Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The U1 antisense morpholino oligonucleotide (AMO) disrupts U1 snRNP structure to promote intronic PCPA modification of pre-mRNAs

ABSTRACT: The U1 antisense morpholino oligonucleotide (AMO) disrupts U1 snRNP structure to promote intronic PCPA modification of pre-mRNAs

PROVIDER: PRJNA793864 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR17385237_1.fastq.gz	Fastqsanger.gz
	SRR17385237_2.fastq.gz	Fastqsanger.gz
	SRR17385238_1.fastq.gz	Fastqsanger.gz
	SRR17385238_2.fastq.gz	Fastqsanger.gz
	SRR17385239_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 148

Similar Datasets

Promoter directionality is controlled by U1 snRNP and polyadenylation signals

Project description:Transcription of the mammalian genome is pervasive, but productive transcription outside of protein-coding genes is limited by unknown mechanisms. In particular, although RNA polymerase II (RNAPII) initiates divergently from most active gene promoters, productive elongation occurs primarily in the sense-coding direction. Here we show in mouse embryonic stem cells that asymmetric sequence determinants flanking gene transcription start sites control promoter directionality by regulating promoter-proximal cleavage and polyadenylation. We find that upstream antisense RNAs are cleaved and polyadenylated at poly(A) sites (PASs) shortly after initiation. De novo motif analysis shows PAS signals and U1 small nuclear ribonucleoprotein (snRNP) recognition sites to be the most depleted and enriched sequences, respectively, in the sense direction relative to the upstream antisense direction. These U1 snRNP sites and PAS sites are progressively gained and lost, respectively, at the 5' end of coding genes during vertebrate evolution. Functional disruption of U1 snRNP activity results in a dramatic increase in promoter-proximal cleavage events in the sense direction with slight increases in the antisense direction. These data suggest that a U1-PAS axis characterized by low U1 snRNP recognition and a high density of PASs in the upstream antisense region reinforces promoter directionality by promoting early termination in upstream antisense regions, whereas proximal sense PAS signals are suppressed by U1 snRNP. We propose that the U1-PAS axis limits pervasive transcription throughout the genome. 3' end sequencing of poly (A) + RNAs in mouse ES cells with and without U1 snRNP inhibition using antisense morpholino oligonucleotides (AMO). Each with two biological replicates.

2013-06-28 | E-GEOD-46433 | biostudies-arrayexpress

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

U1 snRNP complex with cleavage and polyadenylation factors controls mRNA transcription termination

Project description:Full-length transcription in the majority of human genes depends on U1 snRNP (U1) to co-transcriptionally suppress transcription-terminating premature 3’-end cleavage and polyadenylation (PCPA) from cryptic polyadenylation signals (PASs) in introns. However, the mechanism of this U1 activity, termed telescripting, is unknown. Here, we captured a complex, comprising U1 and CPA factors (U1–CPAFs), that binds intronic PASs and suppresses PCPA. U1–CPAFs are distinct from U1-spliceosomal complexes; they include CPA’s three main subunits, CFIm, CPSF, and CstF, lack essential splicing factors, and associate with transcription elongation and mRNA export complexes. Telescripting requires U1:pre-mRNA base-pairing, which can be disrupted by U1 antisense oligonucleotide (U1 AMO), triggering PCPA. U1 AMO remodels U1–CPAFs, revealing changes, including recruitment of CPA-stimulating factors, that explain U1–CPAFs’ switch from repressive to activated states. Our findings outline U1 telescripting mechanism and demonstrate U1’s unique role as central-regulator of pre-mRNA processing and transcription.

2019-07-31 | GSE135140 | GEO

mRNA polyadenylation profile analysis in control and U1 AMO treated HeLa cells

Project description:To globally assess the effect of polyadenylation site (PAS) usage upon functional knockdown of U1 snRNP, we carried out PAS-seq analysis with control and U1 AMO-treated HeLa cells using the QuantSeq Rev 3' mRNA sequencing library prep kit (Cat. 016-24).

2019-01-22 | GSE125397 | GEO

Neuronal stimulation changes U1 snRNP binding and intronic polyadenylation

Project description:Neuronal stimulation changes U1 snRNP binding and intronic polyadenylation

| PRJNA770346 | ENA

CstF64 iCLIP-seq in control and U1 AMO-treated HeLa cells

Project description:To understand the effect of U1 AMO treatment on CstF64 binding profile , we carried out CstF64 iCLIP-seq experiments in HeLa cells treated with either control or U1 AMO.

2023-02-27 | GSE192893 | GEO

wdr33 iCLIP-seq in control and U1 AMO-treated HeLa cells

Project description:To understand the effect of U1 AMO treatment on wdr33 binding profile , we carried out CstF64 iCLIP-seq experiments in HeLa cells treated with either control or U1 AMO.

2023-02-27 | GSE193370 | GEO

The U1 antisense morpholino oligonucleotide (AMO) disrupts U1 snRNP structure to promote intronic PCPA modification of pre-mRNAs.

Project description:Functional depletion of the U1 small nuclear ribonucleoprotein (snRNP) with a 25 nt U1 AMO (antisense morpholino oligonucleotide) may lead to intronic premature cleavage and polyadenylation of thousands of genes, a phenomenon known as U1 snRNP telescripting; however, the underlying mechanism remains elusive. In this study, we demonstrated that U1 AMO could disrupt U1 snRNP structure both in vitro and in vivo, thereby affecting the U1 snRNP-RNAP polymerase II interaction. By performing chromatin immunoprecipitation sequencing for phosphorylation of Ser2 and Ser5 of the C-terminal domain of RPB1, the largest subunit of RNAP polymerase II, we showed that transcription elongation was disturbed upon U1 AMO treatment, with a particular high phosphorylation of Ser2 signal at intronic cryptic polyadenylation sites (PASs). In addition, we showed that core 3'processing factors CPSF/CstF are involved in the processing of intronic cryptic PAS. Their recruitment accumulated toward cryptic PASs upon U1 AMO treatment, as indicated by chromatin immunoprecipitation sequencing and individual-nucleotide resolution CrossLinking and ImmunoPrecipitation sequencing analysis. Conclusively, our data suggest that disruption of U1 snRNP structure mediated by U1 AMO provides a key for understanding the U1 telescripting mechanism.

| S-EPMC10404622 | biostudies-literature

U1 snRNP regulates alternative polyadenylation in DNA damage response

Project description:The DNA damage response (DDR) involves coordinated control of gene expression and DNA repair. Using deep sequencing we found widespread changes of alternative cleavage and polyadenylation (APA) site usage upon UV-treatment in mammalian cells. APA regulation in the 3’ untranslated region (3’UTR) is substantial, leading to both shortening and lengthening of 3’UTRs. Interestingly, a strong activation of intronic APA sites is detected, resulting in widespread expression of truncated transcripts. Intronic APA events are biased to the 5’ end of genes and affect gene groups with important functions in DDR. Moreover, intronic APA site activation during DDR correlates with a decrease in U1 snRNA levels, and this is reversed by U1 snRNA overexpression. Importantly, U1 snRNA overexpression decreases UV-induced apoptosis. Together, these studies describe a significant gene regulatory scheme in DDR where U1 snRNP impacts gene expression via APA.

2016-05-01 | GSE71801 | GEO

ChIP-seq analysis for core 3' processing factors in control and U1 AMO-treated HeLa cells

Project description:To understand the effect of U1 AMO treatment on chromatin binding profiles of core 3' processing factors, we carried out ChIP-seq analysis for several core 3' processing factors after control and U1 AMO treatment

2023-02-27 | GSE193202 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data