Abamectin, soil-born bacterial acaricides, has been intensively used to control Tetranychus urticae. Target site insensitivity and enhanced activity of detoxification enzymes have been considered as major resistance mechanisms. Here, we identified the differentially expressed genes after feeding sublethal dose of abamectin for 36 h by RNA-seq analysis. About 4.9 million reads (± 2,630,543 reads) were assembled into T. urticae. Among a total of 75 genes showing differential transcription, 18 and 14 genes were up- and down-regulated over two fold ratio, respectively. In the validation analysis, the calculated fold change of each genes between RNA-seq and qPCR were moderately correlated (r 2 = 0.661). A cuticular protein was shown as the highest up-regulated gene (192.3-fold) and a chitinase was revealed to be the highest down-regulated (-16.4-fold). Further study would be necessary to validate their roles in T. urticae adaptation to acaricides.

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.

The TSSM is one of the most destructive pests on various orchard trees and garden plants. Abamectin resistance mechanisms in two resistant TSSM strains (PTF, ca. 155-fold; AbaR, ca. 3700-fold) were investigated with an emphasis on target site insensitivity mechanism. Detoxification enzyme assays revealed that metabolic factors contributed by EST and/or P450are involved in abamectin resistance. Synergistic assays showed that enhanced detoxification enzyme activity is not enough to account for the high level of abamectin resistance, further suggestive of the involvement of additional resistance mechanism, most likely target site insensitivity. As a putative target site for abamectin, we cloned the cDNA fragments of glutamate-gated chloride channel (Tuglucl) and determined its full length nucleotide sequences. Amino acid sequence comparison among the four strains showed that the Gly323Asp mutation located in the third transmembrane domainis only found in the AbaR strain, suggesting it is likely associated with the target site insensitivity conferring a high level of abamectin resistance.

Movement behaviors of specimens of mite (Tetranychus urticae) were computationally analyzed after the treatments of pesticide, abamectin, at a low concentration of 0.78ppb. During the observation period, test specimens were placed individually on the bean leaves (diameter=7mm), and their position was recorded in 2-dimension at 0.25 second intervals (8 hours before treatment and 8 hours after treatment). The selected parameters such as speed, angular change, meander, etc, were checked for characterizing response behaviors after the treatments. The difference of mite behavior was accordingly observed after the treatments, and the time spent in the center area appeared to be longer after the treatments. Additional characterization of movement behaviors was computationally checked, and utilization of behavioral monitoring in pest management was further discussed regarding early detection of susceptible or resistant strains.

점박이응애, 간자와응애와 긴털이리응애에 대하여 abanectin 의 독성을 leaf disc 법으로 시험하였다. A-bamectin은 점박이응애나 간자와응애보다 긴털이리응애에 대하여 독성이 매우 낮았다. 긴털이리응애 암컷성충은 처리 농도가 증가할수록 생존율이 크게 감소하였으나, 0.38~6ppm에서 8~78%가 생존하였으며, 산란수도 농도 증가에 따라 크게 감소하였다. 모든 처리 농도에서 긴털이리응애 난의 부화나 생존 유.약충의 발육에는 영향이 없었다. 유.약충의 생존율은 농도 증가에 딸라 감소하여 0.38~3ppm에서 42~90%가 성충으로 우화하였다. 중독된 먹이를 섭식한 긴털이리응애 암컷 성충은 생존율에는 별 영향이 없었지만, 산란수와 차세대의 성비에는 상당한 영향을 받았다. 또한 긴털이리응애에 상대적으로 영향이 적어 아치사농도라할수 있는 0.38~0.75ppm에서의 abamectiondms 점박이응애나 간자와응애의 종합관리에서 긴털이리응애와 식식성응애류의 밀도비율 조절에 유요할것으로 생각된다.

긴덜이리응애와 dicofol 저항성 및 감수성 점박이응애에 대한 아바맥틴의 선택독성을 실험실 내에서 엽침지법으로 조사하였다. 아바멕틴은 긴털이리응애에 대해서는 독성이 낮은 반면, 점박이응애에 대해서는 살균효과가 높았다. 0.12 ppm과 0.6 ppm의 농도에서 점박이응애는 두 계통 모두 침지 후 48시간 0]내에 사망하였고, 0.06 ppm과 0.012 ppm의 낮은 농도에서 120시간 이후에는 77% 이상이 사망하였다. 그러나긴털이리응애의 암컷성충은 0.12ppm에서는 생존솔과 활동력이 영향을 받지 않았고, 0.6ppm과 6ppm의 높은 농도에서도 사망솔이 약 20~23%이었다. 아바맨틴은 산란후 l일 이내의 점박이응애의 난에 대해서는 패화솔에 영향을 미치지 않았으나 산란후 4일된 란에서는 패화솔이 멸소하였다. 반면에0.006-6ppm 용액에 긴털이리응애 난을 침지한경우 난의 패화솔과 그 난에서 부화한 약충의 발육에는 영향이 없었다. 긴털이리응애의 암컷 성충을 0.6 ppm과- 0.12ppm에 침지했을 때 산란수가 줄어들지 않았으나 잠박이응애의 산란수는0.006-0.6 ppm의 농도에서 현저히 감소하였다. 이상과 같이 아바맥틴은 점박이응애와 긴털이리응애에 대한 선택독성이 높은 약제로 점박이응애의 결합방제에 유용하게 이용될 수 있을 것으로 생각되며, 점박이응애에 대한 아치사농도(0.012-0.06 ppm)는 긴털이리응애와 점박이응애의 밀도를 조사하는데 이용될 수 있을 것으로 생각된다.