Abstract
A new study in PLOS Biology finds that interferon (IFN)-induced adenosine deaminase acting on RNA 1 (ADAR1) mRNA is N6-methyladenosine (m6A) modified to promote its translation, enabling ADAR1 to modify self-double-stranded RNAs (dsRNAs) generated during the IFN response and preventing activation of the melanoma differentiation-associated protein 5 (MDA5)-mediated host antiviral response.
Highlights
The cellular RNA deaminase adenosine deaminase acting on RNA 1 (ADAR1) catalyzes the conversion of adenosine to inosine (A-toI) in double-stranded RNA (dsRNA) structures, resulting in single-stranded RNA (ssRNA) that is largely protected from immune sensing [1]
In a new study published in PLOS Biology, Terajima and colleagues seek to understand the intersection of mRNA is N6methyladenosine (m6A) and A-to-I editing, using glioblastoma cells as a model [6]
Previous studies identified a conserved m6A site in the ADAR1 transcript and an inverse relationship between m6A and A-to-I editing, suggesting that a causal link between m6A modification on ADAR1 and A-to-I editing might exist. This new work reveals that the m6A RNA–binding protein called YTH N6-methyladenosine RNA binding protein 1 (YTHDF1A),Uwh:iPchleparsoemnooteteths atYTHDF1ha translation of m6A-containing mRNAs, binds both isoforms of ADAR1 to varying degrees, with strong enrichment seen for the IFN-induced p150 isoform and less enrichment for the basally expressed p110 isoform (Fig 1)
Summary
The cellular RNA deaminase adenosine deaminase acting on RNA 1 (ADAR1) catalyzes the conversion of adenosine to inosine (A-toI) in dsRNA structures, resulting in ssRNA that is largely protected from immune sensing [1]. Modifications to RNA, including m6A and A-to-I editing, can play important and diverse roles in viral infection and the host innate immune response.
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