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Genome-wide analyses of chromatin interactions after the loss of Pol I, Pol II and Pol III [Ocean-C ]

ABSTRACT: Genome binding/occupancy profiling by high throughput sequencing ｜ Expression profiling by high throughput sequencing | Other We analyzed Hi-C, HiChIP, Ocean-C, RNA-seq, ATAC-seq, ChIP-seq and 4C-seq data to provide the most comprehensive evidence to date to demonstrate that transcription plays a marginal role in organizing the 3D genome in mammalian cells: 1) degraded Pol I, Pol II and Pol III proteins in mESCs, and showed their loss results in little or no changes of global 3D chromatin structures for the first time; 2) selected RNA polymerases high abundance binding sites-associated interactions and found they still persist after the degradation; 3) generated higher resolution chromatin interaction maps and revealed that transcription inhibition mildly alters small loop domains; 4) identified Pol II bound but CTCF and Cohesin unbound loops and disclosed that they are largely resistant to transcription inhibition Interestingly, we found that Pol II depletion for a longer time significantly affects the chromatin accessibility and Cohesin occupancy, suggesting RNA polymerases are capable of affecting the 3D genome indirectly. So, the direct and indirect effects of transcription inhibition explain the previous confusing effects on the 3D genome. We conclude that Pol I, Pol II, and Pol III loss only mildly alter chromatin interactions in mammalian cells, suggesting the 3D chromatin structures are preestablished and relatively stable.

ORGANISM(S): Mus musculus

PROVIDER: GSE145794 | GEO | 2020/06/02

REPOSITORIES: GEO

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Genome-wide analyses of chromatin interactions after the loss of Pol I, Pol II and Pol III [4C-seq]

Project description:We analyzed Hi-C, HiChIP, Ocean-C, RNA-seq, ATAC-seq, ChIP-seq and 4C-seq data to provide the most comprehensive evidence to date to demonstrate that transcription plays a marginal role in organizing the 3D genome in mammalian cells: 1) degraded Pol I, Pol II and Pol III proteins in mESCs, and showed their loss results in little or no changes of global 3D chromatin structures for the first time; 2) selected RNA polymerases high abundance binding sites-associated interactions and found they still persist after the degradation; 3) generated higher resolution chromatin interaction maps and revealed that transcription inhibition mildly alters small loop domains; 4) identified Pol II bound but CTCF and Cohesin unbound loops and disclosed that they are largely resistant to transcription inhibition Interestingly, we found that Pol II depletion for a longer time significantly affects the chromatin accessibility and Cohesin occupancy, suggesting RNA polymerases are capable of affecting the 3D genome indirectly. So, the direct and indirect effects of transcription inhibition explain the previous confusing effects on the 3D genome. We conclude that Pol I, Pol II, and Pol III loss only mildly alter chromatin interactions in mammalian cells, suggesting the 3D chromatin structures are preestablished and relatively stable.

2020-06-02 | GSE145784 | GEO

Genome-wide analyses of chromatin interactions after the loss of Pol I, Pol II and Pol III [HiChIP]

Project description:Genome binding/occupancy profiling by high throughput sequencing ｜ Expression profiling by high throughput sequencing | Other We analyzed Hi-C, HiChIP, Ocean-C, RNA-seq, ATAC-seq, ChIP-seq and 4C-seq data to provide the most comprehensive evidence to date to demonstrate that transcription plays a marginal role in organizing the 3D genome in mammalian cells: 1) degraded Pol I, Pol II and Pol III proteins in mESCs, and showed their loss results in little or no changes of global 3D chromatin structures for the first time; 2) selected RNA polymerases high abundance binding sites-associated interactions and found they still persist after the degradation; 3) generated higher resolution chromatin interaction maps and revealed that transcription inhibition mildly alters small loop domains; 4) identified Pol II bound but CTCF and Cohesin unbound loops and disclosed that they are largely resistant to transcription inhibition Interestingly, we found that Pol II depletion for a longer time significantly affects the chromatin accessibility and Cohesin occupancy, suggesting RNA polymerases are capable of affecting the 3D genome indirectly. So, the direct and indirect effects of transcription inhibition explain the previous confusing effects on the 3D genome. We conclude that Pol I, Pol II, and Pol III loss only mildly alter chromatin interactions in mammalian cells, suggesting the 3D chromatin structures are preestablished and relatively stable.

2020-06-02 | GSE145793 | GEO

Genome-wide analyses of chromatin interactions after the loss of Pol I, Pol II and Pol III [ATAC-seq]

2020-06-02 | GSE145785 | GEO

Genome-wide analyses of chromatin interactions after the loss of Pol I, Pol II and Pol III [Hi-C]

2020-06-02 | GSE145873 | GEO

Genome-wide analyses of chromatin interactions after the loss of Pol I, Pol II and Pol III [RNA-seq]

2020-06-02 | GSE145792 | GEO

Genome-wide analyses of chromatin interactions after the loss of Pol I, Pol II and Pol III [ChIP-seq]

2020-06-02 | GSE145791 | GEO

Close Association of RNA Polymerase II and Many Transcription Factors With Pol III Genes

Project description:Transcription of the eukaryotic genomes is carried out by three distinct RNA polymerases I, II and III whereby each polymerase is thought to independently transcribe a distinct set of genes. To investigate a possible relationship of RNA polymerases II and III we mapped their in vivo binding sites throughout the human genome using ChIP Seq in two different cell lines, GM12878 and K562 cells. Pol III was found to bind near many known genes as well as several novel genes. RNA-Seq studies indicate that majority of the genes are expressed although a subset are not suggestive of stalling by RNA polymerase III. Pol II was found to bind near many known Pol III genes, including tRNA, U6, HVG, hY and 7SK and novel Pol III genes. Similarly, in vivo binding studies also reveal that a number of transcription factors normally associated with Pol II transcription, including c-Fos, c-Jun and c-Myc, also tightly associate with most Pol III transcribed genes. Inhibition of Pol II activity using ?-amanitin reduced expression of a number of Pol III genes (e.g. U6, hY, HVG), suggesting that Pol II plays an important role in regulating their transcription. These results indicate that, contrary to previous expectations, polymerases can often work with one another to globally coordinate gene expression. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf This SuperSeries is composed of the SubSeries listed below.

2009-12-31 | GSE19551 | GEO

Genome-wide control of RNA polymerase II activity by cohesin (tiling)

Project description:Cohesin is a well-known mediator of sister chromatid cohesion, but it also influences gene expression and development. These non-canonical roles of cohesin are not well understood, but are vital: gene expression and development are altered by modest changes in cohesin function that do not disrupt chromatid cohesion. To clarify cohesinM-bM-^@M-^Ys roles in transcription, we measured how cohesin controls RNA polymerase II (Pol II) activity by genome-wide chromatin immunoprecipitation and precision global run-on sequencing. On average, cohesin-binding genes have more transcriptionally active Pol II and promoter-proximal Pol II pausing than non-binding genes, and are more efficient, producing higher steady state levels of mRNA per transcribing Pol II complex. Cohesin depletion frequently increases pausing at cohesin-binding genes, indicating that cohesin often facilitates transition of paused Pol II to elongation. In many cases this likely reflects a role for cohesin in transcriptional enhancer function. Strikingly, more than 95% of predicted extragenic enhancers bind cohesin, and cohesin depletion can reduce their association with Pol II, indicating that cohesin facilitates enhancer-promoter contact. Cohesin directly promotes transcription of the myc gene, and cohesin depletion reduces Pol II activity at most Myc target genes. The multiple transcriptional roles of cohesin revealed by these studies likely underlie the growth and developmental deficits caused by minor changes in cohesin activity. We performed ChIP-chip of Rpb3 (representing total Pol II), Ser2P-Pol II (representing elongating Pol II), and Cdk12 and CycT Pol II kinase components in Mock RNAi-treated and cohesin subunit Rad21 RNAi-treated ML-DmBG3-c2 cells, which revealed that cohesin depletion has a variety of effects on Pol II occupancy and modification, as well as on occupancy of Pol II kinases.

2013-04-24 | E-GEOD-42360 | biostudies-arrayexpress

Genome-wide control of RNA polymerase II activity by cohesin (sequencing)

Project description:Cohesin is a well-known mediator of sister chromatid cohesion, but it also influences gene expression and development. These non-canonical roles of cohesin are not well understood, but are vital: gene expression and development are altered by modest changes in cohesin function that do not disrupt chromatid cohesion. To clarify cohesin’s roles in transcription, we measured how cohesin controls RNA polymerase II (Pol II) activity by genome-wide chromatin immunoprecipitation and precision global run-on sequencing. On average, cohesin-binding genes have more transcriptionally active Pol II and promoter-proximal Pol II pausing than non-binding genes, and are more efficient, producing higher steady state levels of mRNA per transcribing Pol II complex. Cohesin depletion frequently increases pausing at cohesin-binding genes, indicating that cohesin often facilitates transition of paused Pol II to elongation. In many cases this likely reflects a role for cohesin in transcriptional enhancer function. Strikingly, more than 95% of predicted extragenic enhancers bind cohesin, and cohesin depletion can reduce their association with Pol II, indicating that cohesin facilitates enhancer-promoter contact. Cohesin directly promotes transcription of the myc gene, and cohesin depletion reduces Pol II activity at most Myc target genes. The multiple transcriptional roles of cohesin revealed by these studies likely underlie the growth and developmental deficits caused by minor changes in cohesin activity. The PRO-seq method was used to measure transcriptionally engaged Pol II genome-wide in two replicates each of mock RNAi-treated, Nipped-B RNAi-treated, and Rad21 RNAi-treated ML-DmBG3-c2 cells.

2013-04-24 | E-GEOD-42397 | biostudies-arrayexpress

Coupling of co-transcriptional splicing and 3’ end Pol II pause during termination in Arabidopsis

Project description:In Arabidopsis, RNA Polymerase II (Pol II) often pauses within a few hundred base pairs downstream of the polyadenylation site, reflecting efficient transcriptional termination, but how such pause is regulated remains largely elusive. Here, we studied Pol II dynamics at gene 3’ end by combining comprehensive experiments with mathematical modelling. We generated high-resolution Ser2P Pol II positioning data specifically enriched at gene 3’ end and defined a 3’ end pause index (3’PI). The position but not the extent of the 3’ end pause correlates with termination window size. The 3’PI is not decreased but even mildly increased in the termination deficient mutant xrn3, indicating 3’ end pause is a regulatory step early during the termination and before XRN3 mediated RNA decay that releases the Pol II. Unexpectedly, 3’PI is closely associated with gene exon numbers and co-transcriptional splicing efficiency. Multiple exons genes often display stronger 3’ end pauses and more efficient on-chromatin splicing than genes with few exons. Chemical inhibition of splicing strongly reduces the 3’PI and disrupts its correlation with exon numbers but does not globally impact 3’ end readthrough levels. These results were further confirmed by fitting Pol II positioning data with a mathematical model, which enables the estimation of parameters that define Pol II dynamics. Our work highlights that the number of exons via co-transcriptional splicing is a major determinant of Pol II pausing levels at gene 3’ end in plants.

2023-05-27 | GSE205545 | GEO

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