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Mus musculus

ABSTRACT: Time-course HoxB4 ChIP-Seq during HSC development from ES cells

OTHER RELATED OMICS DATASETS IN: E-GEOD-33953

PROVIDER: PRJNA156455 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR385644.fastq.gz	Fastqsanger.gz
	SRR385645.fastq.gz	Fastqsanger.gz
	SRR385646.fastq.gz	Fastqsanger.gz
	SRR385647.fastq.gz	Fastqsanger.gz
	SRR385648.fastq.gz	Fastqsanger.gz

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Gene expression profiling and ChIP-Seq study of HoxB4-mediated HSC development from ES cells

Project description:This SuperSeries is composed of the following subset Series: GSE33953: Time-course transcriptome measure of HoxB4-mediated HSC development from ES cells GSE34013: Time-course HoxB4 ChIP-Seq during HSC development from ES cells Refer to individual Series

2012-03-23 | E-GEOD-34014 | biostudies-arrayexpress

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Time-course HoxB4 ChIP-Seq during HSC development from ES cells

Project description:Efficient in vitro generation of hematopoietic stem cells (HSCs) from embryonic stem cells (ESCs) holds great promise for cell-based therapies of hematological diseases. To date, HoxB4 remains to be the most effective transcription factor (TF) whose over-expression in ESCs confers long-term repopulating ability to ESC-derived HSCs. Despite its importance, the components and dynamics of the HoxB4 transcriptional regulatory network is poorly understood, hindering efforts to develop a more efficient protocol for in vitro derivation of HSCs. Towards this goal, we performed global gene expression profiling and chromatin immunoprecipitation coupled with deep sequencing (ChIP-Seq) at four stages of the HoxB4-mediated HSC development. Joint analyses of ChIP-Seq and gene expression profiles unveil a number of global features of the HoxB4 regulatory network. Cells from three time points of the developmental processes were collected, including days 6, 16, and 26. Deep sequencing were done for both IP and input DNA from cells from each time point.

2012-03-23 | E-GEOD-34013 | biostudies-arrayexpress

Time-course transcriptome measure of HoxB4-mediated HSC development from ES cells

Project description:Efficient in vitro generation of hematopoietic stem cells (HSCs) from embryonic stem cells (ESCs) holds great promise for cell-based therapies of hematological diseases. To date, HoxB4 remains to be the most effective transcription factor (TF) whose over-expression in ESCs confers long-term repopulating ability to ESC-derived HSCs. Despite its importance, the components and dynamics of the HoxB4 transcriptional regulatory network is poorly understood, hindering efforts to develop a more efficient protocol for in vitro derivation of HSCs. Towards this goal, we performed global gene expression profiling and chromatin immunoprecipitation coupled with deep sequencing (ChIP-Seq) at four stages of the HoxB4-mediated HSC development. Joint analyses of ChIP-Seq and gene expression profiles unveil a number of global features of the HoxB4 regulatory network. Cells from four time points of the developmental processes were collected, including days 0, 6, 16, and 26. Triplicate microarray hybridizations were done for cells from each time point.

2012-03-23 | E-GEOD-33953 | biostudies-arrayexpress

Downstream Targets of HOXB4 in the primitive hematopoietic progenitor EML Cell line

Project description:Enforced expression of the homeobox transcription factor HOXB4 has been shown to enhance hematopoietic stem cell (HSC) self-renewal and expansion ex vivo and in vivo. In order to investigate the largely unknown downstream targets of HOXB4 in hematopoietic progenitor cells, HOXB4 was constitutively overexpressed in the primitive hematopoietic progenitor cell line, EML. Gene expression differences were compared between KLS (c-Kit+, Lin-, Sca-1+)-EML cells that overexpressed HOXB4 (KLS-EML-HOXB4) to control KLS-EML cells that were transduced with vector alone. ChIP-chip was used to identify promoter regions bound by HOXB4.

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Project description:Overexpression of HOXB4 in hematopoietic stem cells (HSCs) leads to increased self-renewal without causing hematopoietic malignancies in transplanted mice. The molecular basis of HOXB4-mediated benign HSC expansion in vivo is not well understood. To gain further insight into the molecular events underlying HOXB4-mediated HSC expansion, we analyzed gene expression changes at multiple time points in Lin-Sca1+c-kit+ (LSK) cells from mice transplanted with bone marrow (BM) cells transduced with a MSCV-HOXB4-ires-YFP vector. A distinct HOXB4 transcriptional program was reproducibly induced and stabilized by 12 weeks after transplant. Dynamic expression changes were observed in genes critical for HSC self-renewal as well as genes involved in myeloid and B cell differentiation. Prdm16, a transcription factor associated with human acute myeloid leukemia (AML), was markedly repressed by HOXB4 but upregulated by HOXA9 and HOXA10, suggesting that Prdm16 downregulation was involved in preventing leukemia in HOXB4 transplanted mice. Functional evidence to support this mechanism was obtained by enforcing co-expression of sPrdm16 and HOXB4, which led to enhanced self-renewal, myeloid expansion, and leukemia. Altogether, these studies define the transcriptional pathways involved in HOXB4 HSC expansion in vivo and identify repression of Prdm16 transcription as a mechanism by which expanding HSCs avoid leukemic transformation.

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