Low expression levels of nicotinic acetylcholine receptor subunits Boα1 and Boβ1 are associated with imidacloprid resistance in Bradysia odoriphaga.

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Tytuł:: Low expression levels of nicotinic acetylcholine receptor subunits Boα1 and Boβ1 are associated with imidacloprid resistance in Bradysia odoriphaga.
Autorzy:: Shan T; Department of Entomology, China Agricultural University, Beijing, China.
Zhang H; Department of Entomology, China Agricultural University, Beijing, China.
Chen C; Department of Entomology, China Agricultural University, Beijing, China.
Chen A; Department of Entomology, China Agricultural University, Beijing, China.
Shi X; Department of Entomology, China Agricultural University, Beijing, China.
Gao X; Department of Entomology, China Agricultural University, Beijing, China.
Źródło:: Pest management science [Pest Manag Sci] 2020 Sep; Vol. 76 (9), pp. 3038-3045. Date of Electronic Publication: 2020 Apr 29.
Typ publikacji:: Journal Article
Język:: English
Imprint Name(s):: Original Publication: West Sussex, UK : Published for SCI by Wiley, c2000-
MeSH Terms:: Insecticides*/pharmacology
Receptors, Nicotinic*/genetics
Animals ; Insecticide Resistance/genetics ; Neonicotinoids/pharmacology ; Nitro Compounds/pharmacology
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Grant Information:: 201303027 Special Fund for Agro-scientific Research in the Public Interest
Contributed Indexing:: Keywords: Bradysia odoriphaga; imidacloprid; nicotinic acetylcholine receptor; resistance mechanism
Substance Nomenclature:: 0 (Insecticides)
0 (Neonicotinoids)
0 (Nitro Compounds)
0 (Receptors, Nicotinic)
3BN7M937V8 (imidacloprid)
Entry Date(s):: Date Created: 20200415 Date Completed: 20201221 Latest Revision: 20201221
Update Code:: 20240105
DOI:: 10.1002/ps.5854
PMID:: 32285608
: Czasopismo naukowe

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Background: Neonicotinoid insecticide imidacloprid acts on insect nicotinic acetylcholine receptors (nAChRs). The mechanisms of insect resistance to imidacloprid include target-site alteration and increased detoxification metabolism. In Bradysia odoriphaga, cytochrome P450 monooxygenase has been found involved in metabolic resistance to imidacloprid. However, the situation of target-site related resistance to imidacloprid in B. odoriphaga is still unknown.
Results: Nine field-collected B. odoriphaga populations showed various sensitivities to imidacloprid compared with the susceptible (SS) strain, including susceptibility, decreased susceptibility, low resistance, moderate resistance and high resistance. Seven nAChR subunit genes including α1, α2, α3, α7, α8, β1 and β3, were examined for site mutation and changes in transcription levels in field populations. No nAChR polymorphism potentially related to the resistant phenotypes was found. However, differential expression of nAChR subunit genes was found in imidacloprid resistant field population. In high imidacloprid resistant population LC-2 (93.14-fold resistance), the transcription levels of α1, α2 and β1 subunits were significantly down-regulated, while the transcription levels of α3 and α8 subunits were significantly up-regulated, compared with that in SS strain. In addition, imidacloprid acute exposure induced differential expression of nAChR subunit genes in B. odoriphaga. Furthermore, RNA interference (RNAi) suppressed the transcriptional expression of Boα1 and Boβ1, and decreased mortality of B. odoriphaga by 23.03% and 18.69%, respectively, when treated with imidacloprid.
Conclusion: These results indicated that, although no target-site mutation was found in imidacloprid resistant B. odoriphaga population, the reduced expression of α1 and β1 subunits contributed to B. odoriphaga resistance to imidacloprid. © 2020 Society of Chemical Industry.
(© 2020 Society of Chemical Industry.)

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