Frankliniella occidentalis is a notorious polyphagous crop pest causing tremendous economic loss. It damages flowers and leaves of host plants and also carries severe plant viruses. During last few decades, it has spread to all continents via transport of plant materials. Following extensive use of insecticides to control F. occidentalis, it has developed high level of resistance due to its short life cycle and high reproductive potential. In this study, RNA interference (RNAi)-based bioassay system was developed to find an alternative control measure for insecticide-resistant population of F. occidentalis. A variety of genes involved in various physiological mechanisms were selected for the test of dsRNA potency (tubulin, v-ATPase, amylase, aquaporin etc.). Each bioassay unit made by 3D printing has a leaf disc placed on 150 ㎕ of 50 ng/ul dsRNA solution and 20 thrips. The mortality was checked, and the dsRNA and leaf disc were replaced every 24 h for 72 h. Of the 20 genes tesetd, tubulin, v-ATPase, and aquaporin showed 31, 38, 38 and 45% of corrected mortality at 72 h post-treatment, respectively. This result suggests the potential of these genes as candidate lethal genes for RNAi-based F. occidentalis control system.

Recently, the existence of non-neuronal, soluble AChEs with non-classical functions, such as stress response and chemical defense, has been reported in both vertebrates and invertebrates. With this in mind, it is intriguing to hypothesize that fat body is a main tissue to express non-neuronal AChE at least in some insects. As an initial step for the systematic approach to investigate the distribution of non-neuronal AChEs in insect fat body and to elucidate their physiological functions, we have selected 12 different insect species across different orders and isolated fat body tissues from them. Then, the presence or absence of AChE and its solubility nature were determined by native polyacrylamide gel electrophoresis in conjunction with western blot analysis insect-specific AChE1 and 2 antibodies. Among 12 insects examined, soluble AChE1 was determined to be expressed in fat bodies of insects involving honey bees, brown plant hoppers, dynastid beetles, lice, etc, AChE2 in fruit flies, bed bugs, mealworm beetles. However, no AChE was detected in fat bodies of the remaining two species American cockroaches and dragonflies Our findings clearly show that AChE is widely distributed in the fat body tissue of diverse insect species. More extensive investigation on in a wider variety of insect species would be necessary to deduce the evolutionary origin of fat body-specific AChE, which would be the ancestor of AChE with non-neuronal function.

Colony collapse disorder (CCD), a phenomenon of honeybees disappearance, has been reported since 2006. Chronic exposure to neonicotinoid insecticides, particularly imidacloprid, has been suggested to impair forager’s ability for foraging and be a main cause of CCD. Recently, it has been reported that imidacloprid induces insulin resistance in animal cell line by blocking glucose uptake. Similarly to human insulin, insulin-like peptide (ILP) of insects is involved in maintaining blood glucose contents in hemolymph by regulating the concentration of trehalose and glycogen. Therefore, we have hypothesized that sublethal concentration of neonicotinoid may affect the metabolic pathway of honey bees as well. We investigated the transcription levels of the genes involved in the insulin/insulin-like signaling (IIS) pathway, such as AmILP and AmInR, following an acute or a chronic dietary exposure of sublethal concentrations of imidacloprid to foragers. In both experiments, honeybees showed increased expression levels of ILP and InR in a dose-dependent manner. Our results suggest that sublethal dose of imidacloprid likely upregulates IIS pathway, thereby rendering honey bees to become resistant to insulin.