| First Author | Terajima H | Year | 2017 |
| Journal | Nat Genet | Volume | 49 |
| Issue | 1 | Pages | 146-151 |
| PubMed ID | 27893733 | Mgi Jnum | J:261695 |
| Mgi Id | MGI:6151624 | Doi | 10.1038/ng.3731 |
| Citation | Terajima H, et al. (2017) ADARB1 catalyzes circadian A-to-I editing and regulates RNA rhythm. Nat Genet 49(1):146-151 |
| abstractText | It has been proposed that the CLOCK-ARNTL (BMAL1) complex drives circadian transcription of thousands of genes, including Per and Cry family genes that encode suppressors of CLOCK-ARNTL-dependent transcription. However, recent studies demonstrated that 70-80% of circadian-oscillating mRNAs have no obvious rhythms in their de novo transcription, indicating the potential importance of post-transcriptional regulation. Our CLOCK-ChIP-seq analysis identified rhythmic expression of adenosine deaminase, RNA-specific, B1 (Adarb1, also known as Adar2), an adenosine-to-inosine (A-to-I) RNA-editing enzyme. RNA-seq showed circadian rhythms of ADARB1-mediated A-to-I editing in a variety of transcripts. In Adarb1-knockout mice, rhythms of large populations of mRNA were attenuated, indicating a profound impact of ADARB1-mediated A-to-I editing on RNA rhythms. Furthermore, Adarb1-knockout mice exhibited short-period rhythms in locomotor activity and gene expression. These phenotypes were associated with abnormal accumulation of CRY2. The present study identifies A-to-I RNA editing as a key mechanism of post-transcriptional regulation in the circadian clockwork. |
