Insecticide resistance and genetic composition of Myzus persicae (Hemiptera: Aphididae) on field potatoes in New Zealand

Abstract

The prevalence of insecticide resistance mechanisms in populations of Myzus persicae on potatoes in New Zealand was determined in five parthenogenetic aphid lineages raised from individuals collected from Pukekohe in the North Island, and 66 from Canterbury and one from the West Coast in the South Island during mid-summer (January) to early autumn (March) 2005. For each lineage, the genotypes, determined using four microsatellite loci, were compared with the presence or absence of resistance mechanisms assessed using a combination of biochemical tests, polymerase chain reaction-based allelic discrimination and diagnostic dose bioassays. The 72 lineages comprised 23 genotypes (defined using microsatellite markers), with 60% containing one or more mechanisms that confer resistance to between one and three of any of four insecticide classes. In all, 38% contained high or extreme elevated carboxylesterases (E-Carb-R 2 and -R 3) that confer resistance primarily to organophosphates, and some resistance to carbamates and pyrethroids; 19% contained modified acetylcholinesterase (MACE) that gives strong resistance to the di-methyl carbamates, pirimicarb and triazamate; 54% contained a mutation in a voltage-gated sodium channel gene, called knockdown resistance (kdr), that confers resistance to pyrethroids; and 36% contained a second mutation of the gene (super-kdr) that gives enhanced resistance to pyrethroids. In all, 10% of the lineages also showed low-level resistance to neonicotinoids, as shown in imidacloprid diagnostic dose bioassays. Most of the microsatellite genotypes appeared to disclose cycles of sexual reproduction, the clones of which were susceptible to all classes of insecticide chemistry, except two that had acquired MACE possibly by breeding with an invasive MACE genotype or an individual carrying a locally derived MACE mutation. However, lineages carrying multiple resistance mechanisms belonged to two resistant genotypes that formed widely distributed clones. Behavioural bioassays on selected lineages from New Zealand and Europe showed that M. persicae clones from both regions carried E-Carb R 3, or kdr/s-kdr, and showed consistently low responses to the aphid alarm pheromone ( E)- β-farnesene. Methods are discussed for exploiting such putative fitness costs of resistance traits in M. persicae aphids to minimise the development of resistance and restore efficacy to insecticide programmes.