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m6A modification controls the innate immune response to infection by targeting type I interferons
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Journal Article
m6A modification controls the innate immune response to infection by targeting type I interferons
2019
Overview
N
6
-methyladenosine (m
6
A) is the most common mRNA modification. Recent studies have revealed that depletion of m
6
A machinery leads to alterations in the propagation of diverse viruses. These effects were proposed to be mediated through dysregulated methylation of viral RNA. Here we show that following viral infection or stimulation of cells with an inactivated virus, deletion of the m
6
A ‘writer’ METTL3 or ‘reader’ YTHDF2 led to an increase in the induction of interferon-stimulated genes. Consequently, propagation of different viruses was suppressed in an interferon-signaling-dependent manner. Significantly, the mRNA of
IFNB
, the gene encoding the main cytokine that drives the type I interferon response, was m
6
A modified and was stabilized following repression of METTL3 or YTHDF2. Furthermore, we show that m
6
A-mediated regulation of interferon genes was conserved in mice. Together, our findings uncover the role m
6
A serves as a negative regulator of interferon response by dictating the fast turnover of interferon mRNAs and consequently facilitating viral propagation.
RNAs can be dynamically modified by N
6
-methylation of adenosine (m
6
A), which leads to their destabilization. Stern-Ginossar and colleagues demonstrate a role for m
6
A modification of host transcripts encoding type I interferons during viral infection.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
