Award details

The molecular basis of target site and metabolic insecticide resistance

Reference	BBS/E/C/00004343
Principal Investigator / Supervisor	Professor Linda Field
Co-Investigators / Co-Supervisors
Institution	Rothamsted Research
Department	Rothamsted Research Department
Funding type	Research
Value (£)	1,860,549
Status	Completed
Type	Institute Project
Start date	01/04/2000
End date	31/03/2008
Duration	96 months

Abstract

Many pest insect species are subjected to intensive insecticide treatment and this has resulted in the widespread evolution of resistance, which curtails the use of a particular chemical and threatens the success of pest control programmes. Some of the most widespread and potent mechanisms of resistance result from modifications to the proteins targeted by different insecticide groups and our work aims to elucidate these mechanisms at the biochemical and molecular level. The target proteins studied include the voltage-gated sodium channel (the target of DDT and pyrethroids), acetylcholinesterase (AChE; the target of organophosphates and carbamates) and the nicotinic acetylcholine receptor (nAChR; the target of neonicotinyls). The key objectives are to characterise the insensitive proteins using a range of biochemical techniques and to clone the genes that encode the insensitive proteins and identify the mutations underlying the insensitivity. We can confirm the functionality of the mutations by in vitro expression of the cloned genes and site-directed mutagenesis and this highlights key regions/residues that are involved in insecticide binding. Insect species under study include house flies, aphids and whiteflies. An alternative mechanism of resistance involves the detoxification of an insecticide before it reaches the target site and we are studying the esterases responsible for this in a range of pest species. This mainly involves biochemical characterisation of the enymes, including the effects of the synergist piperonyl butoxide. In the case of the aphid Myzus persicae we know that elevated esterases result from gene amplfication and we are studying the involvement of DNA methylation on the regulation and expression of these genes.

Summary

unavailable

Committee	Closed Committee - Biochemistry & Cell Biology (BCB)
Research Topics	X – not assigned to a current Research Topic
Research Priority	X – Research Priority information not available
Research Initiative	X - not in an Initiative
Funding Scheme	X – not Funded via a specific Funding Scheme

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