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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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MRNA decay analysis in the mouse myoblast cell line, C2C12 cells treated with conrtol-, Cugbp1- or Mbnl1-siRNA

ABSTRACT: CUGBP1 and MBNL1 are developmentally regulated RNA-binding proteins that are causally associated with myotonic dystrophy type 1. Using HITS-CLIP anlysis, we found CUGBP1 and MBNL1 preferentially bind to alternatively spliced introns and exons, as well as to the 3' UTRs. To analyze more directly the role of CUGBP1/MBNL1 binding to the 3’ UTR, we performed global analysis of mRNA stability in C2C12 cells using expression arrays, and found that CUGBP1 and MBNL1 regulate decay of endogenous mRNAs. We analyzed total RNA of C2C12 cells treated with control-, Cugbp1- or Mbnl1-siRNA. We analyzed 3 time points after addition of actionmycin D (0, 2.5, 5 hours).

ORGANISM(S): Mus musculus

SUBMITTER: Akio Masuda

PROVIDER: E-GEOD-27583 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Exon array analysis in the mouse myoblast cell line, C2C12 cells treated with control-, Cugbp1- or Mbnl1-siRNA

Project description:CUGBP1 and MBNL1 are developmentally regulated RNA-binding proteins that are causally associated with myotonic dystrophy type 1. Using HITS-CLIP anlysis, we found CUGBP1 and MBNL1 preferentially bind to alternatively spliced introns and exons, as well as to the 3' UTRs. To analyze more directly the role of CUGBP1/MBNL1 binding in alternative splicing, we performed exon array analysis in C2C12 cells using expression arrays. We analyzed total RNA of C2C12 cells treated with control-, Cugbp1- or Mbnl1-siRNA. RNA was harvested 48 hrs after transfection.

2012-01-03 | E-GEOD-29990 | biostudies-arrayexpress

Exon array analysis in the mouse myoblast cell line, C2C12 cells treated with control-, Cugbp1- or Mbnl1-siRNA

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mRNA decay analysis in the mouse myoblast cell line, C2C12 cells treated with conrtol-, Cugbp1- or Mbnl1-siRNA

Project description:CUGBP1 and MBNL1 are developmentally regulated RNA-binding proteins that are causally associated with myotonic dystrophy type 1. Using HITS-CLIP anlysis, we found CUGBP1 and MBNL1 preferentially bind to alternatively spliced introns and exons, as well as to the 3' UTRs. To analyze more directly the role of CUGBP1/MBNL1 binding to the 3’ UTR, we performed global analysis of mRNA stability in C2C12 cells using expression arrays, and found that CUGBP1 and MBNL1 regulate decay of endogenous mRNAs.

2012-01-03 | GSE27583 | GEO

RNA CLIP-seq for Cugbp1, Mbnl1 and Ptbp1 in mouse C2C12 myoblasts

Project description:CUG-binding protein 1 (CUGBP1) and muscleblind-like 1 (MBNL1) are developmentally regulated RNA-binding proteins that are causally associated with myotonic dystrophy type 1. We extensively determined RNA-binding sites of CUGBP1 and MBNL1 to investigate their roles in RNA processing. We also analyzed polypyrimidine tract-binding protein (PTB) as a control. CUGBP1 and MBNL1 preferentially bind to alternatively spliced introns and exons, respectively, and regulate alternative splicing events. Moreover, CUGBP1 and MBNL1 are preferentially bound to the 3' untranslated regions (UTRs), in particular of genes for RNA-binding proteins, and facilitate decay of the bound mRNAs. In addition, CUGBP1 and MBNL1 mutually destabilize mRNA. Precise temporal regulation of CUGBP1 and MBNL1 are likely to be essential for accurate control of destabilization of a broad spectrum of genes as well as of alternative splicing events in cell differentiation and tissue development.

2012-01-04 | E-MTAB-414 | biostudies-arrayexpress

RNA CLIP-seq for Cugbp1, Mbnl1 and Ptbp1 in mouse C2C12 myoblasts

Project description:RNA CLIP-seq for Cugbp1, Mbnl1 and Ptbp1 in mouse C2C12 myoblasts

| PRJEB2614 | ENA

Systematic analysis of cis-elements in unstable mRNAs demonstrates that CUGBP1 is a key regulator of mRNA decay in muscle cells

Project description:This SuperSeries is composed of the following subset Series: GSE21233: Expression data from C2C12 mouse myoblast with treatment actinomycin D GSE21235: mRNA immunoprecipitated with CUGBP1 in C2C12 Refer to individual Series

2010-07-08 | E-GEOD-21236 | biostudies-arrayexpress

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

mRNA immunoprecipitated with CUGBP1 in C2C12

Project description:Dramatic changes in gene expression occur in response to extracellular stimuli and during differentiation. Although transcriptional effects are important, alterations in mRNA decay also play a major role in achieving rapid and massive changes in mRNA abundance. Moreover, just as transcription factor activity varies between different cell types, the factors influencing mRNA decay are also cell-type specific.GREs are recognized by CUGBP1, an RNA-binding protein and instability factor whose function is affected in several neuromuscular diseases. To dectect the mRNA associated with CUGBP1, we utilized RNA immunoprecipitation followed by microarray (RIP-Chip) to identify CUGBP1-associated transcripts. To identify the mRNA associated with CUGBP1, we performed the immunoprecipitation followed by microarray (RIP-Chip)

2010-07-08 | E-GEOD-21235 | biostudies-arrayexpress

Expression profiles of primary cortical neurons after knocking down Cugbp1

Project description:To clarify the functional properties of Cugbp1, we established the differentially expressed alternative exons in Cugbp1-silenced primary cortical neurons by using exon-sensitive microarray technology. We analyzed total RNA of primary motor neuron infected with lentivirus expressing shRNA against mouse Cugbp1 or control. RNA was harvested 11 days after transfection.

2013-04-18 | E-GEOD-46147 | biostudies-arrayexpress

Hepatic transcriptome in CUGBP1 S302A knock-in mice highlights CUGBP1 degradation by Gankyrin through diethylnitrosamine (DEN) activation, leading to fatty liver and liver cancer

Project description:Purpose: CUGBP1 is an important regulator of liver homeostasis, through splicing regulation, stability, and mRNA translation. To aim to characterize the transcriptome of DEN-mediated liver cancer in CUGBP1 knock-in mice with Ser302 mutated to Ala (which mimics unphosphorylated CUGBP1 isoform) through RNA sequencing. Specifically, we compared gene expression levels to identify the impact of DEN-driven activation in both wildtype and CUGBP1 Ser302-to-Ala knock-in mice, focusing on downstream CUGBP1 targets and tumor activating pathways. Methods: Hepatic mRNA profiles were obtained through RNA sequencing of flash-frozen samples obtained at time of sacrifice. Results: We observe an augmentation of up- and downregulated cancer-related genes and pathways in CUGBP1 s302a knock-in mice compared to WT mice. We observe not only changes in expression related to oncogenesis, but also in splicing. Reduction of CUGBP1 protein due to the s302a variant leads to higher sensitivity to the development of liver cancer as a result of alterations in expression of down-stream mRNAs at both the splicing and expression levels. Conclusion: CUGBP1 is a strong tumor suppressor in the liver, and reduction of the CUGBP1 protein accelerates the development of liver cancer.

2017-06-12 | GSE83240 | GEO

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