Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

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


ABSTRACT: 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.

ORGANISM(S): Mus musculus

SUBMITTER: Thomas Doktor 

PROVIDER: E-MTAB-414 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

CUGBP1 and MBNL1 preferentially bind to 3' UTRs and facilitate mRNA decay.

Masuda Akio A   Andersen Henriette Skovgaard HS   Doktor Thomas Koed TK   Okamoto Takaaki T   Ito Mikako M   Andresen Brage Storstein BS   Ohno Kinji K  

Scientific reports 20120104


CUGBP1 and MBNL1 are developmentally regulated RNA-binding proteins that are causally associated with myotonic dystrophy type 1. We globally determined the in vivo RNA-binding sites of CUGBP1 and MBNL1. Interestingly, CUGBP1 and MBNL1 are both preferentially bound to 39 UTRs. Analysis of CUGBP1- and MBNL1-bound 39 UTRs demonstrated that both factors mediate accelerated mRNA decay and temporal profiles of expression arrays supported this. Role of CUGBP1 on accelerated mRNA decay has been previous  ...[more]

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