity to assess precisely both the new adapted phenotypes and the associated genetic changes. A notable feature is that OP resistance is achieved with few genes, and these genes have generally large effects. The molecular events generating such resistance genes are complex (e.g., gene amplification, gene regulation) potentially explaining their low frequency of de novo occurrence. In contrast, migration is a frequent event, including passive transportation between distant populations. This generates a complex interaction between mutations and migration, and promotes competition among resistance alleles. When the precise physiological action of each gene product is rather well known, it is possible to understand the dominance level or the type of epistasis observed. It is however difficult to predict a priori how resistance genes will interact, and it is too early to state whether or not this will be ever possible. These resistance genes are costly, and the cost is variable among them. It is usually believed that the initial fitness cost would gradually decrease due to subsequent mutations with a modifier effect. In the present example, a particular modifier occurred (a gene duplication) at one resistance locus, whereas at the other one reduction of cost is driven by allele replacement and apparently not by selection of modifiers.

A novel acetylcholinesterase gene in mosquitoes codes for the insecticide target and is non–homologous to theacegeneDrosophila

“…Thus ace-1 designates the locus coding for a cholinergic AChE (or AChE1), responsible for OP and carbamate resistance in Cx. pipiens (it was previously named Ace.1; Raymond et al 2001) and ace-2 refers to the second ace locus, not involved in insecticide resistance in Cx. pipiens (previously named Ace.2), its function being unknown in Cx.…”

Increased fecundity of malathion-specific resistant beetles in absence of insecticide pressure

“…The stability of insecticide resistance was found to be the result of subsequent modification of the insect genome (Roush and McKenzie, 1987;McKenzie, 1996;Guillemaud et al, 1998;Raymond et al, 2001). In the sheep blowfly, Lucilia cuprina, there is a fitness cost associated with an allele coding for resistance to diazinon.…”

“…The genes involved in the resistance of the mosquito Culex pipiens to organophosphate insecticides are costly in fitness terms. However, at one resistance locus, a reduction of cost, driven by allele replacement and not by selection of modifiers has been observed (Guillemaud et al, 1998;Raymond et al, 2001). If such modifier genes or allele replacement occurred in T. castaneum malathion-specific resistance, due to the intensive selective pressure with malathion, the increased fecundity of resistance insects may be explained as a pleiotropic effect of the modifier gene or the less costly resistance allele; giving them a reproductive advantage compared to susceptibles.…”

“…Heredity (2002) 89, 425-429. doi:10.1038/sj.hdy.6800167 involved in resistance, from the selection of modifiers that ameliorate the fitness of resistant genotypes in the absence of insecticide (see McKenzie, 1996, and references therein), or from the replacement of the resistance alleles by less costly resistance alleles (Guillemaud et al, 1998;Raymond et al, 2001).…”

Allelic diversity of metallothionein in Orchesella cincta (L.): traces of natural selection by environmental pollution

“…antibiotic resistance) to mammals. A well-known example comes from insecticide (organophosphate) resistance in the mosquito Culex pipiens caused by a modified acetylcholinesterase (Raymond et al, 2001). Lenormand et al (1999) showed that the frequency of 'resistance' alleles was higher in organophosphate-treated areas, and tended to decrease with distance from those treated sites.…”