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Alternative intronic polyadenylation influences cancer metastasis and response to therapy

ABSTRACT: Alternative intronic polyadenylation influences cancer metastasis and response to therapy

PROVIDER: PRJNA369518 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5221950.fastq.gz	Fastqsanger.gz
	SRR5221960.fastq.gz	Fastqsanger.gz
	SRR5221951.fastq.gz	Fastqsanger.gz
	SRR5221961.fastq.gz	Fastqsanger.gz
	SRR5221962.fastq.gz	Fastqsanger.gz

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Alternative intronic polyadenylation influences cancer metastasis and response to therapy [3'-seq]

Project description:We explored the impact of alternative polyadenylation regulation during tumor cell spreading.

2018-01-01 | GSE94373 | GEO

RSC and Bud27 influences chromatin organization and alternative polyadenylation

Project description:RSC and Bud27 influences chromatin organization and alternative polyadenylation

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Coupling between alternative polyadenylation and alternative splicing is limited to terminal introns

Project description:Alternative polyadenylation has been implicated as an important regulator of gene expression. In some cases, alternative polyadenylation is known to couple with alternative splicing to influence last intron removal. However, it is unknown whether alternative polyadenylation events influence alternative splicing decisions at upstream exons. Knockdown of the polyadenylation factors CFIm25 or CstF64 was used as an approach in identifying alternative polyadenylation and alternative splicing events on a genome-wide scale. Although hundreds of alternative splicing events were found to be differentially spliced in the knockdown of CstF64, genes associated with alternative polyadenylation did not exhibit an increased incidence of alternative splicing. These results demonstrate that the coupling between alternative polyadenylation and alternative splicing is usually limited to defining the last exon. The striking influence of CstF64 knockdown on alternative splicing can be explained through its effects on UTR selection of known splicing regulators such as hnRNP A2/B1, thereby indirectly influencing splice site selection. We conclude that changes in the expression of the polyadenylation factor CstF64 influences alternative splicing through indirect effects. HeLa cell line was stably transfected with shRNA plasmids targeting CstF64. Total RNA was isolated from CstF64 KD cells and wild-type control cells using Trizol according to manufacturerâs protocols. Samples were deep sequenced in duplicate using the Illumina GAIIx system.

2016-03-14 | E-GEOD-79157 | biostudies-arrayexpress

Coupling between alternative polyadenylation and alternative splicing is limited to terminal introns

2016-03-14 | GSE79157 | GEO

Alternative polyadenylation alters protein dosage by switching between intronic and 3' UTR sites

Project description:Alternative polyadenylation (APA) creates distinct transcripts from the same gene by cleaving the pre-mRNA at poly(A) sites that can lie within the 3' UTR, introns, or exons. Most studies focus on APA within the 3' UTR, but here we show that CPSF6 insufficiency alters protein levels and causes a developmental syndrome by deregulating APA throughout the transcript. In neonatal humans and zebrafish larvae, CPSF6 insufficiency shifts poly(A) site usage between the 3'UTR and internal sites in a pathway-specific manner. Genes associated with neuronal function undergo mostly intronic APA, reducing their expression, while genes associated with heart and skeletal function mostly undergo 3' UTR APA and are upregulated. This suggests that, in healthy conditions, cells toggle between internal and 3'UTR APA to modulate protein expression.

2022-11-21 | MSV000090759 | MassIVE

Neuronal stimulation changes U1 snRNP binding and intronic polyadenylation

Project description:Synaptic activity induces well-known changes in enhancer-promoter driven gene expression but also induces changes in splicing and polyadenylation that are understudied. Here, we investigate the mechanism of expression for alternative polyadenylation isoform Homer1a, an immediate early gene essential to synaptic plasticity. We report that neuronal activation, in neuronal cultures and in adult mouse brain, depletes the splice factor U1 snRNP from Homer1 pre-mRNA and that this causes shifted utilization of a cryptic polyadenylation signal within intron 5 resulting in Homer1a expression. Because U1 snRNP is a ubiquitous splice factor, we tested the generality of activity-driven U1 snRNP depletion as a mechanism for gene expression using RNA immunoprecipitation sequencing. Analysis reveals that neuronal activity changes U1 snRNP binding to ~2000 transcripts and for a subset of transcripts, a reduction in U1 snRNP binding was accompanied by utilization of a cryptic intronic polyadenylation site. This subset is enriched for transcripts encoding synaptic proteins involved in excitability control. Genes demonstrating activity-dependent reduced U1 snRNP binding often encode a binding motif for Sam68, a neuronal alternative polyadenylation factor. Findings reveal that activity-driven changes in intron utilization for transcript termination serves an important role in synaptic plasticity.

2024-10-08 | GSE185662 | GEO

Alternative intronic polyadenylation influences cancer metastasis and response to therapy

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-01-01 | GSE94375 | GEO

Mouse alternative polyadenylation

Project description:Divergence of alternative polyadenylation in mouse

| PRJEB15336 | ENA

Widespread intronic polyadenylation diversifies immune cell transcriptomes

Project description:Widespread intronic polyadenylation diversifies immune cell transcriptomes

| PRJNA436569 | ENA

Pro-inflammatory polarization and colorectal cancer modulate alternative and intronic polyadenylation in primary human macrophages

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