Journal
INSECT BIOCHEMISTRY AND MOLECULAR BIOLOGY
Volume 43, Issue 11, Pages 1021-1027Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.ibmb.2013.08.005
Keywords
Nilaparvata lugens; Imidacloprid; Resistance mechanisms; P450-monooxygenases; CYP6AY1
Categories
Funding
- National Basic Research Program of China (973 Program) [2010CB126200]
- National High Technology Research and Development Program of China (863 Program) [2012AA101502]
- General Financial Grant from the China Post-doctoral Science Foundation [2012M520853]
- National Science Foundation China Program Grant [31130045, 31171869]
- National Key Technology Research and Development Program [2012BAD19B01]
- Foundation for the Author of National Excellent Doctoral Dissertation of PR China [2007B60]
- Special Fund of Industrial (Agriculture) Research for Public Welfare of China [201003031]
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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. (C) 2013 Elsevier Ltd. All rights reserved.
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