High-resolution genetic mapping combined with transcriptome profiling reveals that both target-site resistance and increased detoxification confer resistance to the pyrethroid bifenthrin in the spider mite Tetranychus urticae
- Author
- Berdien De Beer, Marilou Vandenhole (UGent) , Christine Njiru, Pieter Spanoghe (UGent) , Wannes Dermauw (UGent) and Thomas Van Leeuwen (UGent)
- Organization
- Project
-
- POLYADAPT (Molecular-genetic mechanisms of extreme adaptation in a polyphagous agricultural pest)
- Identification and characterization of salivary effectors in Tetranychus urticae: understanding host plant manipulation in search of novel crop protection tools.
- SuperPests (Innovative tools for rational control of the most difficult-to-manage pests (super pests) and the diseases they transmit)
- Abstract
- Pyrethroids are widely applied insecticides in agriculture, but their frequent use has provoked many cases of resistance, in which mutations in the voltage-gated sodium channel (VGSC), the pyrethroid target-site, were shown to play a major role. However, for the spider mite Tetranychus urticae, it has also been shown that increased detoxification contributes to resistance against the pyrethroid bifenthrin. Here, we performed QTL-mapping to identify the genomic loci underlying bifenthrin resistance in T. urticae. Two loci on chromosome 1 were identified, with the VGSC gene being located near the second QTL and harboring the well-known L1024V mutation. In addition, the presence of an L925M mutation in the VGSC of a highly bifenthrin-resistant strain and its loss in its derived, susceptible, inbred line indicated the importance of target-site mutations in bifenthrin resistance. Further, RNAseq experiments revealed that genes encoding detoxification enzymes, including carboxyl/choline esterases (CCEs), cytochrome P450 monooxygenases and UDP-glycosyl transferases (UGTs), were overexpressed in resistant strains. Toxicity bioassays with bifenthrin (ester pyrethroid) and etofenprox (non-ester pyrethroid) also indicated a possible role for CCEs in bifenthrin resistance. A selection of CCEs and UGTs were therefore functionally expressed, and CCEinc18 was shown to metabolize bifenthrin, while teturUGT10 could glycosylate bifenthrin-alcohol. To conclude, our findings suggest that both target-site and metabolic mechanisms underlie bifenthrin resistance in T. urticae, and these might synergize high levels of resistance.
- Keywords
- bifenthrin, pyrethroids, target-site resistance, metabolic resistance, Tetranychus urticae, carboxyl, choline esterases, UDP-glycosyl transferases
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Citation
Please use this url to cite or link to this publication: http://hdl.handle.net/1854/LU-01GK1XD7DDEAM314N5CPPB9160
- MLA
- De Beer, Berdien, et al. “High-Resolution Genetic Mapping Combined with Transcriptome Profiling Reveals That Both Target-Site Resistance and Increased Detoxification Confer Resistance to the Pyrethroid Bifenthrin in the Spider Mite Tetranychus Urticae.” BIOLOGY-BASEL, vol. 11, no. 11, 2022, doi:10.3390/biology11111630.
- APA
- De Beer, B., Vandenhole, M., Njiru, C., Spanoghe, P., Dermauw, W., & Van Leeuwen, T. (2022). High-resolution genetic mapping combined with transcriptome profiling reveals that both target-site resistance and increased detoxification confer resistance to the pyrethroid bifenthrin in the spider mite Tetranychus urticae. BIOLOGY-BASEL, 11(11). https://doi.org/10.3390/biology11111630
- Chicago author-date
- De Beer, Berdien, Marilou Vandenhole, Christine Njiru, Pieter Spanoghe, Wannes Dermauw, and Thomas Van Leeuwen. 2022. “High-Resolution Genetic Mapping Combined with Transcriptome Profiling Reveals That Both Target-Site Resistance and Increased Detoxification Confer Resistance to the Pyrethroid Bifenthrin in the Spider Mite Tetranychus Urticae.” BIOLOGY-BASEL 11 (11). https://doi.org/10.3390/biology11111630.
- Chicago author-date (all authors)
- De Beer, Berdien, Marilou Vandenhole, Christine Njiru, Pieter Spanoghe, Wannes Dermauw, and Thomas Van Leeuwen. 2022. “High-Resolution Genetic Mapping Combined with Transcriptome Profiling Reveals That Both Target-Site Resistance and Increased Detoxification Confer Resistance to the Pyrethroid Bifenthrin in the Spider Mite Tetranychus Urticae.” BIOLOGY-BASEL 11 (11). doi:10.3390/biology11111630.
- Vancouver
- 1.De Beer B, Vandenhole M, Njiru C, Spanoghe P, Dermauw W, Van Leeuwen T. High-resolution genetic mapping combined with transcriptome profiling reveals that both target-site resistance and increased detoxification confer resistance to the pyrethroid bifenthrin in the spider mite Tetranychus urticae. BIOLOGY-BASEL. 2022;11(11).
- IEEE
- [1]B. De Beer, M. Vandenhole, C. Njiru, P. Spanoghe, W. Dermauw, and T. Van Leeuwen, “High-resolution genetic mapping combined with transcriptome profiling reveals that both target-site resistance and increased detoxification confer resistance to the pyrethroid bifenthrin in the spider mite Tetranychus urticae,” BIOLOGY-BASEL, vol. 11, no. 11, 2022.
@article{01GK1XD7DDEAM314N5CPPB9160,
abstract = {{Pyrethroids are widely applied insecticides in agriculture, but their frequent use has provoked many cases of resistance, in which mutations in the voltage-gated sodium channel (VGSC), the pyrethroid target-site, were shown to play a major role. However, for the spider mite Tetranychus urticae, it has also been shown that increased detoxification contributes to resistance against the pyrethroid bifenthrin. Here, we performed QTL-mapping to identify the genomic loci underlying bifenthrin resistance in T. urticae. Two loci on chromosome 1 were identified, with the VGSC gene being located near the second QTL and harboring the well-known L1024V mutation. In addition, the presence of an L925M mutation in the VGSC of a highly bifenthrin-resistant strain and its loss in its derived, susceptible, inbred line indicated the importance of target-site mutations in bifenthrin resistance. Further, RNAseq experiments revealed that genes encoding detoxification enzymes, including carboxyl/choline esterases (CCEs), cytochrome P450 monooxygenases and UDP-glycosyl transferases (UGTs), were overexpressed in resistant strains. Toxicity bioassays with bifenthrin (ester pyrethroid) and etofenprox (non-ester pyrethroid) also indicated a possible role for CCEs in bifenthrin resistance. A selection of CCEs and UGTs were therefore functionally expressed, and CCEinc18 was shown to metabolize bifenthrin, while teturUGT10 could glycosylate bifenthrin-alcohol. To conclude, our findings suggest that both target-site and metabolic mechanisms underlie bifenthrin resistance in T. urticae, and these might synergize high levels of resistance.}},
articleno = {{1630}},
author = {{De Beer, Berdien and Vandenhole, Marilou and Njiru, Christine and Spanoghe, Pieter and Dermauw, Wannes and Van Leeuwen, Thomas}},
issn = {{2079-7737}},
journal = {{BIOLOGY-BASEL}},
keywords = {{bifenthrin,pyrethroids,target-site resistance,metabolic resistance,Tetranychus urticae,carboxyl,choline esterases,UDP-glycosyl transferases}},
language = {{eng}},
number = {{11}},
pages = {{27}},
title = {{High-resolution genetic mapping combined with transcriptome profiling reveals that both target-site resistance and increased detoxification confer resistance to the pyrethroid bifenthrin in the spider mite Tetranychus urticae}},
url = {{http://doi.org/10.3390/biology11111630}},
volume = {{11}},
year = {{2022}},
}
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