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The splicing activator DAZAP1 integrates splicing control into MEK/Erk regulated cell proliferation and migration

ABSTRACT: DAZAP1 was depleted in culterd HEK 293T cells using shRNA and the resulting poly A RNA were isolated c-DNA library constructed and paired end sequenced on illumina Hi-seq 2000 platform the data was compared to a control shRNA depleted cell

ORGANISM(S): Homo sapiens

PROVIDER: GSE52745 | GEO | 2013/12/25

SECONDARY ACCESSION(S): PRJNA229959

REPOSITORIES: GEO

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The splicing activator DAZAP1 integrates splicing control into MEK/Erk regulated cell proliferation and migration

Project description:DAZAP1 was depleted in culterd HEK 293T cells using shRNA and the resulting poly A RNA were isolated c-DNA library constructed and paired end sequenced on illumina Hi-seq 2000 platform the data was compared to a control shRNA depleted cell Gene expression and splicing switches upon DAZAP1 knockdown

2013-12-25 | E-GEOD-52745 | biostudies-arrayexpress

The splicing activator DAZAP1 integrates splicing control into MEK/Erk-regulated cell proliferation and migration.

Project description:Alternative splicing of pre-messenger RNA (mRNA) is a critical stage of gene regulation in response to environmental stimuli. Here we show that DAZAP1, an RNA-binding protein involved in mammalian development and spermatogenesis, promotes inclusion of weak exons through specific recognition of diverse cis-elements. The carboxy-terminal proline-rich domain of DAZAP1 interacts with and neutralizes general splicing inhibitors, and is sufficient to activate splicing when recruited to pre-mRNA. This domain is phosphorylated by the MEK/Erk (extracellular signal-regulated protein kinase) pathway and this modification is essential for the splicing regulatory activity and the nuclear/cytoplasmic translocation of DAZAP1. Using mRNA-seq, we identify endogenous splicing events regulated by DAZAP1, many of which are involved in maintaining cell growth. Knockdown or over-expression of DAZAP1 causes a cell proliferation defect. Taken together, these studies reveal a molecular mechanism that integrates splicing control into MEK/Erk-regulated cell proliferation.

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Expression data from wild-type and Dazap1 mutant mouse testes

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Project description:The binding of Deleted in Azoospermia Associated Protein 1 (DAZAP1) to splicing mutations in the BRCA1 and NF1 genes that caused exon exclusion suggest a role for DAZAP1 in RNA splicing. To elucidate the biological functions of DAZAP1 and to search for its natural RNA substrates, we compared the exon usages of wild-type and Dazap1 mutant testes by exon microarrays. We used wild-type and Dazap1 mutant mouse testes. Each genotype has three replicates. 6 total samples were analyzed.

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The underlying mechanism by which DAZAP1 exerted carcinogenesis and its potential targets in MM

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