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U4 inhibits premature cleavage and polyadenylation of pre-mRNAs [mRNA-seq]

ABSTRACT: 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

ORGANISM(S): Homo sapiens

PROVIDER: GSE262380 | GEO | 2024/06/26

REPOSITORIES: GEO

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U4 inhibits premature cleavage and polyadenylation of pre-mRNAs [ChIP-seq]

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

U4 inhibits premature cleavage and polyadenylation of pre-mRNAs [mRNA 3'-seq]

Project description:To understand how U4 snRNP regulates premature cleavage and polyadenylation of pre-mRNAs at the transcriptome wide, we conducted 3'-seq analysis on control, U1 and U4-AMO treated samples using the Lexogen mRNA 3'-seq kit (Cat. 016.24), which enables accurate quantification of global PAS usage.

2024-06-26 | GSE262383 | 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

U4 inhibits premature cleavage and polyadenylation of pre-mRNAs

Project description:U4 inhibits premature cleavage and polyadenylation of pre-mRNAs

| PRJNA1091625 | ENA

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

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

U4 inhibits premature cleavage and polyadenylation of pre-mRNAs [ChIP-seq]

Project description:U4 inhibits premature cleavage and polyadenylation of pre-mRNAs [ChIP-seq]

| PRJNA1091630 | ENA

U4 inhibits premature cleavage and polyadenylation of pre-mRNAs [mRNA-seq]

Project description:U4 inhibits premature cleavage and polyadenylation of pre-mRNAs [mRNA-seq]

| PRJNA1091620 | ENA

U4 inhibits premature cleavage and polyadenylation of pre-mRNAs [mRNA 3'-seq]

Project description:U4 inhibits premature cleavage and polyadenylation of pre-mRNAs [mRNA 3'-seq]

| PRJNA1091628 | ENA

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

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