Fig. 1
Evolutionary mechanism of deltamethrin resistance in Aedes albopictus. A An Ae. albopictus laboratory deltamethrin-resistant strain (Lab-R) was derived successfully from the laboratory susceptible strain (Lab-S) in previous work [14]. An F1534S substitution (target-site resistance, F/S) in the voltage-gated sodium channel (vgsc) gene was the first event detected during the emergence of resistance. A second mutation, I1532T (I/T), was subsequently detected accompanied by the emergence of increased metabolic enzyme activity, including cytochrome P450 monooxygenases (P450s), choline/carboxylesterases (CCEs) and the glutathione-S-transferase (GSTs), also likely involved in resistance. The different selected generations are the 6th generation (R6), the 12th generation (R12), the 24th generation (R24) and the 30th generation (Lab-R30) [14]. B Isolation of sub-strains from the Lab-R30 strain. The genotypes of unmated individuals in Lab-R30 were identified by sequencing PCR products. The unmated individuals with the same genotypes were crossed to obtain R30-1532T (1532T/T1534F/F), R30-1534S (1532I/I1534S/S) and R30-M (1532I/I1534F/F) strains. C Larval and adult bioassays of deltamethrin resistance in different strains (n = 10, 20–30 adults per strain in each experiment). Error bars represent 95% CIs. D Target-site resistance (I1532T/F1534S mutations) and metabolic resistance involved in the evolution of resistance to deltamethrin