Two mutations in nAChR beta subunit is associated with imidacloprid resistance in the Aphis gossypii

•We find new case in imidacloprid resistance mechanism in insect.•Mutations confer the resistance phenotype without P450-mediated detoxification.•The L80S mutation along with the R81T mutation in nAChR can be the main player to develop imidacloprid resistance.

The Aphis gossypii imidacloprid-resistant (IR) strain was about 3800-fold resistant to imidacloprid. Synergistic bioassays revealed that metabolic factors were not likely involved in resistance. An isogenic susceptible (IGS) strain was generated and used as references for RNA-seq, qrtPCR and 2DE. There were no noticeable differences between IGS and IR strains in either the transcriptome or proteome profiles, confirming that imidacloprid resistance is likely due to the target site insensitivity. The IR strain was determined to possess a point mutation resulting in an R81T substitution only in the nAChR beta 1 subunit, which had been also reported to be responsible for the reduced sensitivity to imidacloprid in M. persicae. An nAChR beta 1 subunit transcript variant in the N-terminal region was found and an additional point mutation, L80S was also detected along with the R81T mutation in IR strain, suggesting its potential role in resistance. Taken together, the R81T mutation in the nAChR beta 1 subunit, perhaps with the L80S mutation as well, could be the major factor of imidaloprid resistance in the IR strain and can be employed as molecular markers for the detection of imidacloprid resistance in field populations of A. gossypii.

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