A sodium channel point mutation is associated with resistance to DDT and pyrethroid insecticides in the peach-potato aphid, Myzus persicae (Sulzer) (Hemiptera : Aphididae)
D. Martinez-torres et al., A sodium channel point mutation is associated with resistance to DDT and pyrethroid insecticides in the peach-potato aphid, Myzus persicae (Sulzer) (Hemiptera : Aphididae), INSEC MOL B, 8(3), 1999, pp. 339-346
The voltage-gated sodium channel is the primary target site of DDT and pyre
throid insecticides, and point mutations in the domain II region of the cha
nnel protein have been implicated in the knockdown resistant (kdr) phenotyp
e of several insect species. Here, we report that one of these mutations, a
leucine-to-phenylalanine replacement in transmembrane segment IIS6, is als
o found in certain insecticide-resistant clones of the peach-potato aphid,
Myzus persicae, The mutation was present in four clones with amplified E4 e
sterase genes, but was absent from both susceptible clones and those with a
mplified FE4 genes. The inferred presence of kdr-type resistance in the fou
r E4 clones was subsequently confirmed by bioassays that showed this to be
the primary mechanism of resistance to deltamethrin and DDT, although the e
sterase-based mechanism also contributes to the overall level of deltamethr
in resistance. The kdr mutation on its own conferred 35-fold resistance to
deltamethrin and this was enhanced up to 540-fold when it was present in a
high (E4) esterase background. The esterase (FE4) mechanism was far less ef
fective without the kdr mutation, conferring just 3-4-fold resistance to de
ltamethrin. These findings, and the linkage disequilibrium of the kdr mutat
ion within clones overproducing the E4 esterase, have important implication
s for the evolution of resistance in this insect and for the use of pyrethr
oid sprays in the management of M. persicae populations in the field.