Journal
ADVANCED SCIENCE
Volume 8, Issue 15, Pages -Publisher
WILEY
DOI: 10.1002/advs.202100606
Keywords
antiviral immunity; N6‐ methyladenosine modification; methyltransferase‐ like protein 14; mitochondrial antiviral signaling protein; mRNA stability
Categories
Funding
- National Natural Science Foundation of China [31730026, 81930039, 81525012, 31900680]
- National Postdoctoral Program for Innovative Talents [BX201700146]
- Shandong Provincial Natural Science Foundation [ZR2018BC021]
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MAVS mRNA undergoes m(6)A modification through METTL14, affecting its stability and immune response to RNA viruses. Deficiency of METTL14 increases MAVS mRNA stability, leading to enhanced response to RNA virus infection.
Mitochondrial antiviral signaling (MAVS) protein is the core signaling adaptor in the RNA signaling pathway. Thus, appropriate regulation of MAVS expression is essential for antiviral immunity against RNA virus infection. However, the regulation of MAVS expression at the mRNA level especially at the post transcriptional level is not well-defined. Here, it is reported that the MAVS mRNA undergoes N-6-methyladenosine (m(6)A) modification through methyltransferase-like protein 14 (METTL14), which leads to a fast turnover of MAVS mRNA. Knockdown or deficiency of METTL14 increases MAVS mRNA stability, and downstream phosphorylation of TBK1/IRF3 and interferon-beta production in response to RNA viruses. Compared to wild-type mice, heterozygotes Mettl14(+/-) mice better tolerate RNA virus infection. The authors' findings unveil a novel mechanism to regulate the stability of MAVS transcripts post-transcriptionally through m(6)A modification.
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