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Convergent exaptation of Alu and B/ID SINEs for Staufen-mediated mRNA decay

ABSTRACT: Identifying orthologous mRNAs subject to SMD in both mouse and human myoblasts using siRNA depletion of Staufen or Upf1

OTHER RELATED OMICS DATASETS IN: PRJNA352669

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE89588 | GEO | 2017/12/31

SECONDARY ACCESSION(S): PRJNA352669

REPOSITORIES: GEO

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Convergent exaptation of Alu and B/ID SINEs for Staufen-mediated mRNA decay

Project description:Convergent exaptation of Alu and B/ID SINEs for Staufen-mediated mRNA decay

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RIP-Chip of endogenous Staufen and GFP-tagged Staufen from 0-3 hour Drosophila embryos

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RIP-Chip of endogenous Staufen and GFP-tagged Staufen from 0-3 hour Drosophila embryos

Project description:Staufen-associated mRNAs were identified in early Drosophila embryos by RNA-co-immunoprecipitation followed by microarray analysis (RIP-Chip), using two complementary approaches: RIP-Chip from wild-type embryos using a synthetic anti-Staufen antibody, and RIP-Chip from transgenic GFP-Staufen-expressing embryos using an anti-GFP antibody. Genome-wide transcript expression in whole embryos was also assessed for the wild-type and GFP-Staufen lines. There are 18 samples in total. These include 3 replicates each of 1) gene expression profiling from total mRNA isolated from wild-type 0-3 hour embryos, 2) synthetic anti-Staufen antibody RNA co-immunoprecipitations of endogenous Staufen from wild-type 0-3 hour embryos, 3) control synthetic antibody RNA co-immunoprecipitations from wild-type 0-3 hour embryos, 4) gene expression profiling from total mRNA isolated from transgenic GFP-Staufen expressing 0-3 hour embryos, 5) anti-GFP RNA co-immunoprecipitations of GFP-Staufen from transgenic GFP-Staufen expressing 0-3 hour embryos, 6) anti-FLAG control RNA co-immunoprecipitations from transgenic GFP-Staufen expressing 0-3 hour embryos.

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Transcriptome analysis revealed that SMD regulates neuronal differentiation.

Project description:Transcriptome analysis from Staufen-mediated mRNA (SMD) targets during differentiation confirmed that STAU1 was a key factor in neuronal differentiation.

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Project description:Analysis of cellular SMD or NMD substrates that regulated by Upf1 and/or PNRC2 in HeLa cell. The hypothesis tested in the present study was that endogenous SMD or NMD substrates may co-regulated by Upf1 and PNRC2. Results provide important information that vast range of cellular SMD or NMD substrates are reqired PNRC2 for decay. Total RNA obtained from HeLa cells with downregulation of Upf1 or PNRC2 by siRNA. The up- or down-regulated transcripts were compare to control siRNA treated HeLa cell RNA extract. Significant transcripts were confirmed by replication

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Staufen1 regulates a variety of mammalian transcripts

Project description:It is currently unknown how extensively the double-stranded RNA binding protein Staufen (Stau)1 is utilized by mammalian cells to regulate gene expression. To date, Stau1 binding to the 3’ untranslated region (3’UTR) of ARF1 mRNA has been shown to target ARF1 mRNA for Stau1-mediated mRNA decay (SMD). ARF1 SMD depends on translation and recruitment of the nonsense-mediated mRNA decay factor Upf1 to the ARF1 3’UTR by Stau1. Here, we use microarray analyses to examine changes in the abundance of cellular mRNAs that occur when Stau1 is depleted. Results indicate that 1.1% and 1.0% of the 11,569 HeLa-cell transcripts that were analyzed are, respectively, upregulated and downregulated at least two-fold in three independently performed experiments. Additionally, we localize the Stau1 binding site to the 3’UTR of four mRNAs that we define as natural SMD targets. Together, these and substantiating results suggest that Stau1 influences the expression of a wide variety of physiologic transcripts and metabolic pathways. Keywords: Staufen1-mediated mRNA decay; Stau1 downregulation by siRNA.

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Staufen-mediated mRNA decay.

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