Genetics of esterase-mediated insecticide resistance in the aphid Schizaphis graminum

Abstract

The genetics of organophosphate resistance, including the pattern of inheritance and the underlying genetic mechanism, were investigated in the aphid Schizaphis graminum (the greenbug). Resistant greenbugs with pattern 1 (R1) and pattern 2 (R2) esterase and susceptible (S) greenbugs were induced into the sexual cycle and crossed. Each resistance-associated esterase pattern in the greenbug was inherited in a Mendelian fashion as a single gene. An aphid clone that displayed both resistance-associated esterase patterns was produced in the F 1 generation of a cross between R2 and R1 insects, and was designated pattern 3 (R3). DNA from different R1 aphids and the R3 aphid clone displayed a restriction fragment pattern different from that of R2 and S clones, and about a twofold increase in hybridization compared with S aphids. DNA from R2 clones showed no restriction fragment differences or increased hybridization signal compared to S insects. These findings suggest that the mechanism behind the R1 esterase activity may be gene amplification, but that the R2 elevated esterase activity may result from a different genetic mechanism.

Biochemical studies on malathion resistance, inheritance and association of carboxylesterase activity in brown planthopper, Nilaparvata lugens complex in Peninsular Malaysia

“…They suggest that the three esterases are products of a single gene, and the different electromorphs were the result of protease digestion (Chen & Sun, 1994). Other species where organophosphate resistance has been linked to increased esterase enzyme activities are red scale (Grafton‐Cardwell et al ., 1998), sibling species A, B and C of Anopheles culicifacies (Raghavendra et al ., 1998) and the aphid, Schizaphis graminum (Rider et al ., 1998). Esterase‐associated resistance may result from a number of potential mechanisms, including production of a more efficient enzyme (Beeman & Schimidt, 1982; Matsumura & Voss, 1965), a gene duplication of an existing enzyme coding gene such as E4 (esterase‐4) in Myzus persicae (Field & Devonshire, 1992), or to evolution of an existing enzyme‐coding gene that produces a variant of that enzyme, that is, the duplicated FE4 variant or E4 in M. persicae (Devonshire, 1989; Devonshire & Field, 1991; Field & Devonshire, 1992; Field et al ., 1993).…”

Evidence of Sibling Species in the Brown Planthopper Complex (Nilaparvata lugens) Detected from Short and Long Primer Random Amplified Polymorphic DNA Fingerprints

“…This high esterase activity was shown to be correlated to organophosphate resistance in brown planthoppers of rice (Chen and Sun 1994;Hemingway et al 1999). Among other species where organophosphate resistance is associated with increased esterase enzyme activity are sibling species A, B, and C of Anopheles culicifacies (Raghavendra et al 1998) and the aphid Schizaphis graminum (Rider et al 1998). Esterase-associated resistance may be due to the production of a more efficient enzyme (Beeman and Schmidt 1982), or to a gene duplication of an existing enzyme coding gene such as E4 (esterase-4) in Myzus persicae (Field and Devonshire 1992), or to the evolution of an existing enzyme-coding gene to produce a variant of that enzyme, i.e.…”

Landscape genomics of Colorado potato beetle provides evidence of polygenic adaptation to insecticides

“…Current recommendations to manage the evolution of insecticide resistance rely on theoretical predictions based on spatially explicit, single‐ or two‐locus population genetic models, which assume that resistance alleles occur at low frequency in pest populations prior to pesticide exposure due to recent origin or fitness costs in the absence of selection (Caprio & Tabashnik, ; Gould, Kennedy, & Johnson, ; Mallet, ; Mallet & Porter, ; Rosenheim & Tabashnik, ; Roush & McKenzie, ; Tabashnik et al., ). While most studies on the genetic basis of insecticide resistance have concluded that adaptation to insecticides is monogenic and drawing from rare alleles (Beeman, ; Brown, ; Crowder et al., ; Georghiou, ; Halliday & Georghiou, ; Hart, ; Oppenoorth, ; Rider, Wilde, & Kambhampati, ; Roush & Tabashnik, ; Roush et al., ; Shanahan, ; Shetty, Sanil, & Shetty, ; White & Bell, ; Wirth, Walton, & Federici, ), inferences could be improved by integrating data from a broader sample of pest populations and genomes (Wellenreuther & Hansson, ).…”