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H3K79me2 ChIP-seq and RNA-seq analysis of murine AML with DOT1L overexpressed

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE134046 | GEO | 2019/07/10

REPOSITORIES: GEO

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H3K79me2 ChIP-seq analysis of murine AML with DOT1L overexpressed

Project description:We transduced two individual murine KMT2A-MLLT3 AML samples with DOT1L and three days after sorting for DOT1L+ cells were collected for ChIP-Seq. Before beginning the ChIP protocol drosophila melanogaster (S2) cells were spiked in at a 1:2 ratio.

2019-07-10 | GSE134030 | GEO

H3K79me2 ChIP-seq analysis of murine AML with DOT1L overexpressed

Project description:H3K79me2 ChIP-seq analysis of murine AML with DOT1L overexpressed

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H3K79me2 ChIP-seq and RNA-seq analysis of murine AML with DOT1L overexpressed

Project description:H3K79me2 ChIP-seq and RNA-seq analysis of murine AML with DOT1L overexpressed

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Expression profiling and H3K79me2 ChIP-seq in Prostate cancer cells treated with DOT1L inhibitor

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-08-09 | GSE135575 | GEO

The Histone Methyltransferases MLL1 and DOT1L Cooperate with Meningioma-1 to Induce AML

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

2016-01-12 | E-GEOD-76750 | biostudies-arrayexpress

DOT1L-mediated murine neuronal differentiation associates with H3K79me2 accumulation and preserves SOX2-enhancer accessibility.

Project description:During neuronal differentiation, the transcriptional profile and the epigenetic context of neural committed cells is subject to significant rearrangements, but a systematic quantification of global histone modification changes is still missing. Here, we show that H3K79me2 increases and H3K27ac decreases globally during in-vitro neuronal differentiation of murine embryonic stem cells. DOT1L mediates all three degrees of methylation of H3K79 and its enzymatic activity is critical to modulate cellular differentiation and reprogramming. In this context, we find that inhibition of DOT1L in neural progenitor cells biases the transcriptional state towards neuronal differentiation, resulting in transcriptional upregulation of genes marked with H3K27me3 on the promoter region. We further show that DOT1L inhibition affects accessibility of SOX2-bound enhancers and impairs SOX2 binding in neural progenitors. Our work provides evidence that DOT1L activity gates differentiation of progenitors by allowing SOX2-dependent transcription of stemness programs.

| S-EPMC7562744 | biostudies-literature

RNA-seq and ChIP-seq analysis of HA-JICD1 and NICD1 overexpressed Ink4a-/- murine astrocytes

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-02-01 | GSE126855 | GEO

Nucleophosmin 1 regulates H3K79me2 levels and peri-nucleolar heterochromatin organization through interaction with the methyltransferase DOT1L

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-01-01 | GSE223363 | GEO

The Histone Methyltransferases MLL1 and DOT1L Cooperate with Meningioma-1 to Induce AML

Project description:This SuperSeries is composed of the SubSeries listed below.

2016-01-12 | GSE76750 | GEO

DOT1L-mediated H3K79me2 modification critically regulates gene expression during cardiomyocyte differentiation.

Project description:Epigenetic changes on DNA and chromatin are implicated in cell differentiation and organogenesis. For the heart, distinct histone methylation profiles were recently linked to stage-specific gene expression programs during cardiac differentiation in vitro. However, the enzymes catalyzing these modifications and the genes regulated by them remain poorly defined. We therefore decided to identify the epigenetic enzymes that are potentially involved in cardiomyogenesis by analyzing the expression profile of the 85 genes encoding the epigenetic-related proteins in mouse cardiomyocytes (CMs), and then study how they affect gene expression during differentiation and maturation of this cell type. We show here with gene expression screening of epigenetic enzymes that the highly expressed H3 methyltransferase disruptor of telomeric silencing 1-like (DOT1L) drives a transitional pattern of di-methylation on H3 lysine 79 (H3K79) in CMs at different stages of differentiation in vitro and in vivo. Through a genome-wide chromatin-immunoprecipitation DNA-sequencing approach, we found H3K79me2 enriched at genes expressed during cardiac differentiation. Moreover, knockdown of Dot1L affected the expression of H3K79me2-enriched genes. Our results demonstrate that histone methylation, and in particular DOT1L-mediated H3K79me2 modification, drives cardiomyogenesis through the definition of a specific transcriptional landscape.

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