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Genome-wide mapping of RNA polymerase active sites in DOT1L-depleted HCT116 cells by PRO-seq analysis

ABSTRACT: Genome-wide mapping of RNA polymerase active sites in DOT1L-depleted HCT116 cells by PRO-seq analysis

PROVIDER: PRJNA1077998 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28007288_1.fastq.gz	Fastqsanger.gz
	SRR28007288_2.fastq.gz	Fastqsanger.gz
	SRR28007289_1.fastq.gz	Fastqsanger.gz
	SRR28007289_2.fastq.gz	Fastqsanger.gz

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Similar Datasets

Genome-wide mapping of RNA polymerase active sites in DOT1L-depleted HCT116 cells by PRO-seq analysis

Project description:Precision nuclear run-on sequencing (PRO-seq) approach was adopted to evaluate the effect of DOT1L in regulating transcription and RNA polymerase active sites in HCT116 cells

2024-02-24 | GSE256074 | GEO

Heightened DOT1L-AF10 enriches H3K79me3 to promote pro-atherogenic inflammatory endothelial phenotype through NF-κB p65

Project description:DOT1L-catalyzed H3K79 methylation is a hallmark of actively transcribed genes and has been extensively studied in developmental and disease contexts. While DOT1L inhibition has emerged as a promising therapeutic strategy in cancer, its role in pro-atherogenic endothelial inflammation remains unclear. To investigate this, we utilized an in vivo partial carotid artery ligation model and observed increased DOT1L expression and H3K79me3 level. Consistently, in vitro studies employing a 3D-printed human coronary artery model and TNF-α stimulation corroborated these results, showing elevated DOT1L expression and H3K79me3 deposition, while levels of H3K79me and me2 remained unchanged. Further analyses identified key DotCom complex components, AF10 and AF9 (upregulated) and AF17 (downregulated), as contributors to the enhanced H3K79me3 landscape. CUT&RUN sequencing showed prominent H3K79me3 enrichment at the RELA (NF-κB p65) promoter, corresponding with increased NF-κB p65 expression and activation. Notably, inhibition/knockdown of the methyltransferase DOT1L or overexpression of the demethylase FBXL10 significantly reduced H3K79me3 levels, thereby suppressing NF-κB p65 expression and attenuating endothelial inflammation, independent of canonical NF-κB p65 activation. These findings establish DOT1L-mediated H3K79me3 as a crucial epigenetic regulator of endothelial inflammation, highlighting a potential therapeutic avenue for mitigating NF-κB p65-driven pro-atherogenic endothelial dysfunction.

2025-12-16 | GSE295366 | GEO

PRO-seq from HCT116 cells in normoxia and hypoxia

Project description:PRO-seq analysis was used to examine rapid transcriptional changes in response to short-term hypoxia in WT and HIF1A-/- HCT116 cells

2021-01-29 | GSE145567 | GEO

DOT1L-mediated CDK9 methylation is essential for DNA double-strand break repair

Project description:P-TEFb is a key regulator of transcription elongation and is composed of cyclin-dependent kinase 9 (CDK9) and cyclin T1. DOT1L is a histone H3K79 methyltransferase. Here, we show that treatment with the DOT1L inhibitor EPZ-5676 induces transcriptome changes in HCT116 cells. We further demonstrate that DOT1L methylates CDK9 at lysine 56 and that CDK9 methylation-deficient mutant K56A reshapes genome-wide CDK9 occupancy. Notably, changes in CDK9 occupancy are particularly pronounced at double-strand break (DSB)-related genes and are associated with the regulation of their transcription. This idataset includes RNA-seq and ChIP-seq data generated from HCT116 cells.

2025-12-29 | GSE314839 | GEO

Raw RNA-seq data from control and Ki-67-depleted HCT116 human colon cancer cells

Project description:Raw RNA-seq data from control and Ki-67-depleted HCT116 human colon cancer cells

2021-07-23 | GSE159160 | GEO

DOT1L-mediated CDK9 methylation is essential for DNA double-strand break repair [RNA-seq]

2025-12-30 | GSE315014 | GEO

PRO-seq from HCT116 cells in normoxia and hypoxia

Project description:PRO-seq from HCT116 cells in normoxia and hypoxia

| PRJNA607559 | ENA

Common and distinct functions of mouse Dot1l in the regulation of endothelial transcriptome

Project description:Epigenetic mechanisms are mandatory for endothelial cells (ECs) during cardiovascular development. Dot1l-mediated gene transcription in mice is essential for development and function of lymphatic ECs (LECs). The role of Dot1l in development and function of blood ECs (BECs) is unclear. RNA-seq datasets from Dot1l-depleted or -overexpressing BECs and LECs were used to comprehensively analyze regulatory networks of gene transcription and pathways. Dot1l depletion in BECs changed the expression of genes involving cell-to-cell adhesion and immunity-related biological processes. Dot1l overexpression changed the expression of genes involved in different types of cell-to-cell adhesion and angiogenesis-related biological processes. Genes involved in specific tissue development-related biological pathways were altered in Dot1l-depleted BECs and LECs. Vascular endothelial growth factor production-related genes were specifically regulated in BECs by Dot1l. Dot1l overexpression uniquely altered ion transportation-related genes in BECs and immune response regulation-related genes in LECs. Importantly, Dot1l overexpression in BECs led to expression of many genes related to the angiogenesis and mitogen-activated protein kinase signaling pathways. The expression of these genes was unchanged in Dot1l-overexpressing LECs. The findings demonstrate the unique transcriptomic program of ECs and the differential functions of Dot1l in the regulation of gene transcription in BECs and LECs.

2022-10-11 | GSE214945 | GEO

DOT1L regulates pericentromeric heterochromatin

Project description:Many repetitive DNA elements are packaged in heterochromatin, but depend on occasional transcription to maintain long-term silencing. The factors that promote transcription of repeat elements in heterochromatin are largely unknown. Here, we show that DOT1L, a histone methyltransferase that modifies lysine 79 of histone H3 (H3K79), is required for transcription of major satellite repeats to maintain pericentromeric heterochromatin (PCH), and that this function is essential for preimplantation development. DOT1L is a transcriptional activator at single-copy genes but does not have a known role in repeat element transcription. We show that H3K79me3 is specifically enriched at repetitive elements, that loss of DOT1L compromises pericentromeric major satellite transcription, and that this function depends on interaction between DOT1L and the chromatin remodeler SMARCA5. DOT1L inhibition causes chromosome breaks and cell cycle defects, and leads to embryonic lethality. Together, our findings uncover a vital new role for DOT1L in transcriptional activation of heterochromatic repeats.

2023-05-26 | PXD028824 | Pride

Targeting DOT1L and EZH2 synergizes in breaking the germinal center identity of Diffuse Large B Cell Lymphoma

Project description:Differentiation of antigen-activated B cells into pro-proliferative germinal center (GC) B cells depends on the activity of the transcription factors MYC and BCL6, and the epigenetic writers DOT1L and EZH2. GCB-like Diffuse Large B Cell Lymphomas (GCB-DLBCLs) arise from GC B cells and closely resemble their cell of origin. Given the dependency of GC B cells on DOT1L and EZH2, we investigated the role of these epigenetic regulators in GCB-DLBCL cell lines and observed that GCB-DLBCLs synergistically depend on the combined activity of DOT1L and EZH2. Mechanistically, inhibiting both enzymes led to enhanced derepression of PRC2 target genes compared to EZH2 single treatment, along with the derepression of BCL6 target genes and suppression of MYC target genes. The sum of all these alterations results in a ‘cell identity crisis,’ wherein GCB-DLBCLs lose their pro-proliferative GC identity and partially undergo plasma cell differentiation, a state associated with poor survival. In support of this model, combined epi-drugging of DOT1L and EZH2 prohibited the outgrowth of human GCB-DLBCL xenografts in vivo. We conclude that the malignant behavior of GCB-DLBCLs strongly depends on DOT1L and EZH2 and that combined targeting of both epigenetic writers may provide an alternative differentiation-based treatment modality for GCB-DLBCL.

2025-10-14 | PXD056212 | Pride

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