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Effect of CFIm25 knock-out on RNA polymerase II transcription

ABSTRACT: Effect of CFIm25 knock-out on RNA polymerase II transcription

PROVIDER: PRJNA490093 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7812690_1.fastq.gz	Fastqsanger.gz
	SRR7812690_2.fastq.gz	Fastqsanger.gz
	SRR7812691_1.fastq.gz	Fastqsanger.gz
	SRR7812691_2.fastq.gz	Fastqsanger.gz
	SRR7812692_1.fastq.gz	Fastqsanger.gz

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Effect of CFIm25 knock-out on RNA polymerase II transcription

Project description:ChIP-seq of RNA polyerase II and Input in 293 and 293 CFIm25 KO to investigate the effect on pol II of knocking-down by Crispr/Cas9 CFIm25. ChIP-seq was performed after DMSO and DRB treatment (30 minutes, 100 µM)

2018-09-12 | GSE119712 | GEO

Knockdown of CFIm25 or CFIm68 decreases RNA polymerase II pausing and transcription

Project description:Transcription of eukaryotic protein-coding genes by RNA polymerase II (pol II) is highly regulated at initiation, elongation and termination and these steps are coordinated with co-transcriptional processing of the emerging pre-mRNA by capping, splicing, and cleavage and polyadenylation. Polyadenylation (Poly(A)) site recognition, which defines the end of the mRNA, relies on the cleavage and polyadenylation (CPA) complex. It was previously observed that knocking-down proteins of the CPA complex affects not only recognition of the poly(A) site but also results in increased pausing of pol II at the beginning of genes. This finding suggests that the CPA complex plays a role in regulating pol II turnover after transcription initiation. To explore this possibility, we knocked-down two subunits of the cleavage factor I (CFIm), CFIm25 and CFIm68, which are part of the CPA complex and involved in alternative polyadenylation, and performed pol II ChIP-seq. Surprisingly, we found that contrary to the effect of knocking down of other CPA factors, reduction of the level of CFIm25 or CFIm68 decreases pol II pausing and transcription genome-wide in HEK293 cells. These findings indicate that different subunits of the CPA complex have opposite effects on pol II pausing at the start of genes.

2019-06-20 | GSE99955 | GEO

Comparison of genomic binding profile for CFIm25 in control and CFIm25 KD hESCs (H9 cell line)

Project description:To understand how CFIm25 associates with genomic DNA during co-transcriptional mRNA processing,we carried out ChIP-seq analysis for CFIm25 in control and CFIm25 KD cells (CFIm25 KD cells as normalization background)

2022-04-21 | GSE178076 | GEO

poly(A+)-seq profiling of gene expression in control H9 and (CFIm25 KD+ 3Flag-CFIm25 overexpression) H9 cell lines

Project description:We carried out CFIm25 KD experiments in H9 cell line (hESCs). After poly(A+)-seq, we found the expression of hundreds of genes were changed. To investigate if the effect is a direct or indirect effect of CFIm25 KD, we next carried out 3Flag-CFIm25 overexpression in CFIm25 KD cells for gene-rescue experiments. After we obtained this cell line, here we performed poly(A+)-seq in control H9 and (CFIm25 KD+ 3Flag-CFIm25 overexpression)H9 cell lines. The goal of this experiment is to investigate if CFIm25 overexpression could rescue the gene expression phenotype caused by CFIm25 KD.

2022-04-21 | GSE176328 | GEO

Genome wide profiling of RNA Polymerase II upon knock-down or overexpression of RECQL5

Project description:RECQL5 globally effects the distribution of RNA Polymerase II on genes in a dose dependent manner. Knock-down of RECQL5 reduces RNA Polymerase II density in the gene body, while increasing density on TSS and TTS. Overexpression shows exactly the opposite effect. We postulate that RECQL5 acts as a regulator of the elongation rate, more specifically, that the knock-down increases elongation rate while the overexpression decreases it. RNA Polymerase II ChIP-Seq upon knock-down of RECQL5 with either of two specific shRNAs or a CTRL shRNA, and upon Doxycycline induced overexpression of RECQL5 .

2014-06-09 | E-GEOD-49008 | biostudies-arrayexpress

Genome wide profiling of RNA Polymerase II upon knock-down or overexpression of RECQL5

2014-06-09 | GSE49008 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of control, SETD6 Knock-out, SETD3 knock-out and SETD6+SETD3 knock-out HeLa cells Transcriptomes

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of control, SETD6 Knock-out, SETD3 knock-out and SETD6+SETD3 knock-out HeLa cells Transcriptomes

| PRJNA819059 | ENA

ARRDC4 knock out Mouse Heart Analysis

Project description:ARRDC4 knock out Mouse Heart Analysis

| PRJNA773414 | ENA

CFIm25 links alternative polyadenylation to glioblastoma tumour suppression

Project description:Purpose: To identify all of the APA targets of CFIm25 on a global scale and develop an algorithm that can idenitify APA events from standard RNA-seq data Methods: RNA from HeLa cells treated with control siRNA and CFIm25 siRNA were subject to RNA-Seq. Using a custom-designed algorithm to mine RNA-seq data for novel APA events regulated by CFIm25. Results: We identified over 1,400 genes with shortened 3’UTRs after CFIm25 knockdown. Importantly, we show that as a consequence of APA, many of these mRNAs have greatly enhanced protein expression due to the loss of destabilizing features within the 3’UTR. Conclusions: Our study underscored the critical function of the CFIm complex members in governing APA and establish a previously unknown link between APA and metabolic pathways important for tumor progression. Hela cell line mRNA profiles of control treated and CFIm25 Knockdown were generated by RNA-Seq using Illumina GAIIx.

2014-05-15 | E-GEOD-42420 | biostudies-arrayexpress

Comparison of genomic binding profile for RNA polyII in control and CFIm25 KD hESCs (H9 cell line)

Project description:To understand how CFIm25 depletion affects gene expression at the transcription level, we carried out ChIP-seq analysis for RNAPII in control and CFIm25 KD cells.

2022-04-21 | GSE176543 | GEO

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