Mesh : Animals Reactive Oxygen Species / metabolism Inactivation, Metabolic Arylalkylamine N-Acetyltransferase / metabolism genetics Insect Proteins / metabolism genetics Aedes / genetics metabolism Insecticides / pharmacology Gastrointestinal Tract / metabolism

来  源:   DOI:10.1038/s42003-024-06505-x   PDF(Pubmed)

Abstract:
Insecticide resistance has been a problem in both the agricultural pests and vectors. Revealing the detoxification mechanisms may help to better manage insect pests. Here, we showed that arylalkylamine N-acetyltransferase 1 (AANAT1) regulates intestinal detoxification process through modulation of reactive oxygen species (ROS)-activated transcription factors cap\"n\"collar isoform-C (CncC): muscle aponeurosis fibromatosis (Maf) pathway in both the oriental fruit fly, Bactrocera dorsalis, and the arbovirus vector, Aedes aegypti. Knockout/knockdown of AANAT1 led to accumulation of biogenic amines, which induced a decreased in the gut ROS level. The reduced midgut ROS levels resulted in decreased expression of CncC and Maf, leading to lower expression level of detoxification genes. AANAT1 knockout/knockdown insects were more susceptible to insecticide treatments. Our study reveals that normal functionality of AANAT1 is important for the regulation of gut detoxification pathways, providing insights into the mechanism underlying the gut defense against xenobiotics in metazoans.
摘要:
杀虫剂抗性一直是农业害虫和媒介中的问题。揭示解毒机制可能有助于更好地管理害虫。这里,我们表明,芳烷基胺N-乙酰转移酶1(AANAT1)通过调节活性氧(ROS)激活的转录因子cap\“n\”领同工型-C(CncC)调节肠道解毒过程:肌肉膜神经症纤维瘤病(Maf)途径在东方果蝇中,背杆菌,和虫媒病毒载体,埃及伊蚊.敲除/敲除AANAT1导致生物胺的积累,诱导肠道ROS水平降低。中肠ROS水平降低导致CncC和Maf表达降低,导致解毒基因表达水平降低。AANAT1敲除/敲除昆虫更容易受到杀虫剂处理。我们的研究表明,AANAT1的正常功能对于肠道解毒途径的调节很重要。提供对后生动物肠道防御外源性物质的潜在机制的见解。
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