No 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.

No abstract

The whitebacked planthopper, Sogatella furcifera (Horv ath) (Hemiptera: Delphacidae), an economically important rice pest, has developed resistance to many insecticides. Cycloxaprid, a novel cis-nitromethylene neonicotinoid insecticide, has good industrialization prospects because of its high efficiency against rice planthoppers, including imidacloprid-resistant populations. This study focused on the genes involved in xenobiotic detoxification and stress reaction after exposure to doses of cycloxaprid. Ten cytochrome P450 monooxygenase genes (one CYP3, three CYP4, and six CYP6), one microsomal glutathione S-transferase (GST) gene, and one acetylcholinesterase (AChE) gene were up-regulated in response to a high-dose treatment (HD, 85% mortality). Five P450 genes (one CYP4, two CYP6, and one CYP15), one delta-GST gene, and two carboxylesterase genes were up-regulated in response to a low-dose treatment (LD, 15% mortality). These findings were consistent with previous reports showing that CYP4, CYP6, and GSTd were associated with insecticide detoxification in insects and contributed significantly to insecticide resistance. Another interesting finding was that one Hsp70 and one small Hsp (sHsp) were upregulated in response to HD treatment, whereas they were downregulated in response to LD treatment. In order to check the accuracy of transcriptome data, 10 unigenes were randomly selected to compare their expression between treatments. Regulations of related genes in response to cycloxaprid doses could contribute to explaining the quick responses to insecticide stress.

Aphis craccivora (Koch) is an economically important pest that affects legumes in worldwide. Chemical control is still the primary efficient method for A. craccivora management. However, the mechanism underlying insecticide resistance in A. craccivora has not been elucidated. A previous study observed that piperonyl butoxide (PBO) and diethyl maleate (DEM) significantly synergized imidacloprid in A. craccivora field populations, indicating that cytochrome P450 (P450) and glutathione S-transferase (GST) genes may play pivotal roles in imidacloprid resistance. In this study, 38 P450 genes and 10 GST genes were identified in A. craccivora through transcriptomic analysis. The expression levels of these P450 and GST genes were measured in susceptible (SUS) strains of A. craccivora under imidacloprid treatment with LC15, LC50, and LC85 doses. The expression levels of CYP18A1, CYP6CY21, CYP6DA1, CYP6DA2, CYP4CJ1, CYP4CJ2, and CYP380C6 were up-regulated in the three treatments. Most of these genes belong to CYP3 and CYP4 Clans. In addition, the expression levels of all P450 and GST genes in A. craccivora were also measured in the Juye (JY) and Linqing (LQ) field populations. The expression levels of CYP6DA2, CYP4CJ1, and CYP380C6 were up-regulated in the SUS strain after imidacloprid treatment at three doses, and these genes were overexpressed in the JY population. Furthermore, the sensitivity of A. craccivora to imidacloprid was significantly increased after knockdown of CYP380C6 and CYP6DA2 through RNA interference. These results may help to elucidate the mechanisms underlying of imidacloprid resistance in A. craccivora.