Abstract
Insecticide resistance can arise from a variety of mechanisms, including changes to the target site, but is often associated with substantial fitness costs to insects. Here we describe two resistance-associated target-site mutations that have synergistic and compensatory effects that combine to produce high and persistent levels of resistance to fipronil, an insecticide targeting on γ-aminobytyric acid (GABA) receptors. In Nilaparvata lugens, a major pest of rice crops in many parts of Asia, we have identified a single point mutation (A302S) in the GABA receptor RDL that has been identified previously in other species and which confers low levels of resistance to fipronil (23-fold) in N. lugans. In addition, we have identified a second resistance-associated RDL mutation (R300Q) that, in combination with A302S, is associated with much higher levels of resistance (237-fold). The R300Q mutation has not been detected in the absence of A302S in either laboratory-selected or field populations, presumably due to the high fitness cost associated with this mutation. Significantly, it appears that the A302S mutation is able to compensate for deleterious effects of R300Q mutation on fitness cost. These findings identify a novel resistance mechanism and may have important implications for the spread of insecticide resistance.
Highlights
Ligand-gated chloride channels that include receptors for GABA, glutamate and histamine[13] and are important targets for insecticides[14]
Studies demonstrated that resistance to insecticides such as dieldrin and fipronil were a consequence of a single point mutation (A302S), located within the TM2 domain of RDL19,21–23, that confers resistance to fipronil and is widespread in field populations of several important insect pests
14th generation did not result in a further increase in fipronil resistance, with levels remaining close to 230-fold in subsequent generations
Summary
Ligand-gated chloride channels that include receptors for GABA, glutamate and histamine[13] and are important targets for insecticides[14]. The first insect GABA-gated ion channel to be characterized in detail was RDL17, originally identified in Drosophila as being encoded by a gene associated with resistance to the insecticide dieldrin (rdl) ‘resistance to dieldrin’[18,19]. Studies demonstrated that resistance to insecticides such as dieldrin and fipronil were a consequence of a single point mutation (A302S), located within the TM2 domain of RDL19,21–23, that confers resistance to fipronil and is widespread in field populations of several important insect pests. We describe studies examining insecticide resistance mechanisms in Nilaparvata lugens (brown planthopper), a major pest of rice crops throughout Asia Studies with both field populations and laboratory-selected insects have identified a second resistance-associated point mutation (R300Q) in fipronil-resistant N. lugens. It is a phenomenon that is likely to have important implications for the development and spread of resistance to fipronil
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