| The whitefly Bemisia tabaci (Gennadius) is one of the most damaging pests throughoutthe tropical and subtropical regions of the world. It is an important agricultural pest thatfeeds in the phloem and also the most important vector of several plant virus genera. So far,at least 26 biotypes has been characterized, including B-type, Q-type and non-B/Q-type, inwhich the B type B. tabaci is the most serious agricultural pest due to its particularlypolyphagous, highly fecund, strongly adaptability and resistance to many insecticides.Imidacloprid, the first of the neonicotinoid class of insecticides, exhibits strong insecticidalactivity against B. tabaci. But the extensive use of imidacloprid is intensifying strongselection pressure for imidacloprid resistance in the target insects such as B. tabaci. In thispaper, biochemical mechanisms and cross resistance pattern of imidacloprid resistance inB-type Bemisia tabaci were studied in order to provide some theoretical bases for designingresistance monitoring techniques and resistance management tactics.1. Laboratory selection and cross-resistance .pattern of imidacloprid resistance inB-type Bemisia tabaciA strain of B. tabaci (NJ) was collected in Nanjing, Jiangsu Province of China in 2002and the NJ strain was classified as B-type B. tabaci according to the similarity of mtDNACOI gene sequence among Bemisia tabaci biotypes. The NJ-Imi strain was selected fromthe NJ strain with imidacloprid for 15 generations. The NJ-Imi strain exhibited 256-foldresistance to imidacloprid, strong cross resistance to two other neonicotinoids (acetamipridand thiamethoxam), low cross resistance to monosultap and spinosad, but no crossresistance to abamectin and cypermethrin. Resistance to imidacloprid in field populationsof B. tabaci collected from Beijing, Nanjing, Wuhan and Guangdong was monitored withdiscriminating dose method and thcsc populations have developed low to middle levels ofresistance to imidacloprid. 2. Biochemical mechanisms of imidacloprid resistance in the NJ-Imi strain ofBemisia tabaciResistance mechanisms to imidacloprid in the NJ-Imi strain of B. tabaci werepreliminarily studied by using synergist bioassay and quantifying detoxification enzymes.Neither esterase inhibitor DEF nor glutathione S-transferase inhibitor DEM could synergizeimidacloprid at different levels between the resistant NJ-Imi strain and the susceptible NJstrain, however the oxidase inhibitor PBO had synergistic ratio of 2.49-fold in the resistantNJ-Imi strain only. Determination of detoxifying enzymes showed only cytochrome P450oxidase activity increased 2.2-fold in the NJ-Imi strain compared with the NJ strain. Soenhanced detoxifying mediated by P450 oxidases could play some role in imidaclopridresistance in the NJ'Imi strain. Although no difference of binding of [~3H]-Epibatidine tomembrane proteins prepared from the NJ and NJ-Imi strains was detected, which does notexclude the possibility of the involvement of target site insensitivity in imidaclopridresistance in the NJ-Imi strain of B. tabaci.3. Cloning and sequence analyzing of nAChR genes from B-type Bemisia tabaciNicotinic acetylcholine receptors (nAChRs) are import excitatory neurotransmitterreceptors and the target site for neonicotinoids in insects. A nAChR a subunit gene wascloned and sequenced from the whitefly, Bemisia tabaci. The complete cDNA sequence ofthis gene contained 2090bp and encoded a protein of 564 amino acids. This gene wasdesignated as Bta4 (GenBank accession number EF590120) according to its amino acidsimilarity to other insect nAChRs. The putative a subunit encoded by Bta4 included twodomains, the N-terminal extracellular domain and the transmembrane domain. TheN-terminal extracellular domain of Bta4 subunit contains two adjacent cysteine residues(typical character for a-subunit), a cysteine loop and acetylcholine binding regions. Thecurrent study has significance for investigating potential target site resistance mechanism ofB. tabaci to neonicotinoids.
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