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N6-methyladenosine RNA modification suppresses antiviral innate sensing pathways via reshaping double-stranded RNA
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N6-methyladenosine RNA modification suppresses antiviral innate sensing pathways via reshaping double-stranded RNA
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N6-methyladenosine RNA modification suppresses antiviral innate sensing pathways via reshaping double-stranded RNA
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Journal Article
N6-methyladenosine RNA modification suppresses antiviral innate sensing pathways via reshaping double-stranded RNA
2021
Overview
Double-stranded RNA (dsRNA) is a virus-encoded signature capable of triggering intracellular Rig-like receptors (RLR) to activate antiviral signaling, but whether intercellular dsRNA structural reshaping mediated by the
N
6
-methyladenosine (m
6
A) modification modulates this process remains largely unknown. Here, we show that, in response to infection by the RNA virus Vesicular Stomatitis Virus (VSV), the m
6
A methyltransferase METTL3 translocates into the cytoplasm to increase m
6
A modification on virus-derived transcripts and decrease viral dsRNA formation, thereby reducing virus-sensing efficacy by RLRs such as RIG-I and MDA5 and dampening antiviral immune signaling. Meanwhile, the genetic ablation of METTL3 in monocyte or hepatocyte causes enhanced type I IFN expression and accelerates VSV clearance. Our findings thus implicate METTL3-mediated m
6
A RNA modification on viral RNAs as a negative regulator for innate sensing pathways of dsRNA, and also hint METTL3 as a potential therapeutic target for the modulation of anti-viral immunity.
N
6
-methyladenosine (m
6
A) RNA modification regulates RNA metabolism, and has been implicated in immune regulation. Here, the authors show that the m
6
A methyltransferase, METTL3, translocates into the cytoplasm to increase viral RNA m
6
A modification, decreases viral ds RNA content, and thereby dampens the RIG/MDA5-induced anti-viral immunity.
