Cell Reports Reveals Novel Mechanism of Innate Immune Signals Regulating m6A Modification

On February 15, 2022, You Fuping's team from Peking University School of Basic Medicine published a research paper titled "TBK1-METTL3 axis facilitates antiviral immunity" in Cell Reports, reporting that TBK1, a key kinase in the innate immune signaling pathway, can act in virus Directly interacts with METTL3 after infection and enhances the body's type 1 interferon response through dual regulation of METTL3 function

Eukaryotic mRNAs usually carry a variety of chemical modifications, among which N 6 -methyladenosine (m 6 A) is the most common internal mRNA modification

The TBK1-METTL3 axis regulates antiviral innate immunity

In this study, the authors first confirmed the direct interaction between METTL3 and TBK1 through protein profiling analysis, combined with co-immunoprecipitation and microthermophoresis experiments, and that METTL3 could synergize with TBK1 to activate IFNβ expression

To continue to explore the impact of S67 phosphorylation on METTL3 function, we analyzed the protein profiles of wild-type and S67A mutant METTL3

In conclusion, this study revealed a new mechanism by which innate immune signals regulate m 6 A modification, that is, TBK1 is involved in regulating the m 6 A activity and protein translation function of METTL3 at the same time, and promotes the body's type 1 interferon response .

Professor You Fuping from Peking University School of Basic Medicine is the corresponding author of the paper

The project was supported by the National Key R&D Program, the National Natural Science Foundation of China, and the Beijing Natural Science Foundation of China's key research projects

( Peking University School of Basic Medicine )