Convergent exaptation of Alu and B/ID SINEs for Staufen-mediated mRNA decay
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ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA352669
ORGANISM(S): Mus musculus Homo sapiens
PROVIDER: GSE89588 | GEO | 2017/12/31
SECONDARY ACCESSION(S): PRJNA352669
REPOSITORIES: GEO
Similar Datasets
Project description:Convergent exaptation of Alu and B/ID SINEs for Staufen-mediated mRNA decay
| PRJNA352669 | ENA
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.
2013-09-05 | GSE43418 | GEO
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.
2013-09-05 | E-GEOD-43418 | biostudies-arrayexpress
Project description:Primate-specific Alu short interspersed elements (SINEs) as well as rodent-specific B and ID (B/ID) SINEs can promote Staufen-mediated decay (SMD) when present in mRNA 3'-untranslated regions (3'-UTRs). The transposable nature of SINEs, their presence in long noncoding RNAs, their interactions with Staufen, and their rapid divergence in different evolutionary lineages suggest they could have generated substantial modification of posttranscriptional gene-control networks during mammalian evolution. Some of the variation in SMD regulation produced by SINE insertion might have had a similar regulatory effect in separate mammalian lineages, leading to parallel evolution of the Staufen network by independent expansion of lineage-specific SINEs. To explore this possibility, we searched for orthologous gene pairs, each carrying a species-specific 3'-UTR SINE and each regulated by SMD, by measuring changes in mRNA abundance after individual depletion of two SMD factors, Staufen1 (STAU1) and UPF1, in both human and mouse myoblasts. We identified and confirmed orthologous gene pairs with 3'-UTR SINEs that independently function in SMD control of myoblast metabolism. Expanding to other species, we demonstrated that SINE-directed SMD likely emerged in both primate and rodent lineages >20-25 million years ago. Our work reveals a mechanism for the convergent evolution of posttranscriptional gene regulatory networks in mammals by species-specific SINE transposition and SMD.
| S-EPMC5798355 | biostudies-literature
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.
2012-02-28 | GSE26781 | GEO
Project description:Transcriptome analysis from Staufen-mediated mRNA (SMD) targets during differentiation confirmed that STAU1 was a key factor in neuronal differentiation.
2017-02-27 | GSE94948 | GEO
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
2012-02-28 | E-GEOD-26781 | biostudies-arrayexpress
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.
2007-12-26 | GSE6679 | GEO
Project description:Staufen1 (STAU1)-mediated mRNA decay (SMD) is an mRNA degradation process in mammalian cells that is mediated by the binding of STAU1 to a STAU1-binding site (SBS) within the 3'-untranslated region (3'-UTR) of target mRNAs. During SMD, STAU1, a double-stranded (ds) RNA-binding protein, recognizes dsRNA structures formed either by intramolecular base pairing of 3'-UTR sequences or by intermolecular base pairing of 3'-UTR sequences with a long-noncoding RNA (lncRNA) via partially complementary Alu elements. Recently, STAU2, a paralog of STAU1, has also been reported to mediate SMD. Both STAU1 and STAU2 interact directly with the ATP-dependent RNA helicase UPF1, a key SMD factor, enhancing its helicase activity to promote effective SMD. Moreover, STAU1 and STAU2 form homodimeric and heterodimeric interactions via domain-swapping. Because both SMD and the mechanistically related nonsense-mediated mRNA decay (NMD) employ UPF1; SMD and NMD are competitive pathways. Competition contributes to cellular differentiation processes, such as myogenesis and adipogenesis, placing SMD at the heart of various physiologically important mechanisms.
| S-EPMC3711692 | biostudies-literature
Project description:Previous studies have indicated a paucity of SINEs within the genomes of the guinea pig and nutria, representatives of the Hystricognathi suborder of rodents. More recent work has shown that the guinea pig genome contains a large number of B1 elements, expanding to various levels among different rodents. In this work we utilized A-B PCR and screened GenBank with sequences from isolated clones to identify potentially uncharacterized SINEs within the guinea pig genome, and identified numerous sequences with a high degree of similarity (>92%) specific to the guinea pig. The presence of A-tails and flanking direct repeats associated with these sequences supported the identification of a full-length SINE, with a consensus sequence notably distinct from other rodent SINEs. Although most similar to the ID SINE, it clearly was not derived from the known ID master gene (BC1), hence we refer to this element as guinea pig ID-like (GPIDL). Using the consensus to screen the guinea pig genomic database (Assembly CavPor2) with Ensembl BlastView, we estimated at least 100,000 copies, which contrasts markedly to just over 100 copies of ID elements. Additionally we provided evidence of recent integrations of GPIDL as two of seven analyzed conserved GPIDL-containing loci demonstrated presence/absence variants in Cavia porcellus and C. aperea. Using intra-IDL PCR and sequence analyses we also provide evidence that GPIDL is derived from a hystricognath-specific SINE family. These results demonstrate that this SINE family continues to contribute to the dynamics of genomes of hystricognath rodents.
| S-EPMC2670544 | biostudies-literature