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The majority of A-to-I RNA editing is not required for mammalian homeostasis

ABSTRACT: RNAseq of Adult Brain in ADAR1 E861A, ADAR2 knock out, ADAR1 E861A x ADAR2 knock out het, and ADAR1 E861A x ADAR2 knock out mice generated by deep sequencing.

ORGANISM(S): Mus musculus

PROVIDER: GSE132214 | GEO | 2019/10/27

REPOSITORIES: GEO

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The majority of A-to-I RNA editing is not required for mammalian homeostasis.

Project description: Not available

| S-EPMC6900863 | biostudies-literature

RNA sequencing quantitative analysis of RNA editing levels in ADAR1, ADAR2, AIMP2 overexpression and wild type HEK293 cells

Project description:We overexpressed ADAR1, ADAR2 and AIMP2 in HEK293 cells and examined editing using RNA-seq.

2017-10-01 | GSE87198 | GEO

Core binding factor fusion downregulation of ADAR2 RNA editing contributes to acute myeloid leukaemia (AML) leukemogenesis

Project description:Adenosine to inosine (A-to-I) RNA editing, which is catalyzed by adenosine deaminases acting on RNA (ADAR) family of enzymes ADAR1 and ADAR2, has been shown to contribute to multiple cancers. However, other than chronic myeloid leukemia (CML) blast crisis, relatively little is known about its role in other types of hematological malignancies. Here, we found that ADAR2, but not ADAR1 and ADAR3, was specifically downregulated in the core binding factor (CBF) AML with t(8;21) or inv(16) translocations. In t(8;21) AML, RUNX1-driven transcription of ADAR2 was repressed by the RUNX1-ETO AE9a fusion protein in a dominant negative manner. Further functional studies confirmed that ADAR2 could suppress leukemogenesis specifically in t(8;21) and inv16 AML cells dependent on its RNA editing capability. Expression of two exemplary ADAR2-regulated RNA editing targets COPA and COG3 inhibited clonogenic growth of human t(8;21) AML cells. Our findings support a hitherto unappreciated mechanism leading to ADAR2 dysregulation in CBF AML and highlight the functional relevance of loss of ADAR2-mediated RNA editing to CBF AML.

2023-04-01 | GSE220488 | GEO

Adenosine deaminases that act on RNA induce reproducible changes in abundance and sequence of embryonic miRNAs

Project description:We used transgenic mouse embryos that are deficient in the two enzymatically active RNA editing enzymes ADAR1 and ADAR2 to compare relative frequencies but also sequence composition of mature miRNAs in these genetically modified backgrounds to wild-type mice by Illumina next gen sequencing. Deficiency of ADAR2 leads to a reproducible change in abundance of specific miRNAs and their predicted targets. Changes in miRNA abundance seem unrelated to editing events. Additional deletion of ADAR1 has surprisingly little impact on the mature miRNA repertoire, indicating that miRNA expression is primarily dependent on ADAR2. A to G transitions reflecting A to I editing events can be detected at few sites and at low frequency during the early embryonic stage investigated. Again, most editing events are ADAR2 dependent with only few editing sites being specifically edited by ADAR1. Besides known editing events in miRNAs a few novel, previously unknown editing events were identified. Some editing events are located to the seed region of miRNAs opening the possibility that editing leads to their retargeting. GSM852140-8: sequencing of mature miRNAs of wt, ADAR2-/- and ADAR1-/-/ADAR2-/- female mouse embryos at E11.5 GSM863778-81: Gene expression was measured in wiltype, ADAR2-/- and ADAR1-/-/ADAR2-/- E11.5 whole female mouse embryos using Agilent Whole Mouse Genome Oligo Microarrays 8x60K.

2012-02-02 | E-GEOD-34626 | biostudies-arrayexpress

RNA editing is the essential function of ADAR1 and, in the absence of MDA5, is dispensable for normal adult homeostasis [mmPCR-seq]

Project description:Adenosine-to-Inosine (A-to-I) editing of dsRNA by ADAR proteins is a pervasive feature of the epitranscriptome. There are estimated to be over 100 million potential A-to-I editing sites in humans and A-to-I editing can have varying consequences for gene expression. Whilst editing resulting in protein recoding defines the role of ADAR2, ADAR1 has been proposed to have both editing-dependent and -independent functions. The relative contribution of these putative functions to ADAR1 biology is unclear. We demonstrate that the absence of ADAR1-mediated editing is well tolerated when the cytosolic dsRNA sensor MDA5 is deleted. These mice have normal hematopoiesis, tissue patterning and life span. A direct comparison of the complete deletion of ADAR1 and the specific loss of A-to-I editing activity demonstrates that RNA editing is the only essential function of ADAR1 in adult mice. Therefore, preventing MDA5 substrate formation by endogenous RNA is the essential in vivo function of ADAR1-mediated editing.

2017-08-14 | GSE94386 | GEO

RNA editing is the essential function of ADAR1 and, in the absence of MDA5, is dispensable for normal adult homeostasis [RNAseq (Fetal Brain)]

2017-08-14 | GSE94388 | GEO

RNA editing is the essential function of ADAR1 and, in the absence of MDA5, is dispensable for normal adult homeostasis [RNAseq (Adult Brain)]

2017-08-14 | GSE94387 | GEO

Zfr regulates ADAR-mediated RNA editing in mouse primary neurons

Project description:We used RNA-seq of mouse primary cortical neurons transfected with control shRNAs or shRNAs targeting ADAR1, ADAR2, or Zfr to test for A-to-I RNA editing level differences between control and knockdown neurons.

2019-05-08 | GSE126629 | GEO

RNA A>I editing of tau circular RNAs

Project description:tau circular RNAs undergo Adenosine to inosine editing, which promotes their translation. To map editing sites,we cotransfected expression constructs for tau 7->12 and 10->12 circRNAs with expression constructs for GFP, ADAR1, ADAR2 and ADAR3 in HEK293 cells. RNA from these transfected cells was isolated and A>I editing was identified by A>G changes in the cDNA.

2022-11-08 | GSE216791 | GEO

ADAR1-editing in HeLa, p150-KO and ADAR1-KO transcriptomes

Project description:RNAseq analysis of cell lines with ADAR1-p150 and ADAR1-p110 knock-outs and primary human tissue samples (from GSE57353 and GSE99392 data sets) to identify sites of ADAR1 editing

2018-12-04 | GSE115127 | GEO

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