Ontology highlight
ABSTRACT:
PROVIDER: PRJNA644394 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12158445_1.fastq.gz | Fastqsanger.gz | |||
| SRR12158445_2.fastq.gz | Fastqsanger.gz | |||
| SRR12158446_1.fastq.gz | Fastqsanger.gz | |||
| SRR12158446_2.fastq.gz | Fastqsanger.gz | |||
| SRR12158447_1.fastq.gz | Fastqsanger.gz |
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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
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.
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Project description:We overexpressed ADAR1, ADAR2 and AIMP2 in HEK293 cells and examined editing using RNA-seq.
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Project description:RNA editing by adenosine deaminases acting on RNA (ADARs) is an evolutionarily conserved posttranscriptional modification essential for organismal development and normal cell function. Three catalytically active ADARs are conserved in mammals: two isoforms of ADAR1 referred to as ADAR1-p150 and ADAR1-p110, as well as ADAR2. All recognize and edit double-stranded RNA (dsRNA) structures but demonstrate target specificity and selectivity that dictate the unique essential biological functions of the three enzymes. The editing activity of ADAR1-p150 suppresses autoimmune responses against self-RNA structures, whereas ADAR1-p110 and ADAR2 have other primary functions. To better understand the mechanism of target selection by ADARs, we developed TSniffer, which allows accurate de novo identification of edited transcripts and quantification of the extent of editing within each transcript. We found that 17-40% of protein coding transcripts in mice, ferrets, and humans are edited by ADARs. Individual transcripts can harbor hundreds and thousands of editing sites, mostly within inverted retrotransposable elements. For human transcripts, we found differential editing by ADAR1 and ADAR2, aligning with a supportive role for ADAR2, while some targets were dominantly edited by ADAR1. Relying only on RNA-seq data and reference genome, TSniffer represents a novel tool to decipher the role of ADAR editing in different physiological states including disease models. Its unbiased approach is suitable for any organism.
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Project description:RNA editing by adenosine deaminases acting on RNA (ADARs) is an evolutionarily conserved posttranscriptional modification essential for organismal development and normal cell function. Three catalytically active ADARs are conserved in mammals: two isoforms of ADAR1 referred to as ADAR1-p150 and ADAR1-p110, as well as ADAR2. All recognize and edit double-stranded RNA (dsRNA) structures but demonstrate target specificity and selectivity that dictate the unique essential biological functions of the three enzymes. The editing activity of ADAR1-p150 suppresses autoimmune responses against self-RNA structures, whereas ADAR1-p110 and ADAR2 have other primary functions. To better understand the mechanism of target selection by ADARs, we developed TSniffer, which allows accurate de novo identification of edited transcripts and quantification of the extent of editing within each transcript. We found that 17-40% of protein coding transcripts in mice, ferrets, and humans are edited by ADARs. Individual transcripts can harbor hundreds and thousands of editing sites, mostly within inverted retrotransposable elements. For human transcripts, we found differential editing by ADAR1 and ADAR2, aligning with a supportive role for ADAR2, while some targets were dominantly edited by ADAR1. Relying only on RNA-seq data and reference genome, TSniffer represents a novel tool to decipher the role of ADAR editing in different physiological states including disease models. Its unbiased approach is suitable for any organism.
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Project description:Adenosine deaminase acting on RNA 2 (ADAR2) catalyzes adenosine-to-inosine RNA editing and contributes to multiple aspects of post-transcriptional regulation. Proximity-labeling (BioID) studies have previously defined the proximal protein environment of ADAR2. To complement these datasets and identify stably associated proteins, we performed Strep-tag affinity purification coupled to label-free LC–MS/MS. Doxycycline-inducible 293 T-REx cells expressing N-terminally Strep II–HA–tagged ADAR2 were used to isolate ADAR2-containing complexes under native conditions, followed by high-resolution mass spectrometric identification and quantification of co-purifying proteins. The resulting ADAR2 interactome shows significant overlap with our previously defined ADAR1 interaction network, as well as with publicly available ADAR2 proximity-labeling datasets, supporting the robustness and reproducibility of ADAR-associated protein complexes across methods and studies. This dataset provides a focused map of the stable ADAR2 interactome. This proteomic data form the basis of the first figure in the associated ADAR–exosome manuscript and complement existing proximity-labeling data by defining stable ADAR2 protein complexes.
2026-04-30 | PXD071677 | Pride
Project description:RNA modifications, including adenosine-to-inosine (A-to-I) editing, are fundamental for normal brain physiology, as they participate in multiple biological processes and pathological conditions. These modifications can alter RNA secondary structures and affinity for RNA-binding proteins, thereby influencing RNA processing mechanisms such as alternative splicing. In this study, we investigated A-to-I RNA editing and its impact on alternative splicing regulation in the mouse brain using ADAR enzyme-deficient mice. We analyzed the brain transcriptome of ADAR2 knockout (Adar2−/−Gria2R/R), as well as double ADAR1 catalytically inactive / ADAR2 knockout (Adar1E861A/E861A Ifih−/− Adar2−/−Gria2R/R) mice compared to wild-type controls, identifying alternative splicing events associated with the absence of ADAR1 and ADAR2 specific A-to-I editing.
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Project description:Adenosine deaminases acting on RNA (Adar1 and Adar2) catalyze I-to-A RNA editing, a post-transcriptional mechanism involved in multiple cellular functions. The role of Adar1-dependent RNA editing in cardiomyocytes (CMs) remains unclear. Here we show that conditional deletion of Adar1 in CMs results in myocarditis progressively evolving into dilated cardiomyopathy and heart failure at only 6 months of age. Adar1 depletion drives activation of interferon signaling genes (ISGs) in the absence of apoptosis and cytokine activation, and reduces the hypertrophic response of CMs upon pressure overload. Interestingly, ablation of the cytosolic sensor MDA5 prevents cardiac ISG activation and delays disease onset, but does not rescue the long-term lethal phenotype elicited by conditional deletion of Adar1. Retention of a single catalytically inactive Adar1 allele in CMs, in combination with MDA5 depletion, however, completely restores the cardiac function and prevents heart failure. Finally, ablation of interferon regulatory factor 7 (Irf7) attenuates the phenotype of Adar1-deficient CMs to a similar extent as MDA5 depletion, highlighting Irf7 as the main regulator of the immune response triggered by lack of Adar1 in CMs.
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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.
2012-02-02 | GSE34626 | GEO