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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Identification and characterization of Hoxa9 binding sites in hematopoietic cells

ABSTRACT: This SuperSeries is composed of the following subset Series: GSE21299: Expression data from murine cell line transduced with epitope tagged forms of Hoxa9 GSE33509: Identification and Characterization of Hoxa9 Binding Sites in Hematopoietic Cells GSE33517: Epigenetic profiling of histone H3K4me1, H3K4me3, H3K27me3, H3ac, H4ac, CBP and P300 using ChIP-chip Refer to individual Series

ORGANISM(S): Mus musculus

SUBMITTER: Yongsheng Huang

PROVIDER: E-GEOD-33518 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Identification and Characterization of Hoxa9 Binding Sites in Hematopoietic Cells

Project description:The clustered homeobox proteins play crucial roles in development, hematopoiesis and leukemia yet the targets they regulate and their mechanisms of action are poorly understood. Here, we identified the binding sites for Hoxa9 and the Hox cofactor Meis1 on a genome-wide level and profiled their associated epigenetic modifications and transcriptional targets. Hoxa9 and the Hox cofactor Meis1 co-bind at hundreds of highly evolutionarily-conserved sites, most of which are distant from transcription start sites. These sites show high levels of histone H3K4 monomethylation and CBP/P300 binding characteristic of enhancers. Furthermore, a subset of these sites shows enhancer activity in transient transfection assays. Many Hoxa9 and Meis1 binding sites are also bound by PU.1 and other lineage-restricted transcription factors previously implicated in establishment of myeloid enhancers. Conditional Hoxa9 activation is associated with CBP/P300 recruitment, histone acetylation and transcriptional activation of a network of proto-oncogenes including Erg, Flt3, Lmo2, Myb and Sox4. Collectively this work suggests that Hoxa9 regulates transcription by interacting with enhancers of genes important for hematopoiesis and leukemia. To identify the genome-wide binding sites for Hoxa9 and the Hox cofactor Meis1

2011-12-04 | E-GEOD-33509 | biostudies-arrayexpress

Epigenetic profiling of histone H3K4me1, H3K4me3, H3K27me3, H3ac, H4ac, CBP and P300 using ChIP-chip

Project description:The clustered homeobox proteins play crucial roles in development, hematopoiesis and leukemia yet the targets they regulate and their mechanisms of action are poorly understood. Here, we identified the binding sites for Hoxa9 and the Hox cofactor Meis1 on a genome-wide level and profiled their associated epigenetic modifications and transcriptional targets. Hoxa9 and the Hox cofactor Meis1 co-bind at hundreds of highly evolutionarily-conserved sites, most of which are distant from transcription start sites. These sites show high levels of histone H3K4 monomethylation and CBP/P300 binding characteristic of enhancers. Furthermore, a subset of these sites shows enhancer activity in transient transfection assays. Many Hoxa9 and Meis1 binding sites are also bound by PU.1 and other lineage-restricted transcription factors previously implicated in establishment of myeloid enhancers. Conditional Hoxa9 activation is associated with CBP/P300 recruitment, histone acetylation and transcriptional activation of a network of proto-oncogenes including Erg, Flt3, Lmo2, Myb and Sox4. Collectively this work suggests that Hoxa9 regulates transcription by interacting with enhancers of genes important for hematopoiesis and leukemia. Enriched Hoxa9 and Meis1 regions and a selected set of the nearest 360 TSSs were tiled onto Nimblegen custom arrays (Mus musculus 8, Feb 2006) with 50-mer probes (average spacing of 35bp), along with 60 negative control sequences that were selected randomly from the mouse genome

2011-11-09 | E-GEOD-33517 | biostudies-arrayexpress

Genome-wide co-occupancy of Hoxa9 and C/EBPα in Hoxa9/Meis1 transformed HSCs [ChIP-seq]

Project description:Identification of the genome-wide binding sites of Hoxa9 and C/EBPα in a murine myeloblastic cell line transformed by Hoxa9/Meis1. Over 50% of Hoxa9 binding sites are co-bound by C/EBPα, providing mechanistic insight into the requirement of C/EBPα for Hoxa9-mediated leukemogenesis. Additionally, genome-wide occupancy of H3K4 monomethylation and H3K27 trimethylation provide additional information on the functionality of Hoxa9/C/EBPα cobound loci. Examination of two transcription factor binding sites and two histone modifications in a transformed cell line.

2014-06-11 | E-GEOD-58361 | biostudies-arrayexpress

Gene expression changes after loss of Hoxa9 in transformed HSCs [HOXA9 RNA-seq]

Project description:Characterization of gene expression changes 72 hours after withdrawal of tamoxifen in murine hematopoietic progenitors transformed by Hoxa9-ER/Meis1 using RNAseq. In the presence of tamoxifen (4OHT), Hoxa9-ER localizes to the nucleus of cells allowing for transformation, while withdrawal of 4OHT (culture in EtOH) leads to loss of nuclear Hoxa9-ER. Loss of Hoxa9-ER leads to a decrease in cellular proliferation and differentiation along the myeloid lineage. Examination of gene expression by RNAseq in two conditions in biological replicates.

2014-06-11 | E-GEOD-58359 | biostudies-arrayexpress

Gene expression changes after loss of C/EBPα in transformed HSCs [CEBPA RNA-seq]

Project description:RNAseq characterization of gene expression changes 72 hours after genomic excision of Cebpa in murine hematopoietic progenitors from Cebpaf/f;CreER mice transformed by Hoxa9/Meis1. In the presence of tamoxifen (4OHT), Cre-ER localizes to the nucleus of cells allowing for excision of Cebpa and loss of C/EBPα protein levels. Loss of C/EBPα leads to a decrease in cellular proliferation. Examination of gene expression by RNAseq in two conditions in biological replicates.

2014-06-11 | E-GEOD-58360 | biostudies-arrayexpress

Identification of genome wide Hoxa9 binding sites in primary murine and human AML cells

Project description:Relative overexpression of HOXA9 is a key feature of aggressive AML (acute myeloid leukemia). Here we determined genome wide binding sites of Hoxa9 in primary murine cells transformed by Hoxa9 and in a human AML cell line. In addition global H3K4 monomethylation and H3K27acetylation levels were determined in cells transformed by an inducible Hoxa9-ER construct in Hoxa9-active conditions and 72h after Hoxa9 was inactivated.

2019-04-13 | E-MTAB-7108 | biostudies-arrayexpress

Gene expression signature of HoxA9-Meis1 AML cells treated with Pyrydopyrazine

Project description:Pyrydopyrazine A2 induced in vitro the differentiation of leukemic cells (HoxA9-Meis1) into macrophages, we decided to perform a transcriptomic study in order to analyze the GM-CSF pathway regulation. We therefore compared effect with A2 to cells treated with Retinoic acid and D3 Vitamin, a combination known to induce also differentiation of leukemic cells. HoxA9-Meis1 murine AML cells were treated in vitro during 24h, with Pyrydopyrazine( A2) at 3.4μM or a combination of all-trans Retinoic Acid (RA) and 1α-hydroxy-D3 Vitamin (D3V), 10μM each. Gene expression signature was compared to untreated control. One sample was tested for each condition

2015-09-02 | E-GEOD-72635 | biostudies-arrayexpress

Regulation of gene expression through genome-wide co-binding of Hoxa9 and C/EBPα in transformed HSCs

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

2014-06-11 | E-GEOD-58362 | biostudies-arrayexpress

Gene expression profiling of Hox-driven AML overexpressing JMJD1C

Project description:JMJD1C, a Jumonji C (JmjC) domain-containing histone demethylase, has been reported as a direct cofactor of oncogenic transcription factor HOXA9. To identify JMJD1C downstream effectors, we performed a genome-wide gene expression profiling experiment. Our microarray analysis identified a new role for JMJD1C in regulating a cancer metabolic program in HOX-driven AML. GFP+ HOXA9/MEIS1-mediated pre-leukemic stem cells were transduced with retroviruses carrying JMJD1C or empty vector for the microarray experiment. Each group has 4 samples.

2018-12-30 | E-MTAB-5760 | biostudies-arrayexpress

Expression data from miR-223KO and miR-223WT bone marrow cells

Project description:Total bone marrow (BM) from miR-223 knockout (mir-223-/-) and wildtype (miR-223+/+) mice 21 was extracted, prestimulated for 2 days. Then, the BM cells were simultaneously cotransduced with MSCV-Hoxa9-pgk-neomycin and a MSCV-Meis1-IRES-YFP by co-cultivation with irradiated (4,000 cGy) viral producers. HoxA9-Meis1 transduced cells were sorted for YFP expression and continuously selected with neomycin (1.4 mg/ml). Processing of the pre-miRNA through Dicer1 generates a miRNA duplex, consisting of a miRNA and miRNA* strand. Despite the general view that miRNA*s have no functional role, we further investigated miRNA* species in 10 deep sequencing libraries from mouse and human tissue. Comparing miRNA/miRNA* ratios across the miRNA sequence libraries revealed that 50% of the investigated miRNA duplexes exhibit a highly dominant strand. Conversely, 10% of miRNA duplexes show a comparable expression of both strands, while the remaining 40% exhibit variable ratios across the examined libraries as exemplified by miR-223/miR-223* in murine and human cell lines. Functional analyses revealed a regulatory role for miR-223* in myeloid progenitor cells, implying an active role for both arms of the miR-223 duplex. This was further underscored by the demonstration that miR-223 and miR-223* target the IGF1R/PIK3 axis and that high miR-223* levels associate with increased overall survival in acute myeloid leukemia (AML) patients. Thus, we found a supporting role for miR-223* in differentiating myeloid cells in normal as well as the leukemic cell state. The fact that the miR-223 duplex acts through both arms extends the complexity of miRNA-directed gene regulation of this myeloid key miRNA. 2 biological replicates

2011-05-24 | E-GEOD-29453 | biostudies-arrayexpress

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