Use this URL to cite or link to this record in EThOS: https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.755566
Title: Investigating the breakdown of chemical control in brown planthoppers from Asia
Author: Garrood, W. T.
ISNI:       0000 0004 7428 5598
Awarding Body: University of Liverpool
Current Institution: University of Liverpool
Date of Award: 2018
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Abstract:
The brown planthopper (Nilaparvata lugens Stål) is one of the most economically important pests of rice across Asia. The control of this pest has mainly relied upon the use of insecticides. However, rice ecosystems across Asia are being put at severe risk due to the over-reliance on certain insecticides, mainly imidacloprid (neonicotinoid) and ethiprole (phenylpyrazole), which the pest is now showing widespread resistance against. The evolution of resistance represents a tangible threat to the long-term sustainable control of this species. Field strains were placed under selection separately with imidacloprid and ethiprole, leading to increased resistance within these strains. Selection with ethiprole was demonstrated to cause cross-resistance to another phenylpyrazole, fipronil. A de novo transcriptome was generated and was used to search for differentially expressed genes between susceptible and insecticide resistant populations. This transcriptome also allowed assembly of insecticide target sites, that were then screened for mutations. The most recent class of insecticide to show decreased efficacy against the brown planthopper was the phenylpyrazoles (Fiproles). Potential mechanisms for resistance, both metabolic and target site were studied with the use of a model organism, Drosophila melanogaster. These have implicated a mutation, A301S, in the Rdl channel in ethiprole resistance, but not in causing significant fipronil resistance. Point mutations that occurs at the target site for imidacloprid and previously linked with resistance, were not witnessed in the field strains monitored for this PhD. However, it was discovered that a single cytochrome P450 gene (CYP6ER1) was markedly overexpressed in all the imidacloprid resistant strains tested. This gene displayed considerable coding sequence variation between the susceptible and resistant strains. Of the eight CYP6ER1 variants found, two were highly expressed. Studies in vivo showed these CYP6ER1 variants conferred significant resistance to imidacloprid compared to a CYP6ER1 variant from susceptible N. lugens. It was concluded that coding sequence changes in CYP6ER1 were the primary role for imidacloprid resistance, with overexpression contributing in a secondary role.
Supervisor: Ranson, Hilary ; Davies, T. G. Emyr ; Bass, Chris ; Williamson, Martin ; Nauen, Ralf ; Field, Lin Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.755566  DOI:
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