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CTCF is dispensable for cell fate conversion but facilitates acute cellular responses [ATAC-seq]

ABSTRACT: CTCF is dispensable for cell fate conversion but facilitates acute cellular responses [ATAC-seq]

PROVIDER: PRJNA596486 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10734278_1.fastq.gz	Fastqsanger.gz
	SRR10734278_2.fastq.gz	Fastqsanger.gz
	SRR10734279_1.fastq.gz	Fastqsanger.gz
	SRR10734279_2.fastq.gz	Fastqsanger.gz

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CTCF is dispensable for cell fate conversion but facilitates acute cellular responses

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CTCF is dispensable for cell fate conversion but facilitates acute cellular responses [RNA-Seq]

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CTCF is dispensable for cell fate conversion but facilitates acute cellular responses [Hi-C]

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CTCF is dispensable for cell fate conversion but facilitates acute cellular responses [ATAC-seq]

Project description:Studies of genome topology, chromatin state and gene expression dynamic during human B cell to macrophage transdifferentiation with and without CTCF

2020-05-06 | GSE142301 | GEO

CTCF is dispensable for cell fate conversion but facilitates acute cellular responses [ChIP-seq]

Project description:Studies of genome topology, chromatin state and gene expression dynamic during human B cell to macrophage transdifferentiation with and without CTCF

2020-05-06 | GSE142161 | GEO

CTCF is dispensable for cell fate conversion but facilitates acute cellular responses [Hi-C]

Project description:Studies of genome topology, chromatin state and gene expression dynamic during human B cell to macrophage transdifferentiation with and without CTCF

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CTCF is dispensable for cell fate conversion but facilitates acute cellular responses [RNA-Seq]

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CTCF is dispensable for cell fate conversion but facilitates acute cellular responses

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

2020-05-06 | GSE140528 | GEO

Oncogenic fate conversion by PRDM16s causes acute myeloid leukemia

Project description:Oncogenic mutations confer aberrant replicative capacity to cells with little or no replicative capacity, generating cancer stem cells that perpetuate the tumor through extensive self-replication and differentiation blockade. However, whether oncogenes disrupt the cellular identity ofcancer stem cell by altering the developmental potential is unknown. Fate conversion has been demonstrated by ectopic expression of master transcriptional regulators, such as PU.1 and C/EBP alpha that confers myeloid cell fate to other cell types, and PRDM16 that confers brown adipose fate to white adipocytes or myoblasts. Here we show that a transcriptional regulator overexpressed in human myeloid malignancies, PRDM16s, causes oncogenic fate conversion, by transforming cells fated to form platelets and erythrocytes into myeloid leukemia-initiating cells (LICs). Prdm16s expression in hematopoietic progenitor cells caused a myelodysplastic syndrome (MDS)-like disease that progressed to acute myelogenous leukemia (AML). The myeloid diseases caused by Prdm16s exhibited expansion of megakaryocyte-erythroid progenitors (MEPs) but not granulocyte-macrophage progenitors. MEPs from Prdm16s-induced leukemia possessed LIC potential, and expression of Prdm16s in normal MEPs was sufficient to convert them to myeloid LICs and blocked megakaryocytic/erythroid potential. Prdm16s induced the expression of myeloid master regulators, including PU.1 and C/EBP alpha, by interacting with their super enhancers. Ablation of myeloid master regulators attenuated the myeloid potential and reinstalled the megakaryocytic/erythroid potential of leukemic-MEPs in mouse models and in human AML with PRDM16 rearrangement. Our study demonstrates that oncogenic Prdm16 expression converts the fate of MEPs to a malignant myeloid fate by activating myeloid master transcription factors.

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