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Pesticide resistance is a serious problem that poses a major challenge to pest control. One of the most potent resistance mechanisms is the overexpression of genes coding for detoxification enzymes. The expression of detoxification genes is regulated by a series of transcription factors. Previous studies have revealed that the increased expression of detoxification genes contributes to the insecticide tolerance of Bactrocera dorsalis. Our objective was thus to identify the transcription factors involved in this process. Temporal expression profiles showed that the transcription factor MafB and detoxification genes were expressed highly in the fat body. Further analysis showed that the expression of MafB , GSTz2 , and CYP473A3 was induced by abamectin. Disruption of the MafB transcription factor through RNA interference decreased the transcript levels of GSTz2 and CYP473A3 and increased the susceptibility to abamectin significantly. Direct silencing of the expression of GSTz2 also increased susceptibility to abamectin, while CYP473A3 did not. In conclusion, these results suggest that the expression of GSTz2 and CYP473A3 was regulated by the transcription factor MafB , and the up-regulation of GSTz2 via MafB decreased the susceptibility of B. dorsalis to abamectin.

The oriental fruit fly (Bactrocera dorsalis) is a pest that causes large economic losses in the fruit and vegetable industry, so its control is a major challenge. Nuclear receptors (NRs) are a superfamily of ligand-dependent transcription factors that directly combine with DNA to regulate the expression of downstream target genes. NRs are closely associated with multiple physiological processes such as metabolism, reproduction, and development. Through sequence searches and analysis, we identified 21 B. dorsalis NR genes, all of which contained at least one of the two characteristic binding domains. On the basis of the conserved sequences and phylogenetic relationships, we divided the 21 NR genes into seven subfamilies. All members of the NR0 subfamily and BdHR83, which belonged to the NR2E group, lacked ligand-binding domains. The BdDSF and BdHR51, which also belonged to the NR2Egroup, and BdE78 (which belonged to the NR1E group) all lacked DNA-binding domains. The BdDSF and BdHR83 sequences were incomplete, and were not successfully amplified. Development-and tissue-specific expression profiling demonstrated that the transcript levels of the 19 NR genes varied considerably among eggs, larva, pupae, and adults, as well as among larval and adult male and female tissues. Our results will contribute to a better understanding of NR evolution and expand our knowledge of B. dorsalis physiology.Insects 2020, 11, 126 2 of 15 in recognizing hormone response elements. The D domain functions as a hinge between the DBD and the ligand-binding domain (LBD). The LBD (also known as E domain) contains a hydrophobic ligand-binding pocket that is specific to each receptor and is the source of the sequence variability within the LBD. In addition, the LBD domain mediates dimerization and the ligand-dependent transcriptional activation function (AF-2) [4]. The C-terminal contains the F domain, which is not present in all NRs and is highly diverse.A large number of NR gene sets have been characterized from the whole-genome sequence of many animals. For example, 48 NRs were identified in the human genome [5], over 270 NRs have been found in Caenorhabditis elegans [6], and 49 and 47 were found in mouse and rat, respectively [7]. Surprisingly, only 21 NRs were found in Drosophila melanogaster [8], 19 in Bombyx mori [9], 22 in Apis mellifera [10], and 21 in Tribolium castaneum [11].In D. melanogaster, seven NR genes that are regulated directly by 20E have been identified, namely EcR, E75, E78, FTZ-F1, HR3, HR4, and HR39 [12]. Among them, E75 is the primary response gene of 20E. The others are secondary response genes that are maximally expressed after 20E-induced protein synthesis has begun [13]. The ligand-receptor complex of 20E-EcR-USP induces the expression of the 20E primary response gene. Then, the cascade of 20E secondary response genes, which is induced by the transcription factor encoded by the 20E primary response gene, amplifies the 20E signal by regulating the expression of the secondary response genes (e.g., HR3, HR4, and FTZ...