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Chromatin accessibility promotes hematopoietic and leukemia stem cell activity [ATAC-seq]

ABSTRACT: Chromatin accessibility promotes hematopoietic and leukemia stem cell activity [ATAC-seq]

PROVIDER: PRJNA601825 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10906501_1.fastq.gz	Fastqsanger.gz
	SRR10906501_2.fastq.gz	Fastqsanger.gz
	SRR10906502_1.fastq.gz	Fastqsanger.gz
	SRR10906502_2.fastq.gz	Fastqsanger.gz
	SRR10906503_1.fastq.gz	Fastqsanger.gz

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Chromatin accessibility promotes hematopoietic and leukemia stem cell activity

Project description:Chromatin organization is a highly orchestrated process that influences gene expression, in part by modulating access of regulatory factors to DNA and nucleosomes. We found that the chromatin accessibility regulator HMGN1, a target of recurrent DNA copy gains in leukemia, controls myeloid differentiation. HMGN1 amplification was associated with increased accessibility, expression, and histone H3K27 acetylation of loci important for hematopoietic stem cell (HSC) function and AML, such as HoxA cluster genes. In vivo, HMGN1 overexpression was linked to decreased quiescence and increased HSC activity in bone marrow transplantation. HMGN1 overexpression also cooperated with the AML-ETO9a fusion oncoprotein to impair myeloid differentiation and enhance leukemia stem cell (LSC) activity. Inhibition of histone acetyltransferases CBP/p300 relieved the HMGN1-associated differentiation block. These data nominate factors that modulate chromatin accessibility as regulators of HSCs and LSCs and suggest that targeting HMGN1 or its downstream effects on histone acetylation could be therapeutically active in AML.

2020-02-25 | PXD017054 | Pride

Chromatin accessibility promotes hematopoietic and leukemia stem cell activity

Project description:Chromatin accessibility promotes hematopoietic and leukemia stem cell activity

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Chromatin accessibility promotes hematopoietic and leukemia stem cell activity [ATAC-seq]

Project description:In this project, we studied how the nucleosome binding protein HMGN1 affects myeloid differentiation and hematopoietic and leukemia stem cell activity.

2020-02-05 | GSE143840 | GEO

Chromatin accessibility promotes hematopoietic and leukemia stem cell activity [RNA-seq]

Project description:Chromatin accessibility promotes hematopoietic and leukemia stem cell activity [RNA-seq]

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Chromatin accessibility promotes hematopoietic and leukemia stem cell activity [ChIP-seq]

Project description:Chromatin accessibility promotes hematopoietic and leukemia stem cell activity [ChIP-seq]

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Chromatin accessibility promotes hematopoietic and leukemia stem cell activity [ChIP-seq]

Project description:In this project, we studied how the nucleosome binding protein HMGN1 affects myeloid differentiation and hematopoietic and leukemia stem cell activity.

2020-02-05 | GSE143682 | GEO

Chromatin accessibility promotes hematopoietic and leukemia stem cell activity [RNA-seq]

Project description:In this project, we studied how the nucleosome binding protein HMGN1 affects myeloid differentiation and hematopoietic and leukemia stem cell activity

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ATAC-seq data

Project description:A single hematopoietic stem cell can give rise to all blood cells with remarkable fidelity. Here, we define the chromatin accessibility and transcriptional landscape controlling this process in thirteen primary cell types that traverse the hematopoietic hierarchy. Exploiting the finding that enhancer landscapes better reflect cell identity than mRNA levels, we enable "enhancer cytometry" for accurate enumeration of pure cell types from complex populations. We further reveal the lineage ontogeny of genetic elements linked to diverse human diseases. In acute myeloid leukemia, chromatin accessibility reveals distinctive regulatory evolution in pre-leukemic HSCs (pHSCs), leukemia stem cells, and leukemic blasts. These leukemic cells demonstrate unique lineage infidelity, confirmed by single cell regulomes. We further show that pHSCs have a competitive advantage that is conferred by reduced chromatin accessibility at HOXA9 targets and is associated with adverse patient outcomes. Thus, regulome dynamics can provide diverse insights into human hematopoietic development and disease. ATAC-seq profiles of hematopoietic and leukemic cell types, across 13 normal hematopoietic cell types and 3 acute myeloid leukemia cell types. The complete data set contains a total of 132 samples.

2016-06-01 | E-GEOD-74912 | biostudies-arrayexpress

Single-cell chromatin accessibility data using scATAC-seq

Project description:A single hematopoietic stem cell can give rise to all blood cells with remarkable fidelity. Here, we define the chromatin accessibility and transcriptional landscape controlling this process in thirteen primary cell types that traverse the hematopoietic hierarchy. Exploiting the finding that enhancer landscapes better reflect cell identity than mRNA levels, we enable "enhancer cytometry" for accurate enumeration of pure cell types from complex populations. We further reveal the lineage ontogeny of genetic elements linked to diverse human diseases. In acute myeloid leukemia, chromatin accessibility reveals distinctive regulatory evolution in pre-leukemic HSCs (pHSCs), leukemia stem cells, and leukemic blasts. These leukemic cells demonstrate unique lineage infidelity, confirmed by single cell regulomes. We further show that pHSCs have a competitive advantage that is conferred by reduced chromatin accessibility at HOXA9 targets and is associated with adverse patient outcomes. Thus, regulome dynamics can provide diverse insights into human hematopoietic development and disease. Single-cell ATAC-seq of LMPPs, Monocytes, LSCs and Luekemic blast cells.

2016-06-01 | E-GEOD-74310 | biostudies-arrayexpress

Hematopoietic differentiation is required for initiation of acute myeloid leukemia [ATAC-seq]

Project description:Leukemia initiating cells (LICs) of acute myeloid leukemia (AML) may arise from self-renewing hematopoietic stem cells (HSCs) and from committed progenitors. However, it remains unclear how leukemia-associated oncogenes instruct LIC formation from cells of different origins and if differentiation along the normal hematopoietic hierarchy is involved. Here, using murine models with the driver mutations MLL-AF9 or MOZ-TIF2, we found that regardless of the transformed cell types, myelomonocytic differentiation to the granulocyte macrophage progenitor (GMP) stage is critical for LIC generation. Blocking myeloid differentiation through disrupting the lineage-restricted transcription factor C/EBPa eliminates GMPs, blocks normal granulopoiesis, and prevents AML development. In contrast, restoring myeloid differentiation through inflammatory cytokines “rescues” AML transformation. Our findings identify myeloid differentiation as a critical step in LIC formation and AML development, thus guiding new therapeutic approaches. Examination of chromatin accessibility in Cebpa knock-out and control conditions.

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