UGT201H1 overexpression confers cyflumetofen resistance in Tetranychus cinnabarinus (Boisduval).
Pest Manag Sci
; 80(9): 4675-4685, 2024 Sep.
Article
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| MEDLINE
| ID: mdl-38775471
ABSTRACT
BACKGROUND:
Tetranychus cinnabarinus is one of the most common polyphagous arthropod herbivores, and is primarily controlled by the application of acaricides. The heavy use of acaricides has led to high levels of resistance to acaricides such as cyflumetofen, which poses a threat to global resistance management programs. Cyflumetofen resistance is caused by an increase in metabolic detoxification; however, the role of uridine diphosphate (UDP)-glycosyltransferase (UGT) genes in cyflumetofen resistance remains to be determined.RESULTS:
Synergist 5-nitrouracil (5-Nul) significantly enhanced cyflumetofen toxicity in T. cinnabarinus, which indicated that UGTs are involved in the development of cyflumetofen resistance. Transcriptomic analysis and quantitative (q)PCR assays demonstrated that the UGT genes, especially UGT201H1, were highly expressed in the YN-CyR strain, compared to those of the YN-S strain. The RNA interference (RNAi)-mediated knockdown of UGT201H1 expression diminished the levels of cyflumetofen resistance in YN-CyR mites. The findings additionally revealed that the recombinant UGT201H1 protein plays a role in metabolizing cyflumetofen. Our results also suggested that the aromatic hydrocarbon receptor (AhR) probably regulates the overexpression of the UGT201H1 detoxification gene.CONCLUSION:
UGT201H1 is involved in cyflumetofen resistance, and AhR may regulates the overexpression of UGT201H1. These findings provide deeper insights into the molecular mechanisms underlying UGT-mediated metabolic resistance to chemical insecticides. © 2024 Society of Chemical Industry.Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Resistencia a Medicamentos
/
Tetranychidae
/
Acaricidas
Límite:
Animals
Idioma:
En
Revista:
Pest Manag Sci
Asunto de la revista:
TOXICOLOGIA
Año:
2024
Tipo del documento:
Article
País de afiliación:
China
Pais de publicación:
Reino Unido