Tags

Type your tag names separated by a space and hit enter

Reduction in mRNA and protein expression of a nicotinic acetylcholine receptor α8 subunit is associated with resistance to imidacloprid in the brown planthopper, Nilaparvata lugens.
J Neurochem. 2015 Nov; 135(4):686-94.JN

Abstract

Target-site resistance is commonly caused by qualitative changes in insecticide target-receptors and few studies have implicated quantitative changes in insecticide targets in resistance. Here we show that resistance to imidacloprid in a selected strain of Nilaparvata lugens is associated with a reduction in expression levels of the nicotinic acetylcholine receptor (nAChR) subunit Nlα8. Synergism bioassays of the selected strain suggested resistance was conferred, in part, by a target-site mechanism. Sequencing of N. lugens nAChR subunit genes identified no mutations associated with resistance, however, a decrease in mRNA and protein levels of Nlα8 was observed during selection. RNA interference knockdown of Nlα8 decreased the sensitivity of N. lugens to imidacloprid, demonstrating that a decrease in Nlα8 expression is sufficient to confer resistance in vivo. Radioligand binding assays revealed that the affinity of the high-affinity imidacloprid-binding site of native nAChRs was reduced by selection, and reducing the amount of Nlα8 cRNA injected into Xenopus oocytes significantly decreased imidacloprid potency on recombinant receptors. Taken together, these results provide strong evidence that a decrease in Nlα8 levels confers resistance to imidacloprid in N. lugens, and thus provides a rare example of target-site resistance associated with a quantitative rather than qualitative change. In insects, target-site mutations often cause high resistance to insecticides, such as neonicotinoids acting on nicotinic acetylcholine receptors (nAChRs). Here we found that a quantitative change in target-protein level, decrease in mRNA and protein levels of Nlα8, contributed importantly to imidacloprid resistance in Nilaparvata lugens. This finding provides a new target-site mechanism of insecticide resistance.

Links

Publisher Full Text (DOI)

Authors+Show Affiliations

Key Laboratory of Integrated Management of Crop Diseases and Pests (Ministry of Education), College of Plant Protection, Nanjing Agricultural University, Nanjing, China.

Key Laboratory of Integrated Management of Crop Diseases and Pests (Ministry of Education), College of Plant Protection, Nanjing Agricultural University, Nanjing, China.

Key Laboratory of Integrated Management of Crop Diseases and Pests (Ministry of Education), College of Plant Protection, Nanjing Agricultural University, Nanjing, China.

Key Laboratory of Integrated Management of Crop Diseases and Pests (Ministry of Education), College of Plant Protection, Nanjing Agricultural University, Nanjing, China.

Key Laboratory of Integrated Management of Crop Diseases and Pests (Ministry of Education), College of Plant Protection, Nanjing Agricultural University, Nanjing, China.

Department of Biological Chemistry and Crop Protection, Rothamsted Research, Harpenden, Hertfordshire, UK.

Key Laboratory of Integrated Management of Crop Diseases and Pests (Ministry of Education), College of Plant Protection, Nanjing Agricultural University, Nanjing, China.

MeSH

AnimalsCholinergic AgentsDrug ResistanceDrug SynergismGene Expression RegulationImidazolesInsectaInsecticidesNeonicotinoidsNitro CompoundsRNA InterferenceRNA, Double-StrandedRNA, MessengerRadioligand AssayRatsReceptors, NicotinicTritium

Pub Type(s)

Journal Article

Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

26259922

Citation

Zhang, Yixi, et al. "Reduction in mRNA and Protein Expression of a Nicotinic Acetylcholine Receptor Α8 Subunit Is Associated With Resistance to Imidacloprid in the Brown Planthopper, Nilaparvata Lugens." Journal of Neurochemistry, vol. 135, no. 4, 2015, pp. 686-94.

Zhang Y, Wang X, Yang B, et al. Reduction in mRNA and protein expression of a nicotinic acetylcholine receptor α8 subunit is associated with resistance to imidacloprid in the brown planthopper, Nilaparvata lugens. J Neurochem. 2015;135(4):686-94.

Zhang, Y., Wang, X., Yang, B., Hu, Y., Huang, L., Bass, C., & Liu, Z. (2015). Reduction in mRNA and protein expression of a nicotinic acetylcholine receptor α8 subunit is associated with resistance to imidacloprid in the brown planthopper, Nilaparvata lugens. Journal of Neurochemistry, 135(4), 686-94. https://doi.org/10.1111/jnc.13281

Zhang Y, et al. Reduction in mRNA and Protein Expression of a Nicotinic Acetylcholine Receptor Α8 Subunit Is Associated With Resistance to Imidacloprid in the Brown Planthopper, Nilaparvata Lugens. J Neurochem. 2015;135(4):686-94. PubMed PMID: 26259922.

* Article titles in AMA citation format should be in sentence-case

TY - JOUR T1 - Reduction in mRNA and protein expression of a nicotinic acetylcholine receptor α8 subunit is associated with resistance to imidacloprid in the brown planthopper, Nilaparvata lugens. AU - Zhang,Yixi, AU - Wang,Xin, AU - Yang,Baojun, AU - Hu,Yuanyuan, AU - Huang,Lixin, AU - Bass,Chris, AU - Liu,Zewen, Y1 - 2015/09/03/ PY - 2015/07/13/received PY - 2015/08/02/revised PY - 2015/08/04/accepted PY - 2015/8/12/entrez PY - 2015/8/12/pubmed PY - 2016/2/18/medline KW - insecticide resistance KW - nicotinic acetylcholine receptors KW - quantity change KW - target insensitivity SP - 686 EP - 94 JF - Journal of neurochemistry JO - J Neurochem VL - 135 IS - 4 N2 - Target-site resistance is commonly caused by qualitative changes in insecticide target-receptors and few studies have implicated quantitative changes in insecticide targets in resistance. Here we show that resistance to imidacloprid in a selected strain of Nilaparvata lugens is associated with a reduction in expression levels of the nicotinic acetylcholine receptor (nAChR) subunit Nlα8. Synergism bioassays of the selected strain suggested resistance was conferred, in part, by a target-site mechanism. Sequencing of N. lugens nAChR subunit genes identified no mutations associated with resistance, however, a decrease in mRNA and protein levels of Nlα8 was observed during selection. RNA interference knockdown of Nlα8 decreased the sensitivity of N. lugens to imidacloprid, demonstrating that a decrease in Nlα8 expression is sufficient to confer resistance in vivo. Radioligand binding assays revealed that the affinity of the high-affinity imidacloprid-binding site of native nAChRs was reduced by selection, and reducing the amount of Nlα8 cRNA injected into Xenopus oocytes significantly decreased imidacloprid potency on recombinant receptors. Taken together, these results provide strong evidence that a decrease in Nlα8 levels confers resistance to imidacloprid in N. lugens, and thus provides a rare example of target-site resistance associated with a quantitative rather than qualitative change. In insects, target-site mutations often cause high resistance to insecticides, such as neonicotinoids acting on nicotinic acetylcholine receptors (nAChRs). Here we found that a quantitative change in target-protein level, decrease in mRNA and protein levels of Nlα8, contributed importantly to imidacloprid resistance in Nilaparvata lugens. This finding provides a new target-site mechanism of insecticide resistance. SN - 1471-4159 UR - https://www.unboundmedicine.com/medline/citation/26259922/Reduction_in_mRNA_and_protein_expression_of_a_nicotinic_acetylcholine_receptor_α8_subunit_is_associated_with_resistance_to_imidacloprid_in_the_brown_planthopper_Nilaparvata_lugens_ DB - PRIME DP - Unbound Medicine ER -