Abstract: 【Aim】 To clarify the relationship between arrestin gene Btarrestin and imidacloprid resistance in the whitefly Bemisia tabaci MED. 【Methods】 Based on the previous transcriptome data of B. tabaci, the full-length cDNA sequence of Btarrestin was cloned by RT-PCR in B. tabaci MED and then subjected to bioinformatics analysis. The expression levels of Btarrestin at different developmental stages (egg, 1st-2nd instar, 3rd instar and 4th instar nymph, and female and male adult) and in adults exposed to imidacloprid (100 mg/L) were detected by qPCR. After silencing Btarrestin by RNAi, the expression level of Btarrestin and the mortality of B. tabaci MED adults were detected. 【Results】 The cDNA sequence of Btarrestin (GenBank accession no.: MK204377) was cloned from B. tabaci MED. The complete cDNA is 1 127 bp in length encoding 409 amino acids, with the molecular weight of 45.33 kD and the pI value of 8.38. Conserved domain analysis indicated that Btarrestin has conserved domains of the two superfamilies Arrestin_N and Arrestin_C, consistent with the family characteristics of arrestins. Phylogenetic tree analysis showed that Btarrestin shares high homology with the arrestin of Nilaparvata lugens. Developmental stage-specific expression results revealed that the expression level of Btarrestin was increased gradually with its development and reached the peak at the adult stage. The expression level of Btarrestin in adults exposed to 100 mg/L imidacloprid for 24 h increased by 2.39-fold as compared with that in the control. The RNAi results showed that knockdown of Btarrestin in B. tabaci MED increased the mortality of imidacloprid-treated adults by 31.27%. 【Conclusion】 Btarrestin might be involved in imidacloprid resistance in B. tabaci MED.

Key words: Bemisia tabaci MED')">Bemisia tabaci MED, arrestin, drug resistance, imidacloprid, RNA interference