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Homo sapiens

ABSTRACT: ChIP-seq analysis of HeLa cancer stem cells and non-cancer stem cells using Pol II, H3K4me3 and H3K27Ac.

PROVIDER: PRJNA400459 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5985163.fastq.gz	Fastqsanger.gz
	SRR5985164.fastq.gz	Fastqsanger.gz
	SRR5985165.fastq.gz	Fastqsanger.gz
	SRR5985166.fastq.gz	Fastqsanger.gz
	SRR5985167.fastq.gz	Fastqsanger.gz

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ChIP-seq analysis of HeLa cancer stem cells and non-cancer stem cells using Pol II, H3K4me3 and H3K27Ac.

Project description:ChIP-seq analysis of HeLa cancer stem cells and non-cancer stem cells regarding Pol II, H3K4me3 and H3K27Ac.

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Pol II and its associated epigenetic marks are present at pol III-transcribed non-coding RNA genes (I)

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. Chip-Seq experiments for six samples: Pol III, TFIIIB, TFIIIC, H3K4me3 in HeLa cells and Pol III, S2 phos Pol II in CD4+ cells.

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Project description:We report the ChIP-seq analysis of HOXB13, H3K27Ac, H3K27me3, H3K4me3, and RNA POL II in G401 rhabdoid tumor of the kidney cells.

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SETD5 regulates the OGT-catalyzed O-GlcNAcylation of RNA polymerase II, which is involved in the stemness of colorectal cancer cells

Project description:The dosage-dependent recruitment of RNA polymerase II (Pol II) at the promoters of genes related to neurodevelopment and stem cell maintenance is required for transcription by the fine-tuned expression of SET-domain-containing protein 5 (SETD5). Pol II O-GlcNAcylation by O-GlcNAc transferase (OGT) is critical for preinitiation complex formation and transcription cycling. SETD5 dysregulation has been linked to stem cell-like properties in some cancer types; however, the role of SETD5 in cancer cell stemness has not yet been determined. We here show that aberrant SETD5 overexpression induces stemness in colorectal cancer (CRC) cells. SETD5 overexpression causes the upregulation of PI3K-AKT pathway-related genes and cancer stem cell (CSC) markers such as CD133, Kruppel-like factor 4 (KLF4), and estrogen-related receptor beta (ESRRB), leading to the gain of stem cell-like phenotypes. Our findings also revealed a functional relationship between SETD5, OGT, and Pol II. OGT-catalyzed Pol II glycosylation depends on SETD5, and the SETD5-Pol II interaction weakens in OGT-depleted cells, suggesting a SETD5-OGT-Pol II interdependence. SETD5 deficiency reduces Pol II occupancy at PI3K-AKT pathway-related genes and CD133 promoters, suggesting a role for SETD5-mediated Pol II recruitment in gene regulation. Moreover, the SETD5 depletion nullified the SETD5-induced stemness of CRC cells and Pol II O-GlcNAcylation. These findings support the hypothesis that SETD5 mediates OGT-catalyzed O-GlcNAcylation of RNA Pol II, which is involved in cancer cell stemness gain via CSC marker gene upregulation.

2023-11-16 | PXD041141 | Pride

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Project description:Transcriptional elongation by RNA polymerase II (Pol II) is regulated by positive transcription elongation factor b (P-TEFb) in association with Bromodomain-containing protein 4 (BRD4). We used genome-wide chromatin immunoprecipitation sequencing in primary human CD4+ T cells to reveal that BRD4 co-localizes with Ser2-phosphorylated Pol II (Pol II Ser2) at both enhancers and promoters of active genes. Disruption of bromodomain:histone acetylation interactions by JQ1, a small-molecule bromodomain inhibitor, resulted in decreased BRD4 binding, reduced Pol II Ser2, and reduced expression of lineage-specific genes in primary human CD4+ T cells. A large number of JQ1-disrupted BRD4 binding regions exhibited di-acetylated H4 (lysine-5 and -8) and H3K27 acetylation (H3K27ac), which correlated with the presence of histone acetyltransferases and deacetylases. Genes associated with BRD4/H3K27ac co-occupancy exhibited significantly higher activity than those associated with H3K27ac or BRD4 binding alone. Comparison of BRD4 binding in T cells and in human embryonic stem cells revealed that enhancer BRD4 binding sites were predominantly lineage-specific. Our findings suggest that BRD4-driven Pol II phosphorylation at serine 2 plays an important role in regulating lineage-specific gene transcription in human CD4+ T cells. Examination of BRD4, total Pol II, serine 2 phosphorylated Pol II and serine 5 phosphorylated Pol II binding in CD4+ T cells (with and without JQ1 treatment) and BRD4 binding in human embryonic stems cell; PolyA RNA expression in CD4+ T cells( with and without JQ1 treatment) using RNA-seq

2012-11-14 | E-GEOD-33281 | biostudies-arrayexpress

ChIP-seq

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Mitotic Transcriptional Clearance of Actively Engaged Pol II Through Transcriptional Elongation Control

Project description:Chromatin is highly condensed and transcriptionally repressed during mitosis. Although it is established that some general transcription factors are inactivated by phosphorylation at mitosis, many details of mitotic transcriptional repression and its underlying mechanisms are largely unknown. Here, we provide evidence that as cells enter mitosis, genes with transcriptionally engaged RNA Polymerase II (Pol II) can continue transcription until the end of the gene to clear Pol II from mitotic chromatin. Using ChIP-Seq, we find that the transcriptional reinitiation process is globally impaired in early mitosis (prophase/prometaphase), with loss of TFIIB occupancy and nucleosome-free regions at promoters. Pretreatment of nocodazole-arrested mitotic cells with the P-TEFb inhibitor flavopiridol prevents the release of promoter-proximal engaged Pol II. Global nascent RNA sequencing and RNA fluorescence in situ hybridization (FISH) of individual genes demonstrate the existence of transcriptionally engaged Pol II in early mitosis. Chemical and mutational inhibition of P-TEFb in mitosis leads to delays in the progression of cell division. Together, our study reveals a novel mechanism for mitotic transcriptional repression whereby transcriptionally engaged Pol II can progress into productive elongation and finish transcription to allow proper cellular division. ChIP-Seq of Pol II of different forms, TFIIB, H3K4me3 in human HeLa cells at different cell cycle stages. ChIP-Seq of Pol II in HeLa mitotic cells with or without CDK9 inhibitor flavopiridol pretreatment. Nascent RNA-seq in asynchronous and arrested mitotic cells.

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