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

ABSTRACT: 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 .

ORGANISM(S): Homo sapiens

SUBMITTER: Richard Mitter

PROVIDER: E-GEOD-49008 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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RECQL5 controls transcript elongation and suppresses genome instability associated with transcription stress.

Saponaro Marco M Kantidakis Theodoros T Kantidakis Theodoros T Mitter Richard R Kelly Gavin P GP Heron Mark M Williams Hannah H Söding Johannes J Stewart Aengus A Svejstrup Jesper Q JQ

Cell 20140515 5

RECQL5 is the sole member of the RECQ family of helicases associated with RNA polymerase II (RNAPII). We now show that RECQL5 is a general elongation factor that is important for preserving genome stability during transcription. Depletion or overexpression of RECQL5 results in corresponding shifts in the genome-wide RNAPII density profile. Elongation is particularly affected, with RECQL5 depletion causing a striking increase in the average rate, concurrent with increased stalling, pausing, arres ...[more]

PMID: 24836610

Similar Datasets

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.

2014-06-09 | GSE49008 | GEO

RECQL5 Controls Transcript Elongation and Suppresses Transcription-Associated Genome Instability

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-06-09 | E-GEOD-49134 | biostudies-arrayexpress

Enhancer RNAs stimulate Pol II pause release by harnessing multivalent interactions to NELF

Project description:UV-light-induced protein-RNA cross-linking followed by MS analysis was used to identify RNA-binding regions of enhancer RNAs (eRNAs) to the negative elongation factor (NELF) complex, and NELF as part of the paused elongation complex (PEC) of human RNA polymerase II.

2022-03-08 | PXD030569 | Pride

Multiple roles for LEC in initiation and elongation phases of snRNA gene transcription

Project description:The small nuclear RNA (snRNA) genes have been widely used as a model system for understanding transcriptional regulation due to unique aspects of their promoter structure, selectivity for either RNA Polymerase (Pol) II or III and a unique mechanism of termination that is tightly linked with the promoter. Recently, we identified the Little Elongation Complex (LEC) in Drosophila that is required for the expression of Pol II-transcribed snRNA genes. Here, we identify the molecular mechanism by which LEC specifically regulates Pol II-dependent snRNA gene transcription. We present genetic and molecular evidence from both Drosophila and mammals that LEC regulates both initiation and elongation stages of transcription of Pol II-transcribed snRNA genes. In human HCT116 cells we performed: ChIP-seq of ICE1, ICE2, ZC3H8, ELL, and AFF4; total RNA-seq following ICE1 knock-down and non-targeting (GFP) knock-down; ChIP-seq of ICE1 and Pol II following non-targetting (shGFP) and ICE1 knock-down (shICE1). In fly S2 cells we performed: Ice1 ChIP-seq following small hairpin knock-down of GFP (shGFP/non-targeting control) and Ice1 (knock-down of Ice1); ChIP-seq of Pol II following small hairpin knock-down of GFP (shGFP/non-targeting control), Ice1 (knock-down of Ice1), and Ell (knock-down of Ell).

2013-08-08 | E-GEOD-47938 | biostudies-arrayexpress

Structure of transcribing RNA polymerase II-Elongin complex

Project description:Elongin is a hetero-trimeric elongation factor for RNA polymerase (Pol) II transcription that is conserved among metazoa. We solved three structures of human Elongin bound to transcribing Pol II using cryo-EM assisted by crosslinking mass spectrometry. The structures show that Elongin subunit ELOA binds the RPB2 side of Pol II and anchors the ELOB-8 ELOC subunit heterodimer. ELOA contains an N-terminal ‘latch’ that binds between the end of the RPB1 bridge helix and the funnel helices, thereby inducing a conformational change near the Pol II active center. The latch is strictly required for the elongation-stimulatory activity of Elongin, but not for its binding to Pol II, indicating that Elongin functions by allosterically influencing the conformational mobility of the active center. Structural comparisons show that Elongin binding to Pol II is incompatible with association of super elongation complex, the PAF1 complex, and RTF1, which also contains a latch element that stimulates Pol II.

2023-10-11 | PXD045446 | Pride

Global impact of RNA polymerase II elongation inhibition on alternative splicing regulation

Project description:This SuperSeries is composed of the following subset Series: GSE25287: Global impact of RNA polymerase II elongation inhibition on alternative splicing regulation (expression) GSE25494: Global impact of RNA polymerase II elongation inhibition on alternative splicing regulation (ChIP-Seq) Refer to individual Series

2010-12-09 | E-GEOD-25495 | biostudies-arrayexpress

Homo sapiens

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

| PRJNA212573 | ENA

Promoter proximal pausing and its regulation by c-Myc in embryonic stem cells: ChIP-Seq

Project description:Recruitment of the RNA Polymerase II (Pol II) transcription initiation apparatus to promoters by specific DNA binding transcription factors is well recognized as a key regulatory step in gene expression. We describe here evidence that promoter-proximal pausing is a general feature of transcription by Pol II in embryonic stem (ES) cells, and thus an additional step where regulation of gene expression may occur. We report here that c-Myc, which occupies a third of actively transcribed genes in ES cells and is a key regulator of cellular proliferation, binds P-TEFb and contributes to release of promoter-proximal paused Pol II at these genes. ChIP-seq data for Pol II and additional factors controlling pause release in mouse ES cells.

2010-04-02 | E-GEOD-20530 | biostudies-arrayexpress

Global impact of RNA polymerase II elongation inhibition on alternative splicing regulation (ChIP-Seq)

Project description:The rate of RNA polymerase II (pol II) elongation can influence splice site selection in nascent transcripts, yet the extent and physiological relevance of this kinetic coupling between transcription and alternative splicing is not well understood. We performed experiments to perturb pol II elongation and then globally compared alternative splicing patterns with genome-wide pol II occupancy. RNA binding and RNA processing functions were significantly enriched among the genes with pol II elongation inhibition-dependent changes in alternative splicing. Under conditions that interfere with pol II elongation, including cell stress, increased pol II occupancy was detected in the intronic regions flanking the alternative exons in these genes, and these exons generally became more included. A disproportionately high fraction of these exons introduced premature termination codons that elicited nonsense-mediated mRNA decay (NMD), thereby further reducing transcript levels. Our results provide evidence that kinetic coupling between transcription, alternative splicing and NMD affords a rapid mechanism by which cells can respond to changes in growth conditions, including cell stress, to coordinate the levels of RNA processing factors with mRNA levels. To monitor pol II distributions, chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-Seq) was performed using an anti-pol II antibody (4H8) and cross-linked chromatin preparations from Jurkat cells, treated with or without pol II elongation inhibitor 5,6-dichloro-1-β-D-ribofuranosyl-benzimidazole (DRB) at 10 and 25 ug/ml respectively prior to phorbol 12-myristate 13-acetate (PMA) stimulation, for 5000+ alternative splicing events.

2010-12-09 | E-GEOD-25494 | biostudies-arrayexpress

Expression profile and RNA Polymerase II occupancy of transposable elements among knock down of the piRNA pathway components in OSCs

Project description:The PiwiM-bM-^@M-^SpiRNA complex (PiwiM-bM-^@M-^SpiRISC) in Drosophila ovarian somatic cells represses transposons transcriptionally to maintain genome integrity; however, the underlying mechanisms remain obscure. We performed mRNA-seq analysis from OSCs transfected with siRNAs against CG3893, the known piRNA pathway genes, Piwi, Maelstrom, HP1a and Armitage, and the control (EGFP), and PolII ChIP-seqanalysis from OSCs transfected with siRNAs against CG3893, Piwi, Mael and the control (EGFP). This result indicates that CG3893 is a novel factor for primary piRNA pathway in OSCs. RNA levels in wild-type (EGFP control knock-down) ovarian somatic cells (OSC) and RNAi knock-downs of Piwi, Armi, Mael, CG3893, and HP1a. RNA Polymerase II occupancy in wild-type (EGFP control knock-down) ovarian somatic cells (OSC) and RNAi knock-downs of Piwi, Mael, and CG3893.

2013-08-01 | E-GEOD-47006 | biostudies-arrayexpress

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