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Impairment of Muscle Regeneration in Muscleblind-like 3 Isoform Knockout Mice

ABSTRACT: We have performed an RNA-seq experiment to identify expression and alternative splicing differences between WT and Mbnl3 isoform knockout mice E15 forelimbs. We have also identified and characterized transcriptome wide Mbnl3-binding sites in C2C12 cells and E15 forelimbs.

ORGANISM(S): Mus musculus

PROVIDER: GSE46207 | GEO | 2013/05/18

SECONDARY ACCESSION(S): PRJNA198191

REPOSITORIES: GEO

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Impairment of Muscle Regeneration in Muscleblind-like 3 Isoform Knockout Mice

Project description:We have performed an RNA-seq experiment to identify expression and alternative splicing differences between WT and Mbnl3 isoform knockout mice E15 forelimbs. We have also identified and characterized transcriptome wide Mbnl3-binding sites in C2C12 cells and E15 forelimbs. 6 total samples were analyzed: E15 forelimbs from 3 WT and 3 MBNL3 M-NM-^TE2/M-NM-^TE2 female mice (15dpc). For HITS-CLIP, 3 samples each of C2C12 cells, WT E15 forelimbs and Mbnl3 ?E2 forelimbs were analyzed for Mbnl3 binding site analysis.

2013-05-18 | E-GEOD-46207 | biostudies-arrayexpress

Progressive impairment of muscle regeneration in muscleblind-like 3 isoform knockout mice.

Project description: Not available

| S-EPMC3736872 | biostudies-literature

Illumina bead array -/+ UV ASCC3 short isoform knockout cells

Project description:The transcription-related DNA damage response was analyzed on a genome-wide scale with great spatial and temporal resolution. Upon UV irradiation, a slowdown of transcript elongation and restriction of gene activity to the promoter-proximal ~25 kilobases is observed. This is associated with a shift from expression of long mRNAs to shorter isoforms, incorporating alternative last exons (ALEs) that are more proximal to the transcription start site. Notably, this includes a shift from a protein-coding ASCC3 mRNA to a shorter transcript isoform of which the RNA, rather than an encoded protein, is critical for the eventual recovery of transcription. The protein-coding ASCC3 isoform counteracts the function of the non-coding isoform, indicating crosstalk between them. Thus, the ASCC3 gene expresses both coding and noncoding transcript isoforms with opposite effects on transcription recovery after UV-induced DNA damage

2017-02-21 | GSE92325 | GEO

Transcriptome-wide Regulation of Splicing and mRNA Localization by Muscleblind Proteins

Project description:The Muscleblind-like (Mbnl) family of RNA-binding proteins plays important roles in muscle and eye development and in Myotonic Dystrophy (DM), where expanded CUG or CCUG repeats functionally deplete Mbnl proteins. We identified transcriptome-wide functional and biophysical targets of Mbnl proteins in brain, heart, muscle, and myoblasts using RNA sequencing and crosslinking/immunoprecipitation-sequencing approaches. This analysis identified several hundred splicing events whose regulation depended on Mbnl function, in a pattern indicative of functional interchangeability between Mbnl1 and Mbnl2. A nucleotide resolution RNA map associated repression or activation of exon splicing with Mbnl binding near either 3' splice site or near the downstream 5' splice site, respectively. Transcriptomic analysis of sub-cellular compartments uncovered a global role for Mbnls in regulating localization of mRNAs encoding membrane, synaptic and other proteins in both mouse and Drosophila cells, and Mbnls also contribute to protein secretion. These findings hold several new implications for DM pathogenesis. To assess global functions of Muscleblind proteins, RNA-Seq was performed using WT and Mbnl1 KO brain, heart, and muscle (5 mice each). Additionally, C2C12 mouse myoblasts were depleted of Mbnl1, Mbnl2, or both. Subcellular fractionation experiments were performed to analyze mRNA localization following depletion of Mbnl1 and Mbnl2 in C2C12 mouse myoblasts, and following depletion of Mbnl in Drosophila S-2R+ cells. CLIP-Seq was also performed against Mbnl1 in mouse brain, heart, muscle, and C2C12 myoblasts. Finally, ribosome footprinting was performed with C2C12 mouse myoblasts that were depleted of Mbnl1, Mbnl2, or both.

2012-08-17 | E-GEOD-39911 | biostudies-arrayexpress

Quaking isoform depletion in C2C12 myoblasts; direct binding targets of Quaking RNA binding proteins

Project description:Quaking isoform depletion in C2C12 myoblasts; direct binding targets of Quaking RNA binding proteins

| PRJNA398220 | ENA

Muscleblind-like 1 knockout mice reveal novel splicing defects in the myotonic dystrophy brain.

Project description: Not available

| S-EPMC3302840 | biostudies-literature

Isoform-specific depletion of U2AF1

Project description:Isoform-specific depletion of U2AF1

| PRJEB6651 | ENA

Analysis and design of RNA sequencing experiments for identifying mRNA isoform regulation

Project description:Through alternative splicing, most human genes express multiple isoforms that may have distinct or even antagonistic functions. To infer isoform regulation based on data from high-throughput sequencing of cDNA fragments (RNA-Seq), we have developed MISO, a computational model that estimates the expression level of alternatively spliced exons and mRNA isoforms and provides intuitive measures of con?dence in these estimates. Incorporation of the length distribution of inserted cDNA fragments in paired-end RNA-Seq analysis in MISO enables dramatic improvements in estimation of alternative splicing levels relative to previous methods. We show that one lane of paired-end RNA-Seq data can provide far more information about splicing than two lanes of single-end data, depending critically on properties of the distribution of cDNA fragment lengths in the sequenced library. MISO also leads to an intuitive method to detect di?erentially regulated exons or isoforms. Application of this method implicates the RNA splicing factor hnRNP H in regulation of alternative cleavage and polyadenylation, a role that is supported by UV crosslinking/immunoprecipitation/high-throughput sequencing (CLIP-Seq) analysis. Together, our results provide a probabilistic framework for RNA-Seq analysis, derive functional insights into pre-mRNA processing, and yield guidelines for the optimal design of RNA-Seq experiments for studies of gene and isoform expression. CLIPseq of hnRNP H in HEK 293T cells. RNAseq of polyA+ RNA from C2C12 mouse myoblasts stably expressing an empty vector or a vector containing an shRNA against CUGBP1. Libraries of two different insert lengths were created and examined.

2010-11-07 | E-GEOD-23694 | biostudies-arrayexpress

Isoform-specific depletion of U2AF1

Project description:RNA-Seq data of U2AF1 isoform depletion experiments.

2015-03-16 | E-MTAB-2682 | biostudies-arrayexpress

Transcriptome-wide identification of transcripts regulated by MBNL3 in hepatocellular carcinoma cells

Project description:Understanding the roles of splicing factors and splicing events during human tumorigenesis would open new avenues for targeted therapeutics. Here we identify an oncofetal splicing factor MBNL3, which indicates poor prognosis, and promotes hepatocellular carcinoma (HCC) tumorigenesis. Genetic MBNL3 inhibition almost completely abolishes HCC tumorigenesis. Transcriptomic analysis revealed that MBNL3 induces PXN antisense transcript 1 exon 4 inclusion. The transcript lacking exon 4 binds to coding sequences of PXN mRNA, causes dissociation of translation elongation factors from PXN mRNA, thereby inhibiting PXN mRNA translation. Whereas the transcript containing exon 4 preferentially binds to 3' untranslated region of PXN mRNA, protects PXN mRNA from microRNA-24-AGO2 complex-induced degradation, thereby increasing PXN expression. Through inducing exon 4 inclusion, MBNL3 upregulates PXN expression, which mediates the pro-tumorigenic roles of MBNL3. Collectively, these data demonstrate detailed mechanistic links between oncofetal splicing factor, splicing event, and tumorigenesis, and establish splicing factors and splicing events would be potential therapeutic targets.

2017-03-08 | GSE95778 | GEO

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