Role of the kdr and super-kdr sodium channel mutations in pyrethroid resistance: correlation of allelic frequency to resistance level in wild and laboratory populations of horn flies (Haematobia irritans)

Citation
Rc. Jamroz et al., Role of the kdr and super-kdr sodium channel mutations in pyrethroid resistance: correlation of allelic frequency to resistance level in wild and laboratory populations of horn flies (Haematobia irritans), INSEC BIO M, 28(12), 1998, pp. 1031-1037
Citations number
21
Categorie Soggetti
Entomology/Pest Control","Biochemistry & Biophysics
Journal title
INSECT BIOCHEMISTRY AND MOLECULAR BIOLOGY
ISSN journal
09651748 → ACNP
Volume
28
Issue
12
Year of publication
1998
Pages
1031 - 1037
Database
ISI
SICI code
0965-1748(199812)28:12<1031:ROTKAS>2.0.ZU;2-8
Abstract
The kdr and super-kdr point mutations found in the insect sodium channel ge ne are postulated to confer knockdown resistance (kdr) to pyrethroids. Usin g an allele-specific PCR assay to detect these mutations in individual horn flies, Haematobia irritans (L.), we determined the allelic frequency of th e kdr and super-kdr mutations in several wild and laboratory populations. W ild populations with very similar allelic frequencies had resistance levels that ranged widely from 3- to 18-fold relative to a susceptible population . Conversely, the kdr allele frequency in a lab population with 17-fold res istance was nearly double that found in a heavily pressured wild population with Is-fold resistance. We conclude that, although the kdr mutation confe rs significant levels of pyrethroid resistance, a substantial component of resistance in insecticidally pressured populations is conferred by mechanis ms that are PBO-suppressible. High super-kdr allele frequencies were detect ed in two resistant lab populations, but in wild populations with equivalen t resistance the super-kdr allele frequency was very low. Interestingly, in over 1200 individuals assayed, the super-kdr mutation was never detected i n the absence of the kdr mutation. (C) 1998 Published by Elsevier Science L td. All rights reserved.