摘要
Neonicotinoid insecticides target nicotinic acetylcholine receptors (nAChR) in the nervous system of insects but are largely ineffective against ticks. This study aimed to identify the molecular basis for this insensitivity. A homology model of the nAChR binding domain was generated on the basis of the crystal structure of an acetylcholine-binding protein with the insecticide imidacloprid bound. We hypothesized that tick beta-subunits would differ at a critical residue (Arg81) in their D loops. To test this, we sequenced nAChR genes from five tick species and found that instead of the conserved arginine found in insects, a glutamine was present in all the tick sequences.
- 出版日期2012-6-12