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Biochemical mechanisms of imidacloprid resistance in Nilaparvata lugens: over-expression of cytochrome P450 CYP6AY1.
Insect Biochem Mol Biol. 2013 Nov; 43(11):1021-7.IB

Abstract

Imidacloprid is a key insecticide extensively used for control of Nilaparvata lugens, and its resistance had been reported both in the laboratory selected strains and field populations. A target site mutation Y151S in two nicotinic acetylcholine receptor subunits and enhanced oxidative detoxification have been identified in the laboratory resistant strain, contributing importantly to imidacloprid resistance in N. lugens. To date, however, imidacloprid resistance in field population is primarily attributable to enhanced oxidative detoxification by over-expressed P450 monooxygenases. A resistant strain (Res), originally collected from a field population and continuously selected in laboratory with imidacloprid for more than 40 generations, had 180.8-fold resistance to imidacloprid, compared to a susceptible strain (Sus). Expression of different putative P450 genes at mRNA levels was detected and compared between Res and Sus strains, and six genes were found expressed significantly higher in Res strain than in Sus strain. CYP6AY1 was found to be the most different expressed P450 gene and its mRNA level in Res strain was 17.9 times of that in Sus strain. By expressing in E. coli cells, CYP6AY1 was found to metabolize imidacloprid efficiently with initial velocity calculated of 0.851 ± 0.073 pmol/min/pmol P450. When CYP6AY1 mRNA levels in Res strain was reduced by RNA interference, imidacloprid susceptibility was recovered. In four field populations with different resistance levels, high levels of CYP6AY1 transcript were also found. In vitro and in vivo studies provided evidences that the over-expression of CYP6AY1 was one of the key factors contributing to imidacloprid resistance in the laboratory selected strain Res, which might also be the important mechanism for imidacloprid resistance in field populations, when the target site mutation was not prevalent at present.

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Publisher Full Text (DOI)

Authors+Show Affiliations

Ding Z
Key Laboratory of Integrated Management of Crop Diseases and Pests, Nanjing Agricultural University, Ministry of Education, Nanjing 210095, China.
Wen Y
No affiliation info available
Yang B
No affiliation info available
Zhang Y
No affiliation info available
Liu S
No affiliation info available
Liu Z
No affiliation info available
Han Z
No affiliation info available

MeSH

AnimalsCytochrome P-450 Enzyme SystemHemipteraImidazolesInsect ProteinsInsecticide ResistanceInsecticidesNeonicotinoidsNitro Compounds

Pub Type(s)

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

Language

eng

PubMed ID

23994173

Citation

Ding, Zhiping, et al. "Biochemical Mechanisms of Imidacloprid Resistance in Nilaparvata Lugens: Over-expression of Cytochrome P450 CYP6AY1." Insect Biochemistry and Molecular Biology, vol. 43, no. 11, 2013, pp. 1021-7.
Ding Z, Wen Y, Yang B, et al. Biochemical mechanisms of imidacloprid resistance in Nilaparvata lugens: over-expression of cytochrome P450 CYP6AY1. Insect Biochem Mol Biol. 2013;43(11):1021-7.
Ding, Z., Wen, Y., Yang, B., Zhang, Y., Liu, S., Liu, Z., & Han, Z. (2013). Biochemical mechanisms of imidacloprid resistance in Nilaparvata lugens: over-expression of cytochrome P450 CYP6AY1. Insect Biochemistry and Molecular Biology, 43(11), 1021-7. https://doi.org/10.1016/j.ibmb.2013.08.005
Ding Z, et al. Biochemical Mechanisms of Imidacloprid Resistance in Nilaparvata Lugens: Over-expression of Cytochrome P450 CYP6AY1. Insect Biochem Mol Biol. 2013;43(11):1021-7. PubMed PMID: 23994173.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Biochemical mechanisms of imidacloprid resistance in Nilaparvata lugens: over-expression of cytochrome P450 CYP6AY1. AU - Ding,Zhiping, AU - Wen,Yucong, AU - Yang,Baojun, AU - Zhang,Yixi, AU - Liu,Shuhua, AU - Liu,Zewen, AU - Han,Zhaojun, Y1 - 2013/08/29/ PY - 2011/04/07/received PY - 2013/08/13/revised PY - 2013/08/15/accepted PY - 2013/9/3/entrez PY - 2013/9/3/pubmed PY - 2014/5/13/medline KW - CYP6AY1 KW - Imidacloprid KW - Nilaparvata lugens KW - P450-monooxygenases KW - Resistance mechanisms SP - 1021 EP - 7 JF - Insect biochemistry and molecular biology JO - Insect Biochem Mol Biol VL - 43 IS - 11 N2 - Imidacloprid is a key insecticide extensively used for control of Nilaparvata lugens, and its resistance had been reported both in the laboratory selected strains and field populations. A target site mutation Y151S in two nicotinic acetylcholine receptor subunits and enhanced oxidative detoxification have been identified in the laboratory resistant strain, contributing importantly to imidacloprid resistance in N. lugens. To date, however, imidacloprid resistance in field population is primarily attributable to enhanced oxidative detoxification by over-expressed P450 monooxygenases. A resistant strain (Res), originally collected from a field population and continuously selected in laboratory with imidacloprid for more than 40 generations, had 180.8-fold resistance to imidacloprid, compared to a susceptible strain (Sus). Expression of different putative P450 genes at mRNA levels was detected and compared between Res and Sus strains, and six genes were found expressed significantly higher in Res strain than in Sus strain. CYP6AY1 was found to be the most different expressed P450 gene and its mRNA level in Res strain was 17.9 times of that in Sus strain. By expressing in E. coli cells, CYP6AY1 was found to metabolize imidacloprid efficiently with initial velocity calculated of 0.851 ± 0.073 pmol/min/pmol P450. When CYP6AY1 mRNA levels in Res strain was reduced by RNA interference, imidacloprid susceptibility was recovered. In four field populations with different resistance levels, high levels of CYP6AY1 transcript were also found. In vitro and in vivo studies provided evidences that the over-expression of CYP6AY1 was one of the key factors contributing to imidacloprid resistance in the laboratory selected strain Res, which might also be the important mechanism for imidacloprid resistance in field populations, when the target site mutation was not prevalent at present. SN - 1879-0240 UR - https://www.unboundmedicine.com/medline/citation/23994173/Biochemical_mechanisms_of_imidacloprid_resistance_in_Nilaparvata_lugens:_over_expression_of_cytochrome_P450_CYP6AY1_ DB - PRIME DP - Unbound Medicine ER -