Abstract
One view of adaptation is that it proceeds by the slow and steady accumulation of beneficial mutations with small effects. It is difficult to test this model, since in most cases the genetic basis of adaptation can only be studied a posteriori with traits that have evolved for a long period of time through an unknown sequence of steps. In this paper, we show how ace-1, a gene involved in resistance to organophosphorous insecticide in the mosquito Culex pipiens, has evolved during 40 years of an insecticide control program. Initially, a major resistance allele with strong deleterious side effects spread through the population. Later, a duplication combining a susceptible and a resistance ace-1 allele began to spread but did not replace the original resistance allele, as it is sublethal when homozygous. Last, a second duplication, (also sublethal when homozygous) began to spread because heterozygotes for the two duplications do not exhibit deleterious pleiotropic effects. Double overdominance now maintains these four alleles across treated and nontreated areas. Thus, ace-1 evolution does not proceed via the steady accumulation of beneficial mutations. Instead, resistance evolution has been an erratic combination of mutation, positive selection, and the rearrangement of existing variation leading to complex genetic architecture.
Highlights
Adaptation is often envisioned as a slow and regular improvement, a view embodied by Fisher’s geometrical model of adaptation, whereby mutations fix if they bring the current phenotype closer to an optimum [1,2]
The pleiotropic effects of beneficial mutations may be more complex than deleterious. They may trigger the evolution of the genetic architecture and gene number. This paper illustrates these two aspects with the tortuous path taken during the evolution of insecticide resistance in Culex pipiens mosquitoes in southern France
We present in this study just such a tortuous natural selection pathway, which allows the mosquito Culex pipiens to resist organophosphorous insecticides
Summary
Adaptation is often envisioned as a slow and regular improvement, a view embodied by Fisher’s geometrical model of adaptation, whereby mutations fix if they bring the current phenotype closer to an optimum [1,2]. Pleiotropy causes an ‘‘evolutionary inertia’’ [9] whereby beneficial mutations often only ameliorate the side effects of the last beneficial mutation This process of ‘‘amelioration’’ [10] can follow a scenario a la Fisher [11] with modifiers or compensatory mutations occurring at different loci, or with allele replacement at the same locus (Haldane [12]). Both cases have been reported (e.g., [10,13,14,15,16]). The pleiotropic effects of beneficial mutations may be more complex than deleterious They may trigger the evolution of the genetic architecture and gene number.
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