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The peach-potato aphid Myzus persicae (Sulzer) has developed resistance to pyrethroid insecticides as a result of two mutations in the para-type sodium channel protein: L1014F (kdr) and M918T (super-kdr). Two allelic discriminating PCR assays were developed that used fluorescent probes to determine precisely the genotype of these mutations in individuals of M. persicae. These assays were used alongside existing assays for other resistance mechanisms (MACE and elevated carboxylesterase) to investigate the temporal and spatial incidence of insecticide resistance in M. persicae. The kdr mutation and elevated carboxylesterase were found to be widely distributed, being present throughout Europe and in Australia. MACE and super-kdr were widespread in Europe, but were not detected in insects from Australia. A significant deviation from Hardy-Weinberg equilibrium in the populations sampled implied selection against individuals that are homozygous for these resistance mutations. Patterns of distribution in the UK also indicated strong selection against the super-kdr mutation in the absence of insecticide pressure. Significant associations were found between all the different resistance mechanisms, probably promoted by asexual reproduction. The current distribution of the kdr and super-kdr mutations could have arisen by migration from a single source or by independent mutations arising in separate populations. Sequences of intron DNA flanking the mutations showed multiple independent origins of kdr and super-kdr to be the most plausible explanation of these data. |
