Novel function of U7 snRNA in the repression of HERV1/LTR12s and lincRNAs in human cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1038798 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26786726_1.fastq.gz | Fastqsanger.gz | |||
| SRR26786726_2.fastq.gz | Fastqsanger.gz | |||
| SRR26786727_1.fastq.gz | Fastqsanger.gz | |||
| SRR26786727_2.fastq.gz | Fastqsanger.gz | |||
| SRR26786728_1.fastq.gz | Fastqsanger.gz |
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Project description:U7 snRNA is part of the U7 snRNP complex, required for the 3' end processing of replication-dependent histone pre-mRNAs in S phase of the cell cycle. Here, we show that U7 snRNA plays another function in inhibiting the expression of a subset of human endogenous retroviruses of HERV1/LTR12 class and LTR12-containing long intergenic noncoding RNAs (lincRNAs), both bearing sequence motifs that perfectly match the 5’ end of U7 snRNA. We demonstrate that U7 snRNA inhibits HERV1/LTR12 and lincRNA transcription and propose a mechanism in which U7 snRNA hampers the binding/activity of the NF-Y transcription factor to CCAAT motifs within LTR12 elements. Thereby, U7 snRNA plays a protective role in maintaining the silencing of deleterious genetic elements in selected types of cells. In turn, the expression of U7-dependent HERV1/LTR12s and lincRNAs seems to be relevant during early spermatogenesis in testis, where their synthesis is highly upregulated.
2024-08-29 | GSE247500 | GEO
Project description:Thousands of large intervening non-coding RNAs (lincRNAs) have been identified in mammals. To better understand the evolution and functions of these enigmatic RNAs, we used chromatin marks, poly(A)-site mapping and RNA-Seq data, to identify more than 550 distinct lincRNAs in zebrafish. Although these shared many characteristics with mammalian lincRNAs, only 29 had detectable sequence similarity with putative mammalian orthologs, typically restricted to a single short region of high conservation. Other lincRNAs had conserved genomic locations without detectable sequence conservation. Antisense reagents targeting conserved regions of two zebrafish lincRNAs caused developmental defects. Reagents targeting splice sites caused the same defects and were rescued by adding either the mature lincRNA or its human or mouse ortholog. Our study provides a roadmap for identification and analysis of lincRNAs in model organisms and shows that lincRNAs play crucial biological roles during embryonic development with functionality conserved despite limited sequence conservation. H3K4me3, H3K36me3 chromatin maps, 3P-Seq and RNA-Seq were used to identify lincRNAs in the zebrafish genome
2011-12-22 | E-GEOD-32880 | biostudies-arrayexpress
Project description:Thousands of large intervening non-coding RNAs (lincRNAs) have been identified in mammals. To better understand the evolution and functions of these enigmatic RNAs, we used chromatin marks, poly(A)-site mapping and RNA-Seq data, to identify more than 550 distinct lincRNAs in zebrafish. Although these shared many characteristics with mammalian lincRNAs, only 29 had detectable sequence similarity with putative mammalian orthologs, typically restricted to a single short region of high conservation. Other lincRNAs had conserved genomic locations without detectable sequence conservation. Antisense reagents targeting conserved regions of two zebrafish lincRNAs caused developmental defects. Reagents targeting splice sites caused the same defects and were rescued by adding either the mature lincRNA or its human or mouse ortholog. Our study provides a roadmap for identification and analysis of lincRNAs in model organisms and shows that lincRNAs play crucial biological roles during embryonic development with functionality conserved despite limited sequence conservation.
2011-12-22 | GSE32880 | GEO
Project description:Numerous studies over the past decade have elucidated a substantial set of long intergenic noncoding RNAs (lincRNAs). It has since become clear that lincRNAs constitute an important layer of genome regulation across a wide spectrum of species. Yet, the factors governing their evolution and origins remain relatively unexplored. One possible factor that may have shaped lincRNA biology are transposable elements (TEs). Here we set out to comprehensively characterize the TE content of lincRNAs relative to genomic averages and protein coding transcripts. Our analysis of the TE composition across 9241 human lincRNAs revealed that, in sharp contrast to protein coding genes, a striking majority (83%) of lincRNAs contain a TE, and TEs comprise 42% of lincRNA transcript sequences. LincRNA TE composition varies significantly from genomic averages, being depleted of LI and Alu elements and enriched for a broad class of endogenous retroviruses (ERVs). Furthermore, specific TE families occur in biased positions and orientations within lincRNAs, particularly at their transcription start sites, suggesting a role in the origin of those lincRNAs. Finally, we find that TEs can drive gene expression regulation of lincRNAs—we observed a dramatic correlation between lincRNAs containing HERVH elements and almost exclusive expression in pluripotent cells. Conversely, those lincRNAs that are devoid of TEs are more highly expressed in testis. Collectively, TEs pervade lincRNAs and have shaped lincRNA evolution and function via bestowing tissue-specific expression from donated transcriptional regulatory signals. We extracted profiled the transcriptome expression polyadenylated mRNA-Seq. We then used these to reconstruct the transcriptome using de-novo assemblers and identify long non coding RNAs and their expression.
2013-01-22 | E-GEOD-38993 | biostudies-arrayexpress
Project description:PRC2-mediated repression is essential to maintain identity and function of differentiated dopaminergic and serotonergic neurons [snRNA-Seq]
| PRJNA782566 | ENA
Project description:Numerous studies over the past decade have elucidated a substantial set of long intergenic noncoding RNAs (lincRNAs). It has since become clear that lincRNAs constitute an important layer of genome regulation across a wide spectrum of species. Yet, the factors governing their evolution and origins remain relatively unexplored. One possible factor that may have shaped lincRNA biology are transposable elements (TEs). Here we set out to comprehensively characterize the TE content of lincRNAs relative to genomic averages and protein coding transcripts. Our analysis of the TE composition across 9241 human lincRNAs revealed that, in sharp contrast to protein coding genes, a striking majority (83%) of lincRNAs contain a TE, and TEs comprise 42% of lincRNA transcript sequences. LincRNA TE composition varies significantly from genomic averages, being depleted of LI and Alu elements and enriched for a broad class of endogenous retroviruses (ERVs). Furthermore, specific TE families occur in biased positions and orientations within lincRNAs, particularly at their transcription start sites, suggesting a role in the origin of those lincRNAs. Finally, we find that TEs can drive gene expression regulation of lincRNAs—we observed a dramatic correlation between lincRNAs containing HERVH elements and almost exclusive expression in pluripotent cells. Conversely, those lincRNAs that are devoid of TEs are more highly expressed in testis. Collectively, TEs pervade lincRNAs and have shaped lincRNA evolution and function via bestowing tissue-specific expression from donated transcriptional regulatory signals.
2013-01-22 | GSE38993 | GEO
Project description:While thousands of large intergenic non-coding RNAs (lincRNAs) have been identified in mammals, few have been functionally characterized leading to debate about their biological role. To address this, we performed loss-of-function studies on most lincRNAs expressed in mouse embryonic stem cells (ESC) and characterized the effects on gene expression. Here we show that knockdown of lincRNAs have major consequences on gene expression patterns, comparable to knockdown of well-known ESC regulators. Notably, lincRNAs primarily affect gene expression in trans. We identify dozens of lincRNAs whose knockdown causes an exit from the pluripotent state or upregulation of lineage commitment programs. We integrate lincRNAs into the molecular circuitry of ESCs and show that lincRNA genes are regulated by key transcription factors and that lincRNA transcripts physically bind to multiple chromatin regulatory proteins to affect shared gene expression programs. Together, the results demonstrate that lincRNAs have key roles in the circuitry controlling ESC state. We generated five lentiviral-based shRNAs targeting each of the 237 lincRNAs previously identified in ESCs. These shRNAs successfully targeted 147 lincRNAs and reduced their expression by an average of ~75% compared to endogenous levels in ESCs. As positive controls, we generated shRNAs targeting ~50 genes encoding regulatory proteins, including both transcription factor and chromatin factor genes that have been shown to play critical roles in ESC regulation; we obtained validated hairpins against 40 of these genes. As negative controls, we performed independent infections with lentiviruses containing 27 different shRNAs with no known cellular target RNA.
2011-08-29 | E-GEOD-30245 | biostudies-arrayexpress
Project description:While thousands of large intergenic non-coding RNAs (lincRNAs) have been identified in mammals, few have been functionally characterized leading to debate about their biological role. To address this, we performed loss-of-function studies on most lincRNAs expressed in mouse embryonic stem cells (ESC) and characterized the effects on gene expression. Here we show that knockdown of lincRNAs have major consequences on gene expression patterns, comparable to knockdown of well-known ESC regulators. Notably, lincRNAs primarily affect gene expression in trans. We identify dozens of lincRNAs whose knockdown causes an exit from the pluripotent state or upregulation of lineage commitment programs. We integrate lincRNAs into the molecular circuitry of ESCs and show that lincRNA genes are regulated by key transcription factors and that lincRNA transcripts physically bind to multiple chromatin regulatory proteins to affect shared gene expression programs. Together, the results demonstrate that lincRNAs have key roles in the circuitry controlling ESC state.
2011-08-30 | GSE30245 | GEO
Project description:U1 snRNA is the small nuclear RNA that services as the backbone of U1 snRNP. Removing intron from pre-mRNA to produce mature mRNA is the core function of the U1 snRNA. As one of the most abundant small noncoding RNA in human cells – estimated to be in the region of 1x10^6 copies per human cell (Hela) – U1 snRNA level is much more abundant than the other snRNAs. However, the potential role of the different amounts of the snRNAs is still unknown. To study the function of U1 snRNA in human neurons, we used lentivirus vector to overexpression U1 snRNA. We analyzed the gene expression change and identified target genes of U1 snRNA overexpression. We uncovered a novel role of U1 snRNA in regulating gene expression in human neurons.
2020-01-01 | GSE124951 | GEO
Project description:Removal of introns during pre-mRNA splicing, which is central to gene expression, initiates by base pairing of U1 snRNA with a 5' splice site (5'SS). In mammals, many introns contain weak 5'SSs that are not efficiently recognized by the canonical U1 snRNP, suggesting alternative mechanisms exist. Here, we develop a cross-linking immunoprecipitation coupled to a high-throughput sequencing method, BCLIP-seq, to identify NRDE2 (Nuclear RNAi defective-2) and CCDC174 (Coiled-Coil Domain-Containing 174) as novel RNA-binding proteins in mouse ES cells that associate with U1 snRNA and unspliced 5'SSs. Both proteins bind directly to U1 snRNA independently of canonical U1 snRNP specific proteins, and they are required for the selection and effective processing of weak 5'SSs. Our results reveal that mammalian cells use non-canonical splicing factors bound directly to U1 snRNA to effectively select suboptimal 5'SS sequences in hundreds of genes, promoting proper splice site choice and accurate pre-mRNA splicing.
2023-09-07 | PXD029392 | Pride