Effects of Tebufenozide on the Biological Characteristics of Beet Armyworm (Spodoptera exigua Hübner) and Its Resistance Selection

In this article, the selection of tebufenozide to beet armyworm （Spodoptera exigua Htibner） was studied by the treatments to alternative generations＇ 3rd-instar larvae with LC50 dose and to continuous generations＇ larvae with LC10 dose; the effects of tebufenozide on the biological characteristics of current and subsequent generations were examined by the treatments to 3rd-instar larvae and egg pods in different concentrations. After treatments with LC50 dose till F11, the toxicity of tebufenozide to beet armyworm had no significant change, whereas the pupation rate, pupal weight, and fecundity were reduced markedly. After treatments with LC10 dose till Fl9, the beet armyworm only developed 3.52-fold resistance, and the main biological characteristics were nearly accordant in each generation. The livability was reduced 72 h later after treatments to 3rd-instar larvae, respectively in 2.5-40 μg mL^-1, and larval duration, pupation rate, and pupal weight changed considerably with the increase in concentrations. The fecundity, larval livability, larval weight and pupal weight of subsequent generations were reduced as the dose increased over 10 μg mL^-1. The hatching rate of egg pods did not differ with that of the controls obviously after treatment in 10-300 μg mL^-1. But the larval livability, larval weight and pupal weight were reduced when eggs were exposed to 50 μg mL^-1 dose or more. The results indicated that tebufenozide had low resistance risk to the current and subsequent generations of beet armyworm even if tebufenozide had significant effects on the biological characteristics of this insect.

Degradation of furan tebufenozide in laboratory and field trials

Furan tebufenozide is a newly developed insect growth regulator and has been applied as a pesticide in agriculture in China.Its degradation under both laboratory and field conditions was investigated,and the degradation kinetics was fitted by simple first order kinetics (SFO) model and first order double exponential (FOD) model.Laboratory studies were conducted with or without light in five simulated media (sterilized deionized water,river water,soil solution,sterilized soil and natural soil).No dissipations of furan tebufenozide were observed in sterilized aqueous and soil media under light prevented conditions,whereas degradation occurred under all the other conditions in the laboratory.Derived from SFO and FOD models,DT50 in the dark and light laboratory conditions was in the range of 39.7-82.5 and 1.1-8.0 days,respectively.These results indicated that microbes and light were the main factors for the degradation of the pesticide in the laboratory.During field trials,derived from the SFO model,DT50 and DT90 were 30.3 and 100.5 days,while derived from the FOD model,DT50 and DT90 were 28.9 and 274.9 days,respectively.Compared with laboratory experiments,field trials were influenced by multiple factors.Therefore,the SFO model could not fit experimental data as well as the FOD model did in field trials.

Tebufenozide resistance is associated with sex-linked inheritance in Plutella xylostella

The diamondback moth （DBM）, Plutella xylostella （L.）, is a major pest of cruciferous crops. Tebufenozide, a novel nonsteroidal ecdysone agonist, exhibits good efficacy and has played an increasingly important role in the control of Lepidopteran pests in China. For its resistance management, the genetic basis of tebufenozide resistance was studied using a laboratory selected resistant strain of DBM （resistant ratio, RR = 268）. A series of crosses with laboratory susceptible and resistant strains revealed that tebufenozide resistance in this pest was partially biased toward female heredity, with a large difference in RR for F1 （RR = 29） and rF1 progeny （RR = 147）. The dominance calculated for these 2 cross progeny was -0.788 and 0.09, respectively. Further analysis showed that the susceptible male and female larvae were similar in theft sensitivity to tebufenozide, but the resistant female larvae showed significantly higher resistance than the resistant male larvae. The heredity of tebufenozide resistance in DBM might be linked with the W sex chromosome, which suggested that DBM has the ability to develop high levels of resistance to tebufenozide. This is the first report of sex-linked inheritance oftebufenozide resistance in P xylostella （L.）.

Identification of two ABCC transporters involved in malathion detoxification in the red flour beetle,Tribolium castaneum

ABC transporters have been suggested to be involved in insecticide detoxification in different insect species mainly based on the indirect observation of transcriptional upregulation of ABC gene expression in response to insecticide exposure.Previous studies performed by us and others in the red flour beetle,Tribolium castaneum,have analyzed the function of TcABCA-C and TcABCG-H genes using RNA interference(RNAi)and demonstrated that specific TcABCA and TcABCC genes are involved in the elimination of the pyrethroid tefluthrin and the benzoylurea diflubenzuron,because gene silencing increased the beetle's susceptibility to the insecticides.In this study,we focused on the potential functions of TcABCA-C genes in detoxification of the pyrethroid cyfluthrin(CF),the organophosphate malathion(MAL)and the diacylhdyazine tebufenozide(TBF).Analysis of transcript levels of selected TcABCA-C genes in response to treatment with these three chemically unrelated insecticides revealed that some genes were particularly upregulated after insecticide treatment.In addition,the ABC inhibitor verapamil synergized significantly the toxicity of MAL but only negligibly CF and TBF toxicities.Finally,silencing of two TcABCC genes by RNAi revealed a significant increase in susceptibility to MAL.In contrast,we did not observe a significant increase in insecticide-induced mortalities when knocking down TcABC genes in larvae treated with CF or TBF,although they were upregulated in response to insecticide treatment.Our results suggest that two pleiotropic ABCC transporters expressed in metabolic and excretory tissues contribute to the elimination of MAL.