There was no additional external funding received for this study.Ĭompeting interests: The authors have declared that no competing interests exist.įoreign nucleic acids such as phages and viruses pose constant threats to host cells. The content is solely the responsibility of the authors and does not necessarily represent the official views of these agencies. Work in the T.T.’s group was supported by Takeda Science Foundation. įunding: Research in K.O.’s group was supported by the National Research Foundation, Prime Minister’s Office, Singapore under its NRF Fellowship Programme (NRF2011NRF-NRFF001-042), Temasek Life Sciences Laboratory core funding and the JSPS Fund for the Promotion of Joint International Research (Returning Researcher Development Research, 17K20145). The UCSC assembly hubs with the RNAseq mapping tracks are available at and. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.ĭata Availability: The small RNA library data produced for this study are deposited at NCBI SRA under GSE183810. Received: FebruAccepted: JanuPublished: March 30, 2023Ĭopyright: © 2023 Feng et al. PLoS ONE 18(3):Įditor: Sébastien Pfeffer, Institut de Biologie Moleculaire et Cellulaire, FRANCE (2023) A novel eukaryotic RdRP-dependent small RNA pathway represses antiviral immunity by controlling an ERK pathway component in the black-legged tick. We propose that tick sRNA pathways control multiple aspects of immune response via RNAi and regulation of signaling pathways.Ĭitation: Feng C, Torimaru K, Lim MYT, Chak L-L, Shiimori M, Tsuji K, et al. This effect is dependent on Dsor1, suggesting that antiviral immunity is enhanced by RdRP1 knockdown through Dsor1 upregulation. On the other hand, RdRP1 knockdown unexpectedly results in downregulation of viral transcripts. Consistent with viral gene repression by the RNAi mechanism using virus-derived small interfering RNAs, viral transcripts are upregulated by AGO knockdown. Sensor assays demonstrate that Dsor1 is downregulated by RdRP1 through the 3’UTR that contains a target site of RdRP1-dependent repeat-derived sRNAs. Knockdown of some RdRP homologs misregulates genes including RNAi-related genes and the regulator of immune response Dsor1. RdRP1-dependent sRNAs possess 5’-monophosphates and are mainly derived from RNA polymerase III-transcribed genes and repetitive elements. We find abundant classes of ~22nt sRNAs that require specific combinations of RdRPs and sRNA effector proteins (Argonautes or AGOs). Here, we study sRNAs in the ISE6 cell line, which is derived from the black-legged tick, an important vector of human and animal pathogens. Although roles of RNA-dependent RNA Polymerases (RdRPs) in sRNA biology are extensively studied in nematodes, plants and fungi, understanding of RdRP homologs in other animals is still lacking. Small regulatory RNAs (sRNAs) are involved in antiviral defense and gene regulation.
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