ArticleRNA biology2015
Diverse selective regimes shape genetic diversity at ADAR genes and at their coding targets.
Article in RNA biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Unraveling ADAR-Mediated Protein Recoding: A Proteogenomic Exploration in Model Organisms and Human Pathology.International journal of molecular sciences · 2025Review
- Article
- ADAR1 Prevents R-loop Accumulation-Driven ATR Pathway Activation in Ovarian Cancer.Journal of Cancer · 2022Article
- Regulation and functional consequences of mGluRNA (New York, N.Y.) · 2021Article
- ALU non-B-DNA conformations, flipons, binary codes and evolution.Royal Society open science · 2020Review
- Mapping the dsRNA World.Cold Spring Harbor perspectives in biology · 2019Review
- A novel missense mutation of ADAR1 gene in a Chinese family leading to dyschromatosis symmetrica hereditaria and literature review.Journal of genetics · 2017Article
- The evolution and adaptation of A-to-I RNA editing.PLoS genetics · 2017Review
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A-to-I RNA editing operated by ADAR enzymes is extremely common in mammals. Several editing events in coding regions have pivotal physiological roles and affect protein sequence (recoding events) or function. We analyzed the evolutionary history of the 3 ADAR family genes and of their coding targets. Evolutionary analysis indicated that ADAR evolved adaptively in primates, with the strongest selection in the unique N-terminal domain of the interferon-inducible isoform. Positively selected residues in the human lineage were also detected in the ADAR deaminase domain and in the RNA binding domains of ADARB1 and ADARB2. During the recent history of human populations distinct variants in the 3 genes increased in frequency as a result of local selective pressures. Most selected variants are located within regulatory regions and some are in linkage disequilibrium with eQTLs in monocytes. Finally, analysis of conservation scores of coding editing sites indicated that editing events are counter-selected within regions that are poorly tolerant to change. Nevertheless, a minority of recoding events occurs at highly conserved positions and possibly represents the functional fraction. These events are enriched in pathways related to HIV-1 infection and to epidermis/hair development. Thus, both ADAR genes and their targets evolved under variable selective regimes, including purifying and positive selection. Pressures related to immune response likely represented major drivers of evolution for ADAR genes. As for their coding targets, we suggest that most editing events are slightly deleterious, although a minority may be beneficial and contribute to antiviral response and skin homeostasis.
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