Selection for imidacloprid resistance in Nilaparvata lugens: cross‐resistance patterns and possible mechanisms

Abstract

A field population of brown planthoppers (Nilaparvata lugens Stål) was collected and selected for imidacloprid resistance in the laboratory. The resistance increased by 11.35 times in 25 generations and the resistance ratio reached 72.83 compared with a laboratory susceptible strain. The selected resistant strain showed obvious cross-resistance to all the acetylcholine receptor targeting insecticides tested (monosultap 1.44-fold, acetamiprid 1.61-fold, imidacloprid homologues JS599 2.46-fold and JS598 3.17-fold), but not to others. Further study demonstrated that TPP and DEM had no synergism on imidacloprid. However, PBO displayed significant synergism in some different strains, and the synergism increased with resistance (S strain 1.20, field population 1.43 and R strain 2.93). PBO synergism to cross-resistant insecticides was also found in the resistant strain (monosultap 1.25, acetamiprid 1.39, JS598 1.94 and JS599 2.02). We concluded that esterase and glutathione S-transferase play little role in imidacloprid detoxification. The increase of the P450-monooxygenases detoxification is an important mechanism for imidacloprid resistance and target resistance may also exist in this species.

A nicotinic acetylcholine receptor mutation conferring target-site resistance to imidacloprid inNilaparvata lugens(brown planthopper)

“…19. After further selection, the resistance ratio after 35 generations (T35) had increased to 250-fold (20).…”

“…The bidirectional amplification of specific alleles method (23) was used to further characterize the genotype of susceptible and resistant planthoppers at position Y151 in the gene encoding Nl␣1 (Table 1). At generation 25, when resistance to imidacloprid was 73-fold (19), 59 of 70 individuals tested (84%) were heterozygous for Y151S, and the remaining 11 (16%) were homozygous for the mutation. By generation 35, when resistance had reached 250-fold (20), all insects tested were homozygous for the mutation.…”

“…Recently, evidence has been obtained for resistance to imidacloprid in the brown planthopper Nilaparvata lugens, a major rice pest (19). The lack of cross-resistance to other insecticide classes and the lack of marked synergism by inhibitors of detoxifying enzymes suggested that resistance might be due to a mutation within the target site of imidacloprid rather than due to enhanced detoxification (19).…”

“…The lack of cross-resistance to other insecticide classes and the lack of marked synergism by inhibitors of detoxifying enzymes suggested that resistance might be due to a mutation within the target site of imidacloprid rather than due to enhanced detoxification (19). To examine this possibility, five nAChR subunits (Nl␣1-Nl␣4 and Nl␤1) were cloned from N. lugens.…”

Studies on <i>Aphis gossypii</i> cytochrome P450s CYP6CY22 and CYP6CY13 using an <i>in vitro</i> system

“…1), which achieve excellent control of A. gossypii, target nicotinic acetylcholine (ACh) receptors (nAChRs) of insects. [1][2][3][4] Resistance to neonicotinoid insecticides has developed relatively slowly; however, it is recognized as an important issue, 5) particularly because of the resistance of numerous species such as whiteflies (Bemisia tabaci and Trialeurodes vaporariorum), [5][6][7] brown planthoppers (Nilaparvata lugens), 8) Colorado potato beetles (Leptinotarsa decemlineata), 9) and western flower thrips (Frankliniella occidentalis). 10) Resistance to neonicotinoid insecticides is attributed in some cases to mutations in nAChRs or to increased rates of insecticide detoxification.…”