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Wolbachia enhances expression of NlCYP4CE1 in Nilaparvata lugens in response to imidacloprid stress
Author(s) -
Cai Tingwei,
Zhang Yunhua,
Liu Yu,
Deng Xiaoqian,
He Shun,
Li Jianhong,
Wan Hu
Publication year - 2021
Publication title -
insect science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.991
H-Index - 45
eISSN - 1744-7917
pISSN - 1672-9609
DOI - 10.1111/1744-7917.12834
Subject(s) - imidacloprid , brown planthopper , biology , wolbachia , insect , delphacidae , neonicotinoid , toxicology , bacteria , symbiotic bacteria , microbiology and biotechnology , host (biology) , gene , botany , pesticide , genetics , agronomy , pest analysis , symbiosis , homoptera
The brown planthopper, Nilaparvata lugens , is one of the main insect pests of rice. The N. lugens gene NlCYP4CE1 encodes cytochrome P450 monooxygenase (P450), which is a key enzyme in the metabolism of the insecticide imidacloprid. Previous research has suggested that the expression of NlCYP4CE1 is induced by imidacloprid stress, but the effect of bacterial symbionts on its expression has not been determined. The results of this study show that exposure to subtoxic imidacloprid changed the structure of the bacterial symbiont community in N. lugens . Specifically, the total bacterial content increased, but the bacterial species diversity significantly decreased. Wolbachia accounted for the largest proportion of bacteria in N. lugens ; its abundance significantly increased after subtoxic imidacloprid exposure. The transcript level of NlCYP4CE1 was significantly increased by imidacloprid, but this effect was significantly weakened after Wolbachia was cleared with tetracycline. This result suggests that Wolbachia enhances the expression of NlCYP4CE1 to promote the detoxification metabolic response to imidacloprid stress. Understanding the effect of bacterial symbionts on gene expression in the host provides a new perspective on interactions between insecticides and their target insect pests, and highlights that subtoxic imidacloprid exposure may raise the risk of insecticide resistance by altering the structure of bacterial symbiont communities.