Figure 4.

Esterase overproduction in Cx pipiens mosquitoes and the SA4B4 isogenic strain. The overproduction of detoxifying carboxylesterases in Cx pipiens is achieved through the tandem amplification of two paralogous esterase loci esterase-3 (encoding for the esterase A) and esterase-2 (esterase B). These two genes are in strong linkage disequilibrium and are commonly referred to as an Ester superlocus (Berticat et al. 2001). The amplicon on which this superlocus occurs is however much larger (30–60 kb) than the esterase containing region (∼10 kb, Hemingway et al. 2002; Guillemaud et al. 1997). The ensemble of the esterase-containing amplicons that are repeated plus their flanking region in the mosquito constitutes an Ester-resistant allele. To construct the SA4B4 strain, a homozygous strain for the Ester⁴ allele (Poirie et al. 1992) was introgressed into a susceptible reference line (SLAB) by a repeated backcross procedure (Berticat et al. 2002). Several scenarios may explain the higher immune phenotype observed in the SA4B4 strain. A first scenario (option 1) involves the existence of an immunoregulatory gene within the amplicon, which would result in it being amplified to a higher extent in SA4B4 mosquitoes than in field-caught mosquitoes. Other genes have already been shown to be hitchhiked and co-amplified by this tandem repetition (Guillemaud et al. 1997; Hemingway et al. 2002). A second scenario (option 2) involves the existence of a strong immunoregulatory allelic variant in linkage disequilibrium with the Ester⁴ allele. Such strong immunoregulatory variant may have been present in the original (VIM) strain. A third scenario (option 3) is that the immune phenotype is the result of epistatic interactions between one of these immunoregulatory factors (option 1 or option 2) and the SLAB genetic background. Dashed lines represent the SLAB genetic background in which the Ester⁴ allele is expressed.