共 44 条
A point mutation in the glutamate-gated chloride channel of Plutella xylostella is associated with resistance to abamectin
被引:71
作者:
Wang, X.
[1
]
Wang, R.
[1
,2
]
Yang, Y.
[1
]
Wu, S.
[1
]
O'Reilly, A. O.
[3
]
Wu, Y.
[1
]
机构:
[1] Nanjing Agr Univ, Coll Plant Protect, Nanjing 210095, Jiangsu, Peoples R China
[2] Beijing Acad Agr & Forestry Sci, Inst Plant & Environm Protect, Beijing, Peoples R China
[3] Liverpool John Moores Univ, Sch Nat Sci & Psychol, Liverpool L3 5UX, Merseyside, England
基金:
中国国家自然科学基金;
关键词:
resistance;
abamectin;
glutamate-gated chloride channel;
target site mutation;
molecular docking;
GENE SUPERFAMILY;
DIAMONDBACK MOTH;
LEPIDOPTERA;
IVERMECTIN;
HELIX;
POPULATIONS;
ACID;
D O I:
10.1111/imb.12204
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
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.
引用
收藏
页码:116 / 125
页数:10
相关论文