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Describing a Transcription Factor Dependent Regulation of the MicroRNA Transcriptome
Published on: June 15, 2016
Post-transcriptional regulation of UGT349A13 through a microRNA, PC-5p-86205_18, influences afidopyropen
Yuanxue Yang1, Aiyu Wang1, Chao Xue1
1Institute of Industrial Crops, Shandong Academy of Agricultural Sciences, Jinan, Shandong 250100, China.
Abstract:
As key detoxification enzymes, UDP-glycosyltransferases (UGTs) are known to underpin insecticide tolerance in pests such as Aphis craccivora. Yet, their post-transcriptional regulation by microRNAs (miRNAs) remains largely unexplored in this major crop pest. In the present study, we conducted a genomic analysis that identified 37 UGTs in Aphis craccivora. To investigate their role in susceptibility to the afidopyropen, we performed synergism bioassays following LC50 concentration of afidopyropen exposure, combined with UGT activity measurements, revealed a critical contribution of UGTs to afidopyropen susceptibility. Exposure to afidopyropen resulted in more than a 2-fold increase in the expression levels of UGT343A37 and UGT349A13. Functional validation via RNA interference (RNAi) confirmed that suppression of UGT349A13 alone significantly increased the sensitivity of A. craccivora to afidopyropen. To elucidate the upstream regulatory mechanism, bioinformatic prediction identified candidate miRNAs targeting UGT349A13. To validate regulatory function, A. craccivora fed the synthetic agomir-PC-5p-86205_18, which reduced UGT349A13 transcript levels, correlating with increased susceptibility to afidopyropen. Then, molecular interaction specificity between PC-5p-86205_18 and UGT349A13 was definitively established by dual luciferase reporter assay. This finding demonstrated that PC-5p-86205_18 contributes to afidopyropen susceptibility in A. craccivora by post-transcriptionally regulating UGT349A13. This finding not only deepens our understanding of detoxification mechanisms but also provides a potential molecular target for developing strategies to manage afidopyropen resistance.
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