Reduced susceptibility and neural sensitivity to pyrethroids in the absence of the kdr genotype

The fall armyworm (FAW), Spodoptera frugiperda, is a major pest to row crops causing significant economic losses annually. This damage has led efforts to investigate the genetic and molecular mechanisms driving insecticide resistance. We determined neuronal sensitivity of neurotoxic insecticides via neurophysiological recordings and assessed toxicity ratios between lab and field strains of FAW. Topical toxicity of l-cyhalothrin resulted in a resistance ratio (RR) of 767-fold in field collected FAW when compared to the lab strain and this RR was verified through neurophysiological recordings that showed a 1750-fold reduction in l-cyhalothrin potency. Interestingly, point mutations in the voltage-gated sodium channel, known to confer pyrethroid resistance, were not identified in our study. To expand these data, we studied the RR of the organophosphate chlorpyrifos that had an RR of 12 and the field strain was 8-fold less sensitive in neurophysiological recordings. For the ace gene, 80% of larvae had nucleotide sequences interchangeable to other susceptible strains for A201S and F290V mutations. However, 40% were heterozygous for the G227A mutation. Our data indicates that point mutations known to confer resistance did not contribute to the l-cyhalothrin RRs seen across our field-collected FAW population but ACE point mutations were strongly correlated to chlorpyrifos resistance. These data suggests that the kdr genotype is not the sole predictor of the reduced neuronal sensitivity and resistance to l-cyhalothrin and thus, phenotypic assays in addition to genotypic assays should be employed against field populations to predict resistance phenotypes and product failures more accurately in the field.