Similar Datasets
Project description:Identification of Pol II(G) target genes in mouse liver [ChIP-seq]
| PRJNA603065 | ENA
Project description:RNA polymerase II (Pol II) subunits are thought to be involved in various transcription-associated processes, but it is unclear whether they play different regulatory roles in modulating gene expression. Here, we performed nascent and mature transcript sequencing after the acute degradation of 12 mammalian Pol II subunits and profiled their genomic binding sites and protein interactomes to dissect their molecular functions. We found that Pol II subunits contribute differently to Pol II cellular localization and transcription process and preferentially regulate RNA processing (such as RNA splicing and 3’ end maturation). Genes sensitive to the depletion of different Pol II subunits tend to be involved in diverse biological functions and show different RNA half-lives. Sequences, associated protein factors, and RNA structures are correlated with Pol II subunit-mediated differential gene expression. These findings collectively suggest that the heterogeneity of Pol II and different genes appear to depend on some of the subunits.
2022-08-09 | PXD035866 | iProX
Project description:Under current models for signal-dependent transcription in eukaryotes, DNA-binding activator proteins regulate the recruitment of RNA polymerase II (Pol II) to a set of target promoters. Yet, recent studies, as well as our results herein, show that Pol II is widely distributed (i.e., "preloaded") at the promoters of many genes prior to specific signaling events. How Pol II recruitment and Pol II preloading fit within a unified model of gene regulation is unclear. In addition, the mechanisms through which cellular signals activate preloaded Pol II across mammalian genomes remain largely unknown. Here we show that the predominant genomic outcome of estrogen signaling is the post-recruitment regulation of Pol II activity through phosphorylation, rather than recruitment of Pol II. Furthermore, we show that negative elongation factor (NELF) binds to estrogen target promoters in conjunction with preloaded Pol II and represses gene expression until the appropriate signal is received. Finally, our studies reveal that the estrogen-dependent activation of preloaded Pol II facilitates rapid transcriptional and post-transcriptional responses which play important physiological roles in regulating estrogen signaling itself. Our results reveal a broad use of post-recruitment Pol II regulation by the estrogen signaling pathway, a mode of regulation that is likely to apply to a wide variety of signal-regulated pathways. ChIP-chip analysis for RNA Pol II, Ser5 phosphorylated RNA Pol II and NELF-A in MCF7 breast cancer cells.
2010-05-14 | E-GEOD-13051 | biostudies-arrayexpress
Project description:Under current models for signal-dependent transcription in eukaryotes, DNA-binding activator proteins regulate the recruitment of RNA polymerase II (Pol II) to a set of target promoters. Yet, recent studies, as well as our results herein, show that Pol II is widely distributed (i.e., "preloaded") at the promoters of many genes prior to specific signaling events. How Pol II recruitment and Pol II preloading fit within a unified model of gene regulation is unclear. In addition, the mechanisms through which cellular signals activate preloaded Pol II across mammalian genomes remain largely unknown. Here we show that the predominant genomic outcome of estrogen signaling is the post-recruitment regulation of Pol II activity through phosphorylation, rather than recruitment of Pol II. Furthermore, we show that negative elongation factor (NELF) binds to estrogen target promoters in conjunction with preloaded Pol II and represses gene expression until the appropriate signal is received. Finally, our studies reveal that the estrogen-dependent activation of preloaded Pol II facilitates rapid transcriptional and post-transcriptional responses which play important physiological roles in regulating estrogen signaling itself. Our results reveal a broad use of post-recruitment Pol II regulation by the estrogen signaling pathway, a mode of regulation that is likely to apply to a wide variety of signal-regulated pathways.
2009-01-12 | GSE13051 | GEO
Project description:Bmi-1, Ring1B, H3K27me3, Ser2 Pol II, Ser 5 Pol II binding pattern in WT and Psip1 KO MEFs Menin occupancy is studied over Hox genes and several non-hox genes Bmi-1, Ring1B, H3K27me3, Ser2 Pol II, Ser 5 Pol II ChIPs from WT and Psip1 KO MEFs
2014-06-27 | E-GEOD-49181 | biostudies-arrayexpress
Project description:Purpose: We used ChIP-seq to analyze daily transcription and regulation of Pol II pausing within the mouse liver. Methods: Livers of young mice were processed for Pol II and Nelf-A ChIP-seq at 4-h interval across the day. The binding pattern was analyzed by MACS. Tag pileup within promoter and gene body regions were also obtained to calculate Pol II TR. Results: We obtained > 10 million high quality sequencing reads per time points per sample after quality control and alignments. MACS identified nearly 10,000 Pol II peaks genomewide throughout the day. Nelf-A peaks varied from a few hundreds to 10,000 across the day. A genomewide Nelf-A binding rhythm was evident. We also quantitated bindings within the TSS region and/or gene body and analyzed the quantitation results with ARSER for rhythm detection. We found Pol II binding within the TSS region and gene body show discordant changes. While most genes had peak TSS Pol II binding around dawn, Pol II binding within the gene body showed more scattered distribution, with two peaks around dawn and dusk, respectively. Pol II traveling ratio also showed daily changes, with most genes having a higher TR around dawn. Conclusions: Our study revealed discordant Pol II rhythms in the TSS region and within the gene body, and indicated that Pol II initiation and pause release could have distinct roles in the generation of transcription rhythms within the mouse liver.
2018-12-20 | GSE96773 | GEO
Project description:We reported a diurnal changes in the recruitment of HDAC3, Rev-erbα, NCoR and Pol II to the mouse liver genome as well as H3K9 acetylation in vivo at ZT10 and ZT22. ChIP-Seq profiling of HDAC3, Rev-erbα, NCoR and Pol II binding and H3K9Ac in mouse liver harvested at 2 different times (ZT10 and ZT22) of the day
2011-03-11 | E-GEOD-26345 | biostudies-arrayexpress
Project description:Epigenetic control is an important aspect of gene regulation. Despite detailed understanding of many examples, the transcription of non-coding RNA genes by RNA polymerase (pol) III is less well characterized. Here we profile the epigenetic features of pol III target genes throughout the human genome. This reveals that the chromatin landscape of pol III-transcribed genes resembles that of pol II templates in many ways, although there are also clear differences. Our analysis also discovered an entirely unexpected phenomenon, namely that pol II co-localizes with the majority of genomic loci that are bound by pol III. RNA-seq experiment for total RNA in CD4+ cells.
2010-04-25 | E-GEOD-20071 | biostudies-arrayexpress
Project description:Mass Spectrometry with DTME Crosslinking (MSDC) based on label-free mass spectrometry to assess changes in the post-initiation Pol II complex.
2024-07-04 | PXD052484 | Pride
Project description:Nucleosomes restrict the access of transcription factors to chromatin. RSC is a SWI/SNF-family chromatin-remodeling complex from yeast that repositions and ejects nucleosomes in vitro. Here, we examined these activities and their importance in vivo. We utilized array-based methods to examine nucleosome occupancy and positioning at more than 200 locations in the genome following the controlled destruction of the catalytic subunit of RSC, Sth1. Loss of RSC function caused pronounced and general reductions in transcription from Pol I, II, and III genes. At Pol III genes, Sth1 loss conferred a general gain in nucleosome density and an accompanying reduction in RNA Pol III occupancy. In contrast, we observed primarily single nucleosome changes, including movement, at Pol II promoters. Importantly, a greater number of changes were observed near the transcription start sites of RSC-occupied promoters than non-occupied promoters. These changes are distinct from those due to general loss of transcription. Thus, RSC action affects both nucleosome density and positioning in vivo, but applies these remodeling modes differently at Pol II and Pol III genes. Keywords: ChIP-chip, nucleosome, mononucleosome, RSC, transcription
2007-12-01 | GSE8862 | GEO