Mitochondrial hypoxic stress induces widespread RNA editing by APOBEC3G in lymphocyte

Sharma, Shraddha; Wang, J; Portwood, Scott; Cortes-Gomez, Eduardo; Maguire, Orla; Ph, Basse; Wang, Eunice S.; Be, Baysal

doi:10.1101/389791

Cited by 3 publications

(1 citation statement)

References 63 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Later the same group went on to describe the RNA editing capabilities for A3G, again in the HEK293T cell system [18]. They also suggest that there is an increase in RNA editing as a response to mitochondrial stress in NK cells and lymphocytes [154].…”

Section: Apobec3mentioning

confidence: 99%

RNA Editors, Cofactors, and mRNA Targets: An Overview of the C-to-U RNA Editing Machinery and Its Implication in Human Disease

Lerner

Papavasiliou

Pecori

2018

Genes

View full text Add to dashboard Cite

One of the most prevalent epitranscriptomic modifications is RNA editing. In higher eukaryotes, RNA editing is catalyzed by one of two classes of deaminases: ADAR family enzymes that catalyze A-to-I (read as G) editing, and AID/APOBEC family enzymes that catalyze C-to-U. ADAR-catalyzed deamination has been studied extensively. Here we focus on AID/APOBEC-catalyzed editing, and review the emergent knowledge regarding C-to-U editing consequences in the context of human disease.

show abstract

Section: Apobec3mentioning

confidence: 99%

RNA Editors, Cofactors, and mRNA Targets: An Overview of the C-to-U RNA Editing Machinery and Its Implication in Human Disease

Lerner

Papavasiliou

Pecori

2018

Genes

View full text Add to dashboard Cite

show abstract

MultiEditR: An easy validation method for detecting and quantifying RNA editing from Sanger sequencing

Kluesner

Arnold

Lerner

et al. 2019

Preprint

View full text Add to dashboard Cite

RNA editing is the base change that results from RNA deamination by two predominant classes of deaminases; the APOBEC family and the ADAR family. Respectively, deamination of nucleobases by these enzymes are responsible for endogenous editing of cytosine to uracil (Cto-U) and adenosine to inosine (A-to-I). RNA editing is known to play an essential role both in maintaining normal cellular function, as well as altered cellular physiology during oncogenesis and tumour progression. Analysis of RNA editing in these important processes, largely relies on RNA-seq technology for the detection and quantification of RNA editing sites. Despite the power of these technologies, multiple sources of error in detecting and measuring base editing still exist, therefore additional validation and quantification of editing through Sanger sequencing is still required for confirmation of editing. Depending on the number of RNA editing sites that are of interest, this validation step can be both expensive and time-consuming. To address this need we developed the tool MultiEditR which provides a simple, and cost-effective method of detecting and quantifying RNA editing form Sanger sequencing. We expect that MultiEditR will foster further discoveries in this rapidly expanding field.

show abstract

Mitochondrial hypoxic stress induces widespread RNA editing by APOBEC3G in natural killer cells

et al. 2019

Self Cite

View full text Add to dashboard Cite

Background Protein recoding by RNA editing is required for normal health and evolutionary adaptation. However, de novo induction of RNA editing in response to environmental factors is an uncommon phenomenon. While APOBEC3A edits many mRNAs in monocytes and macrophages in response to hypoxia and interferons, the physiological significance of such editing is unclear. Results Here, we show that the related cytidine deaminase, APOBEC3G, induces site-specific C-to-U RNA editing in natural killer cells, lymphoma cell lines, and, to a lesser extent, CD8-positive T cells upon cellular crowding and hypoxia. In contrast to expectations from its anti-HIV-1 function, the highest expression of APOBEC3G is shown to be in cytotoxic lymphocytes. RNA-seq analysis of natural killer cells subjected to cellular crowding and hypoxia reveals widespread C-to-U mRNA editing that is enriched for genes involved in mRNA translation and ribosome function. APOBEC3G promotes Warburg-like metabolic remodeling in HuT78 T cells under similar conditions. Hypoxia-induced RNA editing by APOBEC3G can be mimicked by the inhibition of mitochondrial respiration and occurs independently of HIF-1α. Conclusions APOBEC3G is an endogenous RNA editing enzyme in primary natural killer cells and lymphoma cell lines. This RNA editing is induced by cellular crowding and mitochondrial respiratory inhibition to promote adaptation to hypoxic stress. Electronic supplementary material The online version of this article (10.1186/s13059-019-1651-1) contains supplementary material, which is available to authorized users.

show abstract

Mitochondrial hypoxic stress induces widespread RNA editing by APOBEC3G in lymphocyte

Cited by 3 publications

References 63 publications

RNA Editors, Cofactors, and mRNA Targets: An Overview of the C-to-U RNA Editing Machinery and Its Implication in Human Disease

RNA Editors, Cofactors, and mRNA Targets: An Overview of the C-to-U RNA Editing Machinery and Its Implication in Human Disease

MultiEditR: An easy validation method for detecting and quantifying RNA editing from Sanger sequencing

Mitochondrial hypoxic stress induces widespread RNA editing by APOBEC3G in natural killer cells

Contact Info

Product

Resources

About