Rooker, S., Guillemaud, T., Bergé, J., Pasteur, N., Michel Raymond, Laboratoire de biologie des invertébrés, Institut National de la Recherche Agronomique (INRA), Institut des Sciences de l'Evolution de Montpellier (UMR ISEM), Centre de Coopération Internationale en Recherche Agronomique pour le Développement (Cirad)-École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université de Montpellier (UM)-Institut de recherche pour le développement [IRD] : UR226-Centre National de la Recherche Scientifique (CNRS), INRA, Génétique moléculaire des Invertébrés, Centre de Coopération Internationale en Recherche Agronomique pour le Développement (Cirad)-École pratique des hautes études (EPHE)-Université de Montpellier (UM)-Institut de recherche pour le développement [IRD] : UR226-Centre National de la Recherche Scientifique (CNRS), École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université de Montpellier (UM)-Centre de Coopération Internationale en Recherche Agronomique pour le Développement (Cirad)-Centre National de la Recherche Scientifique (CNRS)-Institut de recherche pour le développement [IRD] : UR226, ProdInra, Migration, and Pasteur, Nicole
International audience; In Culex pipiens mosquitoes, resistance to organophosphorous insecticides often results from increased detoxification by two types of esterases, A and B, which are closely linked. Overproduction of all esterases B so far investigated (B1, B2, B4, B5 and B6) is from gene amplification. An esterase A gene (esterase A2) has recently been cloned from mosquitoes with the overproduced esterases A2 and B2, and amplification of this gene has also been reported. We describe the cDNA sequences of three additional esterase genes from insecticide-resistant strains of Culex pipiens originating from France and California which show at least 93 per cent homology with the esterase A2 gene sequence. Restriction enzyme mapping shows that the esterase A gene lies within 2.2 kb of the esterase B gene. In mosquitoes with overproduced esterases A2 and B2, the amplification level of esterase A is equal to that of esterase B suggesting that the genes are coamplified. Furthermore, we show that in one strain with an overproduced A esterase (A1), gene amplification cannot account for the increased protein level. This indicates that overproduction of esterases A can be achieved through two different mechanisms: gene amplification and a regulatory mechanism - the nature of which remains to be identified.