Insecticide Resistance Mechanisms In Populations Research Articles

Transcriptomic modulation in response to an intoxication with deltamethrin in a population of Triatoma infestans with low resistance to pyrethroids.

Triatoma infestans is the main vector of Chagas disease in the Southern Cone. The resistance to pyrethroid insecticides developed by populations of this species impairs the effectiveness of vector control campaigns in wide regions of Argentina. The study of the global transcriptomic response to pyrethroid insecticides is important to deepen the knowledge about detoxification in triatomines. We used RNA-Seq to explore the early transcriptomic response after intoxication with deltamethrin in a population of T. infestans which presents low resistance to pyrethroids. We were able to assemble a complete transcriptome of this vector and found evidence of differentially expressed genes belonging to diverse families such as chemosensory and odorant-binding proteins, ABC transporters and heat-shock proteins. Moreover, genes related to transcription and translation, energetic metabolism and cuticle rearrangements were also modulated. Finally, we characterized the repertoire of previously uncharacterized detoxification-related gene families in T. infestans and Rhodnius prolixus. Our work contributes to the understanding of the detoxification response in vectors of Chagas disease. Given the absence of an annotated genome from T. infestans, the analysis presented here constitutes a resource for molecular and physiological studies in this species. The results increase the knowledge on detoxification processes in vectors of Chagas disease, and provide relevant information to explore undescribed potential insecticide resistance mechanisms in populations of these insects.

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

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.