The melon and cotton aphid Aphis gossypii Glover (Hemiptera; Aphididae) is one of the most serious pests worldwide. We surveyed insecticide susceptibility in A. gossypii field populations to 12 insecticides (6 neonicotinoids, 3 pyrethroids and 3 others) to examine resistance ratios. The levels of insecticide resistance were extremely high, especially to neonicotinoids, such as acetamiprid, clothianidin, thiacloprid and imidacloprid. To identify the neonicotinoid resistance mechanisms, we used an imidacloprid-resistant (IMI-R) strain as a model strain. IMI-R showed an extremely high resistance ratio and also cross-resistance to all the test neonicotinoids. However, there was little or no cross-resistance to the other insecticides, including sulfoxaflor. Synergist tests and enzyme activity assays suggested the absence of resistance mechanisms based on enhanced detoxification enzymes, such as cytochrome P450, esterase and glutathione S-transferase. One point mutation was found in the beta1 subunit loop D region of the nicotinic acetylcholine receptor (nAChR) of the IMI-R strain. This R81T point mutation was also found in field populations collected from 5 regions. Therefore, the R81T point mutation was identified as an important mechanism of imidacloprid resistance in A. gossypii.

The two-spotted spider mite, Tetranychus urticae Koch (Acari: Tetranychidae), is one of the most important pest species devastating many horticultural, ornamental crops and fruit trees. Difficulty in managing this mite is largely attributed to its ability to develop resistance to many acaricides. Development of 3,700 folds resistance to etoxazole was found in the population of T. urticae collected from rose greenhouses in Buyeo, Chungnam Province in August 2000. This population has been selected for eleven years with etoxazole (over 500 times), and increased over 5,000,000 fold in resistance as compared with susceptible strain (S). Etoxazole-resistant strain was shown to be maternally inherited. The objective of this study was to determine whether resistance of T. urticae to etoxazole was linked with point mutations in the mitochondrial gene. DNA sequencing of cytochrome c oxidase subunit I (COX1), COX2, COX3, cytochrome b (CYTB), NADH dehydrogenase subunit 1 (ND1), ND2, ND3, ND4, ND5, and ND6 were analyzed by comparing two isogenic etoxazole-susceptible (EtoS) and etoxazole-resistant (EtoR) strains. As a result, all genes revealed no point mutations between the two strains.

The molecular mechanisms and genetics of abamectin resistance mediated by target site insensitivity in the two-spotted spider mite, Tetranychus urticae, were investigated by comparing two isogenic AbaS and AbaR strains. Cloning and sequencing of full-length cDNA fragments of GABA-gated chloride channel genes revealed no polymorphisms between the two strains. However, sequence comparison of the full-length cDNA fragment of a T. urticae glutamate-gated chloride channel gene (TuGluCl) identified a G323D point mutation as being tentatively related with abamectin resistance. In individual F2 progenies obtained by backcrossing, the G323D genotype was confirmed to correlate with abamectin resistance. Bioassays using progeny from reciprocal crossings revealed that the abamectin resistance trait due to TuGluCl insensitivity is incompletely recessive.

Molecular mechanisms of monocrotophos resistance in the two-spotted spider mite (TSSM), Tetranychus urticae Koch, were investigated. The resistant (AD) strain showed ca. 3,565-fold resistance compared to a susceptible (UD) strain. No significant differences in the esterase and gluthathion-S-transferase activities were found between two strains whereas AD showed a 1.9-fold higher mixed function oxidase activity. Acetylcholinesterase (AChE) inhibition assay revealed that the AChE from AD strain is 91-fold less sensitive to monocrotophos, suggestive of the target site insensitivity mechanism. Three point mutations (G228S, A391T and F439W/Y) in the AChE gene (tssmace) appeared to primarily contribute to the reduced sensitivity of AChE as judged by the correlation study of mutation frequency versus resistance levels (LC50) of several field populations. The resulting correlation coefficients of the G228S and F439W mutations were 0.711 and 0.300, respectively, suggesting that G228S mutation may play a more significant role in resistance. The A391T mutation, saturated in all field populations examined, appears to provide a base line resistance.