A point mutation in the glutamate-gated chloride channel of Plutella xylostella is associated with resistance to abamectin
文献类型: 外文期刊
第一作者: Wang, X.
作者: Wang, X.;Wang, R.;Yang, Y.;Wu, S.;Wu, Y.;Wang, R.;O'Reilly, A. O.
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关键词: resistance;abamectin;glutamate-gated chloride channel;target site mutation;molecular docking
期刊名称:INSECT MOLECULAR BIOLOGY ( 影响因子:3.585; 五年影响因子:3.215 )
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收录情况: SCI
摘要: The diamondback moth, Plutella xylostella, is a global pest of cruciferous vegetables. Abamectin resistance in a field population of P. xylostella was introgressed into the susceptible Roth strain. The resulting introgression strain Roth-Abm showed 11000-fold resistance to abamectin compared with Roth. An A309V substitution at the N-terminus of the third transmembrane helix (M3) of the glutamate-gated chloride channel of P. xylostella (PxGluCl) was identified in Roth-Abm. The frequency of the V309 allele of PxGluCl was 94.7% in Roth-Abm, whereas no such allele was detected in Roth. A subpopulation of Roth-Abm was kept without abamectin selection for 20 generations to produce a revertant strain, Roth-Abm-D. Abamectin resistance in Roth-Abm-D declined to 1150-fold compared with Roth, with the V309 allele frequency decreased to 9.6%. After treatment of the Roth-Abm-D strain with 80 mg/l abamectin the V309 allele frequency in the survivors increased to 55%. This demonstrates that the A309V mutation in PxGluCl is strongly associated with a 10-fold increase in abamectin resistance in Roth-Abm relative to Roth-Abm-D. Homology modelling and automated ligand docking results suggest that the A309V substitution allosterically modifies the abamectin-binding site, as opposed to directly eliminating a key binding contact. Other resistance mechanisms to abamectin in Roth-Abm are discussed besides the A309V mutation of PxGluCl.
分类号: R47
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