Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA148757 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Adar1 is an essential gene for mouse embryonic development. Adar1 null mouse embryos dies around E11.5 because of massive apoptosis. Small RNA: 4 samples examined: wild type E11.0, ADAR1 null E11.0, wild type E11.5, ADAR1 null E11.5, mRNA-seq: wild type E11.5, ADAR1 null E11.5.
2013-05-01 | E-GEOD-33473 | biostudies-arrayexpress
Project description:Adar1 is an essential gene for mouse embryonic development. Adar1 null mouse embryos dies around E11.5 because of massive apoptosis.
2013-05-01 | GSE33473 | GEO
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:Total mRNA seq was perfomed on widtype and Ret null mouse embryonic gut at 2 stages of devlopment- E11.5 and E12.5
2016-09-30 | GSE84145 | GEO
Project description:Transcriptome profile of wildtype and Ret homozygote null mouse guts at E11.5 and E12.5
| PRJNA328144 | ENA
Project description:The ADAR RNA editing enzymes deaminate adenosine bases to inosines in cellular RNAs, recoding open reading frames. Human ADAR1 mutations cause Aicardi-Goutieres Syndrome (AGS) and Adar1 mutant mice showing an aberrant interferon response and death by embryonic day E12.5 model the human disease. Searches have not identified key ADAR1 RNA editing sites recoding immune/haematopoietic proteins but editing is widespread in Alu sequences. We show that Adar1 embryonic lethality is rescued in Adar1; Mavs double mutant mice in which general antiviral responses to cytoplasmic dsRNA are prevented. We propose that inosine bases are epigenetic marks identifying cellular RNA as innate immune ÒselfÓ. Consistent with this idea we show that an editing-active cytoplasmic ADAR is required to prevent aberrant immune responses in Adar1 mutant mouse embryo fibroblasts. No dramatic increase in repetitive transcripts is observed. AGS mutations in ADAR1 affect editing by the interferon-inducible cytoplasmic ADAR1 isoform. RNA-seq expression profiling in Adar1 and Adar1/Mavs knockout mice embryos.
2014-12-19 | E-GEOD-62917 | biostudies-arrayexpress
Project description:Ribosomes have been suggested to directly control gene regulation, however regulatory roles for ribosomal RNA (rRNA) remain largely unexplored. Expansion segments (ESs) consist of multitudes of tentacle-like rRNA structures extending from the core ribosome in eukaryotes. ESs are remarkably variable in sequence and size across eukaryotic evolution with a largely unknown function. In characterizing ribosome binding to a regulatory element within a Homeobox (Hox) 5’ UTR, we unexpectedly identify a modular stem-loop within this element that binds to a single ES, ES9S. Here, we described the raw data of the relative quantification proteomic analysis using tandem mass tag mass spectrometry of the ribonucleoprotein (RNP) complexes enriched from affinity pulldown of the 4xS1m-aptamer fusion constructs with the lysate components of C3H/10T1/2 cells and mouse embryo. 4xS1m pulldown is performed by combining mouse Hoxa9 mRNA elements (P3 and P4) with C3H/10T1/2 cell lysates, and by combining a9 IRES180 and an unrelated viral IRES with E11.5 FVB mouse embryo lysates. The aptamer alone served as a negative control. RNPs in the eluate were released by RNAse A treatment and were subjected to TMT 6plex labelling.
2020-11-19 | PXD021678 | Pride
Project description:E11.5 metanephric mesenchyme and ureteric bud were dissected from the E11.5 kidney rudiment using fine manual microdissection (ureteric bud only) or both fine manual microdissection and laser capture microdissection (metanephric mesenchyme) to define the gene expression profiles of these structures. Additionally, HoxA11, HoxD11 compound null E11.5 metanephric mesenchyme was obtained through laser capture microdissection allowing analysis of possible Hox targets in kidney development. Targets from multiple biological replicates of each were generated and the expression profiles were determined using Affymetrix MOE430_v2 arrays. Using microdissection techniques, ureteric bud and metanephric mesenchyme were dissected from E11.5 kidney rudiments allowing the identificated genes specifically regulated in either structure. In addition, Hoxa11, Hoxd11 compound null E11.5 metanephric mesenchyme were normalized to wild type embryonic controls allowing the identification of potential Hox targets in normal kidney development. Each structure/genotype were represented in biological (seperate embryo) replicate.
2007-12-07 | E-GEOD-3822 | biostudies-arrayexpress
Project description:Purpose: The goals of this study are to compare WT and ADAR1 knockout mouse B cell transcriptome profiling (RNA-seq) Methods: Cells are sorted from bone marrow of WT and ADAR1 KO mice and mRNA profiles were generated by deep sequencing using Illumina Hiseq. Results: Using an optimized data analysis workflow, we confirmed over hundrad differential expressed genes by KEGG pathway analysis with 185 up-regulated genes and 136 down-regulated genes. Conclusions: Our study represents the first detailed analysis of B cell mRNA profile from WT and ADAR1 KO mice using RNA-Seq. We conclude that ADAR1 plays important roles during early B cell development.
2023-12-31 | GSE196304 | GEO
Project description:Cellular senescence plays a causal role in ageing and, in mouse, depletion of p16INK4a-expressing senescent cells delays ageing-associated disorders. Adenosine deaminases acting on RNA (ADARs) RNA editing enzymes are also implicated as important regulators of human ageing and ADAR inactivation causes age-associated pathologies such as neurodegeneration in model organisms. However, the role, if any, of ADARs in cellular senescence is unknown. Here we show that ADAR1 is post-transcriptionally downregulated by autophagic degradation to promote senescence through upregulating p16INK4a. ADAR1 is downregulated during senescence post-transcriptionally by autophagy-lysosomal pathway and the downregulation is sufficient to drive senescence in both in vitro and in vivo models. Senescence induced by ADAR1 downregulation is p16INK4a dependent and independent of its RNA editing function. Mechanistically, ADAR1 promotes SIRT1 expression by affecting its RNA stability through HuR, an RNA binding protein that increases the half-life and steady state levels of its target mRNAs. And SIRT1, in turn, antagonizes translation of mRNA encoding p16INK4a. Hence, downregulation of ADAR1 and SIRT1 mediates p16INK4aupregulation by enhancing its mRNA translation. Finally, Adar1 is downregulated during ageing of mouse tissues such as brain, ovary, and intestine, and Adar1 expression correlates with Sirt1 expression in these tissues in mice. Together, our study reveals an RNA-editing independent role of ADAR1 in regulating senescence by post-transcriptionally controlling p16INK4a expression.
2022-04-25 | GSE179423 | GEO