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The landscape of A-to-I RNA editome in mouse embryonic development

ABSTRACT: The landscape of A-to-I RNA editome in mouse embryonic development

PROVIDER: PRJNA507248 | ENA |

REPOSITORIES: ENA

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The landscape of A-to-I RNA editome in mouse embryonic development

Project description:A-to-I editing, as a post-transcriptional modification process mediated by ADAR, plays a crucial role in many biological process in metazoans.The study of RNA editing in mouse early embryonic development can understand the dynamic changes of RNA editing during mouse early embryonic development, and further reveal the role of RNA editing in mouse early embryo development.We found that as embryonic developing, RNA editome in mice is getting more and more. Besides, RNA editome in mouse embryonic development is stage specified.

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The landscape of A-to-I RNA editome from 462 individuals human genomes

Project description:A-to-I editing, as a post-transcriptional modification process mediated by ADAR, plays a crucial role in many biological process in metazoans. However, how and to what extent that A-to-I editing diversifies and shapes the population diversity at the RNA level is largely unknown. We employed 462 mRNA-sequencing data from five populations of the Geuvadis Project and identified 16,518 A-to-I editing sites, forming a landscape of RNA editome of the human genome. By exploration of RNA editing within and between populations, we discovered non-adaption of nonsynonymous editing in the evolution, and revealed geographic restriction of rare editing sites. Moreover, we showed that RNA editing can characterize the subtle but substantial divergence between different populations, especially those from different continents. Altogether, we demonstrated RNA editing can well depict the nature and structure of populations at RNA level, which provides insights into the process of how A-to-I editing shapes population diversity at transcriptomic level. Our work will facilitate the understanding of the landscape of RNA editome at population-scale, and be helpful to interpret difference in the distribution and prevalence of disease among individuals and across populations.

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Project description:Adenosine deaminase acting on RNA (ADAR) (also known as ADAR1) promotes A-to-I conversion in double-stranded and highly structured RNAs. ADAR1 has two isoforms transcribed from different promoters: ADAR1p150, which is mainly cytoplasmic and interferon-inducible, and constitutively expressed ADAR1p110 that is primarily localized in the nucleus. Mutations in ADAR1 cause Aicardi – Goutières syndrome (AGS), a severe autoinflammatory disease in humans associated with aberrant IFN production. In mice, deletion of ADAR1 or selective knockout of the p150 isoform alone leads to embryonic lethality driven by overexpression of interferon-stimulated genes. This phenotype can be rescued by concurrent deletion of cytoplasmic dsRNA-sensor MDA5. These findings indicate that the interferon-inducible p150 isoform is indispensable and cannot be rescued by the ADAR1p110 isoform. Nevertheless, editing sites uniquely targeted by ADAR1p150 but also mechanisms of isoform- specificity remain elusive. To identify ADAR1 isoform-specific ‘editome’, we transfected A-to-I editing deficient mouse embryonic fibroblasts (MEFs) with ADAR1p150- or ADAR1p110- or RFP-editing negative control. We subjected the samples to RNA sequencing and detected editing at known-editing sites.

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