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Genome wide mapping of polyadenylation sites in proliferating and contact-inhibited cells and cells with knockdown of cleavage and polyadenylation factors

ABSTRACT: Genome wide mapping of polyadenylation sites in proliferating and contact-inhibited cells and cells with knockdown of cleavage and polyadenylation factors

PROVIDER: PRJNA480879 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7516120.fastq.gz	Fastqsanger.gz
	SRR7516130.fastq.gz	Fastqsanger.gz
	SRR7516121.fastq.gz	Fastqsanger.gz
	SRR7516131.fastq.gz	Fastqsanger.gz
	SRR7516122.fastq.gz	Fastqsanger.gz

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Similar Datasets

Global mapping of polyadenylation site use in proliferating and quiescent (contact-inhibited and serum-starved) cells

Project description:Purpose: To determine genes that undergo alternative polyadenylation in proliferating versus quiescent fibroblasts. Methods: Three different biological replicates (fibroblast strains, 10-1, 12-1, and 12-2) were used for generating proliferating and quiescent (7-day contact inhibited and 7-day serum-starved) cells. RNA extracted from these cells were used for library preparation. cDNA fragments were enriched for the junction between the poly(A) site and the end of the 3' UTR using a modified high throughput sequencing protocol (GnomeGen). cDNA libraries were created according to Gnome-Gen RNA-seq library preparation kit for RNA profiling except Amgen Ampure XP beads were used instead of the Gnome-gen size selector product to remove ligation reaction products before proceeding to the reverse transcription step. The libraries were sequenced on an Illumina HiSeq 2000 instrument. The sequencing reaction wasa run for 147 cycles. Reads from pol(A) enriched cDNA libraries were aligned to the genome using the STAR alignment algorithm after the computational removal of untemplated adenosines. Results: Polyadenylation site selection was significantly altered in approximately 10% of genes in quiescent compared with proliferating fibroblasts. Contact inhibited and serum starved fibroblasts had similar polyadenylation site selection profiles. Conclusions: Quiescence is associated with changes in polyadenylation site selection.

2018-07-19 | GSE117337 | GEO

Genome wide mapping of polyadenylation sites in proliferating and contact-inhibited cells and cells with knockdown of cleavage and polyadenylation factors

Project description:Purpose: Quiescence is a state of reversible cell cycle exit. Levels of polyadenylation factors decreases when proliferating cells become quiescent. The goals of this study are to determine the differential use of polyadenylation sites (changes in alternative polyadenylation) in quiescent vs. proliferating cells and also upon knockdown of polyadenylation factors. Methods: Two biological replicates of human dermal fibroblasts (12-1 and 12-3) were used for polyadeylation-site enriched RNA-seq on an Illumina HiSeq 2500 to compare quiescent vs. proliferating cells and polyadenylation factor knockdown vs. control cells. The reads were aligned to the human genome (hg19) uisng Tophat (2.0.14). The resulting bam files were used as an input to a python script provided by Gruber et al. (PMID: 27382025) to determine the counts for each polyadenylation site. Results: We observed a shift toward greater use of distal polyadenylation sites when the fibroblasts entered quiescence. We observed significant overlap between the genes that shift to greater distal site use with quiescence and CstF-64 or CPSF73 knockdown. Conclusions: The shift to greater distal site use with quiescence may reflect in part the reduced levels of cleavage and polyadenylation factors.

2018-08-28 | GSE117033 | GEO

Global mapping of polyadenylation site use in proliferating and quiescent (contact-inhibited and serum-starved) cells

Project description:Global mapping of polyadenylation site use in proliferating and quiescent (contact-inhibited and serum-starved) cells

| PRJNA481778 | ENA

Development of gene expression signatures for contact-inhibited and adipogenic-differentiated 3T3-L1 and NIH3T3 fibroblasts

Project description:Given previous works showing that, in the process of adipogenic differentiation of 3T3-L1 fibroblasts, the cells need to be cultured to confluency followed by additional incubation before initiating differentiation, we hypothesized that contact inhibition of proliferation (CIP) is requisite for making the cells prone to the differentiation. We screened upregulated genes in contact-inhibited 3T3-L1 fibroblasts, as well as NIH3T3 fibroblasts that are also sensitive to contact inhibition, by a whole genome microarray analysis. We also screened the genes that undergo rapid downregulation after the initiation of adipogenic differentiation. To investigate the mechanism of contact inhibition of proliferation and adipogenic differentiation of 3T3-L1 and NIH3T3 fibroblasts, we have employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to distinguish proliferating and contact-inhibited cells and cells that undergo adipogenic differentiation. Total RNAs from 80% confluent (3T3-L1_80%, NIH3T3_80%) and overconfluent (3T3-L1_overconfluent, NIH3T3_overconfluent) cells and cells stimulated with the adipogenic differentiation medium (ZenBio) for 2 hours (3T3-L1_adipo diff med 2 hours, NIH3T3_adipo diff med 2 hours) were harvested and subjected to the microarray analysis.

2015-05-28 | E-GEOD-69320 | biostudies-arrayexpress

To investigate the decay constants (half-lives) of transcript isoforms generated by alternative polyadenylation in proliferating and quiescent cells

Project description:Purpose: Alternative polyadenylation (APA) can result in the generation of transcripts that terminate at different locations within the gene, which can result in different 3' UTRs. 3´ UTRs are known to contain RNA stabilizing and destabilizing motifs that provide a platform for binding of RNA binding proteins. Changes in 3´ UTRs for the different APA-generated isoforms of a gene could allow for inclusion or exclusion of these RNA stability elements. The goal of this study is determine the stability (half-lives based on transcript decay) of APA isoforms in proliferating and quiescent cells. Methods: The proliferating and quiescent (7-day contact inhibited) cells were treated with actinomycin D to stop transcription and the cells were harvested at different time points (0. 2, 4, 8 hours) for RNA isolation and global sequencing of 3´ ends. The adaptors and polyA sequenced were trimmed from each read. The reads were aligned to the human genome (hg19) using TopHat (v2.0.14). The aligned read files were used to determine the counts of APA isoforms of each gene using the code provided by Gruber et al. (PMID: 27382025). The counts of the APA isoforms were fit to an exponential decay model to obtain half-lives. The entire workflow was performed for two biological replicates: 12-1 and 12-3 strains of human dermal fibroblasts. Results: In two different fibroblast strains (12-1 and 12-3), we found that isoforms terminating at distal polyadenylation sites were more stable than isoforms terminating at proximal polyadenylation sites in quiescent, but not proliferating, fibroblasts. Conclusions: The transition from shorter to longer isoforms in quiescent cells is associated with stabilization of the transcripts.

2018-08-28 | GSE117121 | GEO

Genome-wide analysis of differential gene expression of contact-inhibited versus proliferating endothelial cells

Project description:Brief summary: Analysis of gene expression in endothelial cells upon contact-inhibition. With this experiments we aimed to identify genes that are associated with the induction of cellular quiescence. Abstract from the associated publication: In contrast to the growing insight in the metabolic reprogramming underlying the angiogenic switch, little is known about the metabolic changes accompanying the quiescence of endothelial cells (ECs). Nonetheless, when dysfunctional, quiescent ECs (QECs) contribute to multiple diseases. Here, we report that QECs are not hypometabolic, but upregulate fatty acid β-oxidation (FAO), not for energy or biomass production, but for redox homeostasis. Hence, inhibition of CPT1a, a rate-controlling step of fatty acid breakdown, promotes a pro-thrombotic and pro-inflammatory signature of QECs by increasing oxidative stress. EC-specific genetic loss similarly elevates oxidative stress in vivo. Compared to proliferating ECs (PECs), QECs switch on a broad “vasculoprotective” metabolic program, involving (i) NAPDH production by the oxidative pentose phosphate pathway (oxPPP) and nicotinamide nucleotide transhydrogenase (NNT), and (ii) prostacyclin synthesis. Molecularly, pro-quiescent Notch signaling elevates FAO by upregulating CPT1a gene transcription. Thus, QECs switch on vasculoprotective metabolic reactions to ensure vascular health.

2018-10-24 | GSE89174 | GEO

Paf1C plays novel subunit-specific roles in alternative cleavage and polyadenylation

Project description:The PAF complex (Paf1C) has been shown to regulate chromatin modifications, gene transcription, and PolII elongation. Here, we provide the first genome-wide analysis of chromatin occupancy by the entire PAF complex in mammalian cells. We show that Paf1C is recruited not only to promoters and gene bodies, but also to regions downstream of cleavage/polyadenylation (pA) sites at 3â ends, a profile that sharply contrasted with the yeast complex. Remarkably, our studies identified novel, subunit-specific links between Paf1C and regulation of alternative cleavage and polyadenylation (APA) and upstream antisense transcription. Moreover, we found that depletion of Paf1C subunits also resulted in the accumulation of RNA polymerase II (PolII) over gene bodies, which coincided with APA. Depletion of specific Paf1C subunits leads to global loss of histone H2B ubiquitylation, but surprisingly, there is little impact of Paf1C depletion on other histone modifications, including the tri-methylation of histone H3 on lysines 4 and 36 (H3K4me3 and H3K36me3), previously associated with this complex. Our results provide surprising differences with yeast, while unifying observations that link Paf1C with PolII elongation and RNA processing, and suggest that Paf1C could play a role in protecting transcripts from premature cleavage by preventing PolII accumulation at TSS-proximal pA sites. ChIP-seq, RNA-seq and 3'READS of Paf1C factors in mouse C2C12 myoblast cells

2016-01-15 | E-GEOD-72574 | biostudies-arrayexpress

Uncoupling from transcription protects polyadenylation site cleavage from inhibition by DNA damage

Project description:We studied the regulation of pre-messenger RNA 3'-end processing (i.e., cleavage at polyadenylation sites) in response to ultraviolet C irradiation in human cells.

2023-02-06 | GSE203517 | GEO

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-seq]

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

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