U6 snRNP inhibits the premature cleavage and polyadenylation of pre-mRNAs (ChIP-Seq)
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1053389 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27227463_1.fastq.gz | Fastqsanger.gz | |||
| SRR27227463_2.fastq.gz | Fastqsanger.gz | |||
| SRR27227464_1.fastq.gz | Fastqsanger.gz | |||
| SRR27227464_2.fastq.gz | Fastqsanger.gz | |||
| SRR27227465_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 34 |
Similar Datasets
Project description:U6 snRNP inhibits the premature cleavage and polyadenylation of pre-mRNAs (RNA-Seq)
| PRJNA1053391 | ENA
Project description:Transcription and splicing are intricately linked processes, with emerging evidence highlighting the involvement of splicing factors mediating their coupling. U1 small nuclear ribonucleoprotein particle (U1 snRNP), a key splicing factor, not only serves as the initial component of the spliceosome but also plays a crucial role in preventing premature cleavage and polyadenylation, facilitating long-distance transcription elongation. Here, we show that U1 snRNP regulates alternative promoter usage through inhibition of premature polyadenylation. Inhibiting U1 snRNP with antisense oligonucleotides or introducing a premature polyadenylation leads to a significant decrease in downstream promoter activity in genes with premature polyadenylation sites in between two promoters. Conversely, restoring U1 snRNP activity or inhibiting premature polyadenylation sites using a gene-specific U1 snRNP rescues downstream promoter activity. Mechanistically, U1 snRNP inhibition correlates with reduced chromatin accessibility and serine 5 phosphorylation levels of RNA polymerase II at downstream promoters. Our findings propose a model where U1 snRNP facilitates productive transcription from upstream promoters, triggering downstream promoter activation by destabilizing nucleosomes and promoting promoter escape.
2025-05-19 | GSE284680 | GEO
Project description:Transcription and splicing are intricately linked processes, with emerging evidence highlighting the involvement of splicing factors mediating their coupling. U1 small nuclear ribonucleoprotein particle (U1 snRNP), a key splicing factor, not only serves as the initial component of the spliceosome but also plays a crucial role in preventing premature cleavage and polyadenylation, facilitating long-distance transcription elongation. Here, we show that U1 snRNP regulates alternative promoter usage through inhibition of premature polyadenylation. Inhibiting U1 snRNP with antisense oligonucleotides or introducing a premature polyadenylation leads to a significant decrease in downstream promoter activity in genes with premature polyadenylation sites in between two promoters. Conversely, restoring U1 snRNP activity or inhibiting premature polyadenylation sites using a gene-specific U1 snRNP rescues downstream promoter activity. Mechanistically, U1 snRNP inhibition correlates with reduced chromatin accessibility and serine 5 phosphorylation levels of RNA polymerase II at downstream promoters. Our findings propose a model where U1 snRNP facilitates productive transcription from upstream promoters, triggering downstream promoter activation by destabilizing nucleosomes and promoting promoter escape.
2025-05-19 | GSE284682 | GEO
Project description:Transcription and splicing are inherently intertwined. Accumulating evidence support a role of splicing factors in mediating this coupling. U1 small nuclear ribonucleoprotein particle (U1 snRNP), a key splicing factor, acts as the initial building block of the spliceosome, interacting with nascent pre-mRNA at 5' splice sites. In addition to its role in splicing, U1 snRNP is crucial for preventing premature cleavage and polyadenylation, enabling long-distance transcription elongation. Here, we show that U1 snRNP can regulate the usage of alternative promoters through its role in inhibiting premature polyadenylation. Using antisense oligonucleotides to inhibit U1 snRNP, we first observed a markedly decrease in downstream promoter activity at the newly synthesized RNA level. Interestingly, U1 snRNP inhibition selectively impacts downstream promoters of genes featuring premature polyadenylation sites located between two promoters. Overexpressing a wild-type U1 snRNP or a gene-specific U1 snRNP designed to inhibit premature polyadenylation sites restores downstream promoter activity. Conversely, introducing a premature polyadenylation site between two promoters reduces downstream promoter activity. Exploring the underlying molecular mechanisms, we identified a substantial decrease in serine 5 phosphorylation levels in newly recruited RNA polymerase II at downstream promoters following U1 snRNP inhibition, and reduced chromatin accessibility in the vicinity of downstream promoters. Overall, our model is consistent with productive transcription from upstream promoters triggering downstream promoter activation in the presence of U1 snRNP by destabilizing nucleosomes and promoting promoter escape at downstream promoters.
2025-05-19 | GSE252389 | GEO
Project description:Transcription and splicing are inherently intertwined. Accumulating evidence support a role of splicing factors in mediating this coupling. U1 small nuclear ribonucleoprotein particle (U1 snRNP), a key splicing factor, acts as the initial building block of the spliceosome, interacting with nascent pre-mRNA at 5' splice sites. In addition to its role in splicing, U1 snRNP is crucial for preventing premature cleavage and polyadenylation, enabling long-distance transcription elongation. Here, we show that U1 snRNP can regulate the usage of alternative promoters through its role in inhibiting premature polyadenylation. Using antisense oligonucleotides to inhibit U1 snRNP, we first observed a markedly decrease in downstream promoter activity at the newly synthesized RNA level. Interestingly, U1 snRNP inhibition selectively impacts downstream promoters of genes featuring premature polyadenylation sites located between two promoters. Overexpressing a wild-type U1 snRNP or a gene-specific U1 snRNP designed to inhibit premature polyadenylation sites restores downstream promoter activity. Conversely, introducing a premature polyadenylation site between two promoters reduces downstream promoter activity. Exploring the underlying molecular mechanisms, we identified a substantial decrease in serine 5 phosphorylation levels in newly recruited RNA polymerase II at downstream promoters following U1 snRNP inhibition, and reduced chromatin accessibility in the vicinity of downstream promoters. Overall, our model is consistent with productive transcription from upstream promoters triggering downstream promoter activation in the presence of U1 snRNP by destabilizing nucleosomes and promoting promoter escape at downstream promoters.
2025-05-19 | GSE252387 | GEO
Project description:Transcription and splicing are inherently intertwined. Accumulating evidence support a role of splicing factors in mediating this coupling. U1 small nuclear ribonucleoprotein particle (U1 snRNP), a key splicing factor, acts as the initial building block of the spliceosome, interacting with nascent pre-mRNA at 5' splice sites. In addition to its role in splicing, U1 snRNP is crucial for preventing premature cleavage and polyadenylation, enabling long-distance transcription elongation. Here, we show that U1snRNP can regulate the usage of alternative promoters through its role in inhibiting premature polyadenylation. Using antisense oligonucleotides to inhibit U1 snRNP, we first observed a markedly decrease in downstream promoter activity at the newly synthesized RNA level. Interestingly, U1 snRNP inhibition selectively impacts downstream promoters of genes featuring premature polyadenylation sites located between two promoters. Overexpressing a wild-type U1 snRNP or a gene-specific U1 snRNP designed to inhibit premature polyadenylation sites restores downstream promoter activity. Conversely, introducing a premature polyadenylation site between two promoters reduces downstream promoter activity. Exploring the underlying molecular mechanisms, we identified a substantial decrease in serine 5 phosphorylation levels in newly recruited RNA polymerase II at downstream promoters following U1 snRNP inhibition, and reduced chromatin accessibility in the vicinity of downstream promoters. Overall, our model is consistent with productive transcription from upstream promoters triggering downstream promoter activation in the presence of U1 snRNP by destabilizing nucleosomes and promoting promoter escape at downstream promoters.
2025-05-19 | GSE252391 | GEO
Project description:To understand how U4 snRNP regulates premature cleavage and polyadenylation of pre-mRNAs at the transcriptome wide, we conducted RNAPII ChIP-seq analysis on control, U1 and U4-AMO treated samples.
2024-06-26 | GSE262384 | GEO
Project description:To understand how U4 snRNP regulates premature cleavage and polyadenylation of pre-mRNAs at the transcriptome wide, we conducted mRNA-seq analysis on control, U1 and U4-AMO treated HeLa cells
2024-06-26 | GSE262380 | GEO
Project description:To investigate the extent to which U6 inhibits premature cleavage and polyadenylation at the transcriptome level. we performed 3’-seq in control, U1 and U6-AMO treated sample using lexogen 3’-seq kit (Cat. 016.24) that could accurately quantify the global PAS usage. Indeed, we found both U1 and U6 could globally suppress intronic PCPA.
2025-01-29 | GSE250342 | GEO
Project description:RNAPII ChIP-seq analysis in U2 and U6 antisense morpholino oligonucleotide (AMO)-treated HeLa cells in comparison to negative control (NC) AMO To investigate if U2 or U6 AMO treatment caused transcription defect, we carried out RNAPII ChIP-seq analysis in control, U2 and U6 AMO treated HeLa cells
2025-01-29 | GSE250343 | GEO