LncRNA-GAS5 negative regulation of YAP-target genes expression
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA532331 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8881853_1.fastq.gz | Fastqsanger.gz | |||
| SRR8881853_2.fastq.gz | Fastqsanger.gz | |||
| SRR8881854_1.fastq.gz | Fastqsanger.gz | |||
| SRR8881854_2.fastq.gz | Fastqsanger.gz | |||
| SRR8881855_1.fastq.gz | Fastqsanger.gz |
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Project description:Analysis of RNA-seq-based differential expression after overexpression of GAS5 or knockdown of YAP revealed a highly significant overlap of common targets.
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Project description:Long non-coding RNAs (lncRNAs) are a class of transcribed RNA molecules greater than 200 nucleotides long. Though do not encode proteins, they play functional roles in gene expression regulation. LncRNAs are notably abundant in the brain, however, their neural functions are largely unknown. Here we demonstrate that repeated short- and long-term cocaine administrations all decreased the expression of lncRNA Gas5 in the nucleus accumbens (NAc) of adult male mice. To illustrate the functional role of Gas5, we performed viral mediated overexpression of Gas5 in the NAc and found decreased cocaine-induced conditioned place preference. Furthermore, Gas5 overexpression also led to decreased drug intake, lower motivation, repressed compulsivity to acquire cocaine, and faster extinction of drug during cocaine self-administration. Transcriptome profiling identified numerous Gas5 mediated gene expression changes that are enriched in relevant neural function categories. Interestingly, these Gas5 regulated gene expression changes significantly overlap with chronic cocaine induced transcriptome alterations, which suggests that Gas5 may serve as a main transcription regulator of cocaine response. Our study therefore displays a novel lncRNA based molecular mechanism of cocaine action.
2020-06-26 | GSE146005 | GEO
Project description:Long noncoding RNAs (lncRNAs) represent a multidimensional class of regulatory molecules that are involved in many aspects of brain function. Emerging evidence indicates that lncRNAs are localized to the synapse; however, a direct role for their activity in this subcellular compartment in memory formation has yet to be demonstrated. Using lncRNA capture-seq, we identified a Gas5 variant that accumulate in the synaptic compartment within the infralimbic prefrontal cortex of adult male C57/Bl6 mice. Gas5 RNA immunoprecipitation followed by mass spectrometry revealed that this Gas5 isoform, in association with the RNA binding proteins G3BP2 and CAPRIN1, regulates the activity-dependent trafficking and clustering of RNA granules. In addition, we found that cell-type-specific, activity-dependent, and synapse-specific knockdown of this Gas5 variant led to impaired fear extinction memory. These findings identify a new mechanism of fear extinction that involves the dynamic interaction between local lncRNA activity and RNA condensates in the synaptic compartment.
2023-11-20 | PXD046479 | Pride
Project description:In this study monoclonal cell lines carrying mutations in the small nucleolar RNA host-gene GAS5 were obtained. Next, Poly(A) RNA-seq and Small RNA-seq analyses of obtained cell lines were performed on an Illumina NextSeq 500 platform. Poly(A) RNA-seq libraries was constructed on polyA mRNA-enriched fraction. Small RNA-seq libraries was constructed on small RNA fraction (<200 nucleotide length). The reads were aligned via STAR to the human genome (GRCh37). The comparison of the mRNA levels of genes and small RNA levels in RNA-Seq experiments was carried out using CuffDiff tool. Sashimi plots for RNA-Seq analyses of isoform expression were generated by IGV. It was shown that specific mutations in SNORD74 led to the downregulation of all GAS5-encoded SNORDs and GAS5 lncRNA. Obtained results demonstrate the SNORD-dependent manner of the GAS5 maturation.
2023-11-14 | E-MTAB-13515 | biostudies-arrayexpress
Project description:In addition to protein-coding genes, the human genome makes a large amount of noncoding RNAs, including microRNAs and long noncoding RNAs (lncRNAs). Both microRNAs and lncRNAs have been shown to have a critical role in the regulation of cellular processes such as cell growth and apoptosis, as well as cancer progression and metastasis. Although it is well known that microRNAs can target a large number of protein-coding genes, little is known whether microRNAs can also target lncRNAs. In the present study, we determine whether miR-21 can regulate lncRNA expression. Using the lncRNA RT-PCR (reverse transcription-polymerase chain reaction) array carrying 83 human disease-related lncRNAs, we show that miR-21 is capable of suppressing the lncRNA growth arrest-specific 5 (GAS5). This negative correlation between miR-21 and GAS5 is also seen in breast tumor specimens. Of interest, GAS5 can also repress miR-21 expression. Whereas ectopic expression of GAS5 suppresses, GAS5-siRNA increases miR-21 expression. Importantly, there is a putative miR-21-binding site in exon 4 of GAS5; deletion of the miR-21-binding site abolishes this activity. Experiments with in vitro cell culture and xenograft mouse model suggest that GAS5 functions as a tumor suppressor. We further show that the biotin-labeled GAS5-RNA probe is able to pull down the key component (AGO2) of the RNA-induced silencing complex (RISC) and we subsequently identify miR-21 in this GAS5-RISC complex, implying that miR-21 and GAS5 may regulate each other in a way similar to the microRNA-mediated silencing of target mRNAs. Together, these results suggest that miR-21 targets not only tumor-suppressive protein-coding genes but also lncRNA GAS5.
| S-EPMC3792431 | biostudies-other
Project description:YAP is an oncogene and an inducer of Epithelial-to-Mesenchymal Transition (EMT). We used microarrays to detail the global program of gene expression to identify YAP target genes. PUBLICATION ABSTRACT: The Hippo pathway defines a novel signaling cascade regulating cell proliferation and survival in Drosophila, which involves the negative regulation of the transcriptional coactivator Yorkie by the kinases Hippo and Warts. We have recently shown that the human ortholog of Yorkie, YAP, maps to a minimal amplification locus in mouse and human cancers, and that it mediates dramatic transforming activity in MCF10A primary mammary epithelial cells. Here we show that LATS proteins (mammalian orthologs of Warts) interact directly with YAP in mammalian cells and that ectopic expression of LATS1, but not LATS2, effectively suppresses the YAP phenotypes. Furthermore, shRNA-mediated knockdown of LATS1 phenocopies YAP overexpression. Since this effect can be suppressed by simultaneous YAP knockdown, it suggests that YAP is the primary target of LATS1 in mammalian cells. Expression profiling of genes induced by ectopic expression of YAP or by knockdown of LATS1 reveals a subset of potential Hippo pathway targets implicated in epithelial-to-mesenchymal transition (EMT), suggesting that this is a key feature of YAP signaling in mammalian cells. Keywords: vector vs. YAP comparison
2008-01-31 | GSE10196 | GEO
Project description:Microarray analyses with cells/tissues overexpressing YAP have revealed many transcription targets of YAP (Dong et al, 2007; Zhao et al, 2008). However, as YAP induces transformation of non-cancerous cells, we thought many of known targets of YAP may be indirect consequence of transforming property of YAP. To identify the immediate transcription targets for YAP, we utilized immortalized mammary epithelial MCF-10A cells expressing a tamoxifen inducible, hyperactive (S127/381A) YAP mutant (MCF-10A ERT2-YAP 2SA). MCF-10A ERT2 and MCF-10A ERT2-YAP 2SA are generated. Each cell line was treated with 0.1% of ethanol (solvent) or 1uM of 4-hydroxytamoxifen for 2 or 6 hours. This makes 6 samples per set. The experiments were done in duplicate. The expression data from MCF-10A ERT2 and MCF-10A ERT2-YAP 2SA before tamoxifen treatment can serve as control.
2015-11-23 | E-GEOD-60579 | biostudies-arrayexpress
Project description:Constitutively Active YAP/TAZ Target Genes
| PRJNA489431 | ENA