Genetic bases and robustness of the toxicological response to spinosad and lambda-cyhalothrin in Drosophila melanogaster.

Insecticides are valuable and widely used tools for the control of insect pests. However, we know very little about the genes and processes involved in the key steps of the poisoning sequence. Besides, the excessive and indiscriminate use of insecticides is generating mechanisms of resistance in various insect pests. To improve our understanding of insecticide toxicity, we need a powerful model organism to help describe the processes underlying insecticide poisoning and the use of genomic tools to identify and analyze the genetic basis of the toxicological response of the insecticides. In this context, we associate variation in toxicological response with genomic variation, to identify genetic polymorphisms underlying the different steps of the insect (genotype)-response (phenotype)-insecticide (environment) interaction. We investigate the genetic factors involved in the toxicological response of D. melanogaster lines when exposed to spinosad and lambda-cyhalothrin through the measured of KT50 in adult males. Since the genomes of all lines evaluated are completely sequenced, we performed a Genome Wide Association Study that enabled us to identify genetic polymorphisms and candidate genes responsible for the overall phenotypic variation. Most of the candidate genes detected exhibited insecticide-specific effect and play roles in the toxicodynamics as AstC-R1, Dh44-R, stan, Ca-β, AgmNAT, Acox57D-d, Btk, CarT, dpr8, Pkd2, and Shab and the toxicokinetics like for example ckd, Hr38, robo2, Toll-4, Eglp2, and Prip of spinosad and lambda-cyhalothrin. Finally our results suggest that in the case of lambda-cyhalothrin genotypes exhibiting resistance phenotypes (higher KT50) also displaying a less constant (robust) response.