Mutation of a nicotinic acetylcholine receptor beta subunit is associated with resistance to neonicotinoid insecticides in the aphid Myzus persicae

A - Papers appearing in refereed journals

Bass, C., Puinean, A. M., Andrews, M., Cutler, P., Daniels, M., Elias, J., Paul, V. L., Crossthwaite, A. J., Denholm, I., Field, L. M., Foster, S. P., Lind, R., Williamson, M. S. and Slater, R. 2011. Mutation of a nicotinic acetylcholine receptor beta subunit is associated with resistance to neonicotinoid insecticides in the aphid Myzus persicae. BMC Neuroscience. 12 (51).

AuthorsBass, C., Puinean, A. M., Andrews, M., Cutler, P., Daniels, M., Elias, J., Paul, V. L., Crossthwaite, A. J., Denholm, I., Field, L. M., Foster, S. P., Lind, R., Williamson, M. S. and Slater, R.
Abstract

Background
Myzus persicae is a globally important aphid pest with a history of developing resistance to insecticides. Unusually, neonicotinoids have remained highly effective as control agents despite nearly two decades of steadily increasing use. In this study, a clone of M. persicae collected from southern France was found, for the first time, to exhibit sufficiently strong resistance to result in loss of the field effectiveness of neonicotinoids.

Results
Bioassays, metabolism and gene expression studies implied the presence of two resistance mechanisms in the resistant clone, one based on enhanced detoxification by cytochrome P450 monooxygenases, and another unaffected by a synergist that inhibits detoxifying enzymes. Binding of radiolabeled imidacloprid (a neonicotinoid) to whole body membrane preparations showed that the high affinity [3H]-imidacloprid binding site present in susceptible M. persicae is lost in the resistant clone and the remaining lower affinity site is altered compared to susceptible clones. This confers a significant overall reduction in binding affinity to the neonicotinoid target: the nicotinic acetylcholine receptor (nAChR). Comparison of the nucleotide sequence of six nAChR subunit (Mpα1-5 and Mpβ1) genes from resistant and susceptible aphid clones revealed a single point mutation in the loop D region of the nAChR β1 subunit of the resistant clone, causing an arginine to threonine substitution (R81T).

Conclusion
Previous studies have shown that the amino acid at this position within loop D is a key determinant of neonicotinoid binding to nAChRs and this amino acid change confers a vertebrate-like character to the insect nAChR receptor and results in reduced sensitivity to neonicotinoids. The discovery of the mutation at this position and its association with the reduced affinity of the nAChR for imidacloprid is the first example of field-evolved target-site resistance to neonicotinoid insecticides and also provides further validation of exisiting models of neonicotinoid binding and selectivity for insect nAChRs.

Year of Publication2011
JournalBMC Neuroscience
Journal citation12 (51)
Digital Object Identifier (DOI)doi:10.1186/1471-2202-12-51
Open accessPublished as ‘gold’ (paid) open access
FunderBiotechnology and Biological Sciences Research Council
Funder project or codeCentre for Sustainable Pest and Disease Management (PDM)
BBSRC Institute Career Path Fellowship: A genomic approach to understanding insecticide resistance in crop pests
Publisher's version
File Access Level
Open
Output statusPublished
Publication dates
Online31 May 2011
Publication process dates
Accepted31 May 2011
ISSN1471-2202
PublisherBiomed Central Ltd

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