Fig. 2

PxylOR16 knockout mutants show impaired electrophysiological responses to heptanal. A Schematic diagram of the sgRNA target in Exon II of PxylOR16. The target sequence is shown in blue, the PAM sequence is marked in red, and the non-homologous insertion in the genome in yellow. Deleted bases are represented by dashes. PxylOR16 mutants show impaired electrophysiological responses to heptanal. B Electrophysiological responses measured as electroantennograms of Plutella xylostella antennae to heptanal and trans-2-hexen-1-ol in wild-type (WT) animals and in PxylOR16 knockout mutants generated by CRISPR/Cas9 (PxylOR16^−/−). Left, dose-dependent electroantennographic (EAG) responses of female and male moths. Heptanal was used at doses ranging from 10 ng to 10 μg. WT female and male antennae exhibited dose-dependent EAG responses to heptanal, with responses increasing with increasing heptanal doses. EAG responses of female and male PxylOR16^−/− moths to heptanal were far lower than those of WT female and male moths at all heptanal doses. Right, as a control, we tested the responses of female and male moths to trans-2-hexen-1-ol, which is not a ligand of PxylOR16. As expected, we observed no differences in the responses to this compound between PxylOR16^−/− moths and WT moths. Error bars indicate SEM (n = 10). Different letters indicate significant differences among insects (two-way ANOVA followed by Tukey’s pairwise test; P < 0.05)