Inheritance of L1014F and M918T sodium channel mutations associated with pyrethroid resistance in Myzus persicae

Abstract

Two amino acid substitutions (L1014F and M918T) in the voltage-gated sodium channel confer target-site resistance to pyrethroid insecticides in the peach potato aphid, Myzus persicae. Pyrethroid-resistant and -susceptible M. persicae clones with various combinations of these mutations were crossed under laboratory conditions, and the genotypes of aphid progeny were analysed by direct DNA sequencing of the IIS4-S6 region of the sodium channel gene. Segregation patterns showed that in aphids heterozygous for both L1014F and M918T, both mutations were present in the same resistance allele. Despite these mutations appearing largely recessive in other pest species, such aphids exhibited strong resistance to pyrethroids in leaf-dip bioassays. These results have important implications for the spread and management of pyrethroid resistance in field populations.

The Molecular Genetics of Insecticide Resistance

“…This phenomenon was first shown in houseflies where a single amino acid replacement, knockdown resistance (kdr), confers low levels of pyrethroid resistance, but a second amino acid replacement is required in the same polypeptide to confer higher levels of resistance or super-kdr (Miyazaki et al 1996;Williamson et al 1996). These two mutations have occurred repeatedly in different species; for example, both kdr and super-kdr are also found together in the same pyrethroid resistance allele in Myzus persicae (Eleftherianos et al 2008). Similarly, several independent origins of the kdr mutation alone have been documented in the malaria vector Anopheles gambiae by looking at flanking nucleotide sequence variation in different alleles collected from across Africa (Pinto et al 2007).…”

An evolutionarily‐unique heterodimeric voltage‐gated cation channel found in aphids

“…Further evidence supporting a heterodimeric Na v 1 organization in aphids was obtained by amplification of full-length H1 cDNAs from pyrethroid-resistant M. persicae ( Supplementary Table 2 ), using primers unique to the 5′ and 3′ termini of H1. This yielded H1 amplicons containing the classic DII L1014F and M918T amino acid substitutions associated with pyrethroid-resistance [8] , demonstrating the amplification of a functional gene that has been subjected to recent evolutionary modification [15] rather than a pseudogene. Taken together all of this evidence strongly supports the view that aphids have a 4x6TM Na v channel encoded by two genes.…”

“…Given this well-maintained gene organization in the aphid genomes, one could speculate that expression of these subunits may be controlled by regulatory elements such as enhancers which can work in a bidirectional manner [16] , so the “back-to-back” orientation of the two genes may be highly instrumental in allowing the simultaneous co-expression of the two genes. Notably, the H1 prediction for clone G006 also contains both pyrethroid-resistance associated mutations [8] .…”

“…In contrast, all insects thus far studied have only one 4x6TM Na v gene, with alternative splicing of exons imparting functional variability [7] and all channel variants exhibiting high sensitivity to TTX. The 4x6TM Na v s also characteristically bind modulatory drugs and other neurotoxins including local anaesthetics, voltage-sensor disabling scorpion toxins and insecticides such as DDT and the synthetic pyrethroids [8] .…”

Genetic characterization of field-evolved resistance to phosphine in the rusty grain beetle, Cryptolestes ferrugineus (Laemophloeidae: Coleoptera)

“…The novel resistance factors observed in C. ferrugineus could be new copies of already described weak or strong resistance genes resulting from gene duplication [32], or multiple mutations within the same gene as has occurred in several field insect pests [33][34][35], or they could be unique minor factors [31,36]. These additional factors may contribute to the ability of C.…”