Submitted to: Journal of Insect Biochemistry and Molecular Biology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/21/1998
Publication Date: N/A
Citation: N/A Interpretive Summary: Many agricultural insect pest species have developed resistance to the extensively used family of pyrethroid insecticides. Resistance in several species, including the horn fly (Haematobia irritans), has been associated with two point mutations in the para-sodium channel gene. These mutations, known as kdr and super-kdr, have been postulated to confer pyrethroid resistance, but the extent to which they directly confer resistance is unknown. Using a PCR-based assay to detect the presence of kdr and super- kdr alleles in individual flies, we have determined the mutation frequencies (percentage of individuals with mutations) in several wild and laboratory populations. Comparison of mutation frequency and bioassay determined cyhalothrin resistance levels indicates that the kdr mutation confers a significant level of pyrethroid resistance. However, suppression of resistance by PBO in a highly resistant laboratory strain indicates extensive involvement of monooxygenases, but only in the presence of consistent insecticide pressure. Additionally, in over 1,200 wild and laboratory-reared flies assayed, no individuals were encountered with the super-kdr mutation in the absence of the kdr mutation. This suggests that the super-kdr mutation may be lethal. This is the first report of this finding, which indicates a complex relationship between the two mutations.
Technical Abstract: The kdr and super-kdr point mutations found in the insect sodium channel gene are postulated to confer knockdown resistance (kdr) to pyrethroids. Using an allele-specific PCR assay to detect these mutations in individual horn flies, Haematobia irritans (L.), we determined the frequency of the kdr and super-kdr mutations in several wild and laboratory populations. Wild populations with very similar mutation frequencies had resistance levels that ranged widely from 3- to 18-fold relative to a susceptible population. Conversely, the kdr frequency in a lab population with 17-fold resistance was nearly double that found in a heavily pressured wild population with 18-fold resistance. We conclude that, although the kdr mutation confers significant levels of pythrethroid resistance, a substantial component of resistance in insecticidally pressured populations is conferred by mechanisms that are PBO-suppressible. High super-kdr frequencies were detected in resistant lab populations, but in wild populations with equivalent resistance the super-kdr frequency was very low. Interestingly, all individuals bearing the super-kdr mutation also bore the kdr mutation, suggesting that without the kdr mutation the effect of the super-kdr mutation may be lethal.