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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Genome-wide Myb chromatin occupancy in murine myeloid progenitor cells

ABSTRACT: We report genome-wide pattern of Myb chromatin occupancy in vivo. We used ERMYB, a myeloid progenitor cell line derived by transformation of primary cells by ER-Myb fusion protein, as our model system. In these cells, activation of the ER-Myb fusion protein by estrogen is required to maintain a proliferative progenitor-like phenotype. We performed ChIP-seq with biological duplicate samples from ERMYB cells with Myb either “on” or “off” (i.e. + or - ?-E2 for 6 hr). By comparing enrichment signals between Myb-on, Myb-off and isotype control samples, we identified 7,646 high-confidence Myb binding regions, which can be assigned to 4,892 annotated genes according to their distances to the nearest transcriptional start sites. Examination of Myb chromatin occupany in myeloid cells transformed by a switchable form of Myb

ORGANISM(S): Mus musculus

SUBMITTER: Evgeny Glazov

PROVIDER: E-GEOD-22095 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Integrated genome-wide chromatin occupancy and expression analyses identify key myeloid pro-differentiation transcription factors repressed by Myb.

Zhao Liang L Glazov Evgeny A EA Pattabiraman Diwakar R DR Al-Owaidi Faisal F Zhang Ping P Zhang Ping P Brown Matthew A MA Leo Paul J PJ Gonda Thomas J TJ

Nucleic acids research 20110211 11

To gain insight into the mechanisms by which the Myb transcription factor controls normal hematopoiesis and particularly, how it contributes to leukemogenesis, we mapped the genome-wide occupancy of Myb by chromatin immunoprecipitation followed by massively parallel sequencing (ChIP-Seq) in ERMYB myeloid progenitor cells. By integrating the genome occupancy data with whole genome expression profiling data, we identified a Myb-regulated transcriptional program. Gene signatures for leukemia stem c ...[more]

PMID: 21317192

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Gene expression signature of MYB-GATA overexpression plus GATA1 down regulation in undifferentiated or differentiated UT7 cells

Project description:Acute basophilic leukemia is a rare subtype of acute myeloblastic leukemia. We recently described a recurrent t(X;6)(p11;q23) translocation occurring in male infants with acute basophilic leukemia, generating a MYB-GATA1 fusion gene. To better understand the role of MYB-GATA1 in the leukemogenesis of acute basophilic leukemias, we expressed this chimeric transcription factor in the UT-7 cell line under normal or differentiating conditions. A gene expression analysis revealed 9 genes deregulated by both MYB-GATA1 and the basophilic differentiation. Three of these genes (CCL23, IL1RL1 and NTRK1) were also increased by MYB-GATA1 in CD34-positive cells, as indicated by quantitative RT-PCR. Two independant experiments (A and S) were performed. For each experiment, UT7 cells were transduced with two lentivirus: a lentivirus carrying the MYB-GATA1 (or a control) coding sequence, and a lentivirus carrying a GATA1 (or control) shRNA. Cells transduced with both lentiviruses were selected, and kept in culture under standard or differentiating conditions for 7 days before RNA extraction.

2016-09-01 | E-GEOD-72913 | biostudies-arrayexpress

c-Myb inhibits myoblast fusion

Project description:The study of the effects of modification of c-Myb expression on differenatiation of C2C12 cells

2013-10-21 | E-MTAB-1376 | biostudies-arrayexpress

Transcription profiling by array of mouse promyelocyte granulocytes with activated MYC-ER protein

Project description:The mouse promyelocyte (MPRO) granulocyte cell model expressing the MYC-ER fusion protein encoding transgene was used as a system to perform gene expression profiling in a granulocytic cell setting of low endogenous MYC expression (differentiated MYC-ER MPROs, D4) where we then activated the MYC-ER protein for 24 h with 4-OHT (D5T) as compared to a EtOH vehicle treated control (D5E).

2011-06-01 | E-MEXP-2794 | biostudies-arrayexpress

MYB silencing in CD14-myeloblasts

Project description:The c-Myb transcription factor is highly expressed in immature hematopoietic cells and down-regulated during differentiation. To define the role of c-Myb during the terminal differentiation of hematopoietic precursors, we studied the effects of its silencing in human primary CD14-myeloblasts, which maintain a granulo-monocyte differentiation bipotentiality. c-Myb-silenced myeloblasts were blocked in the G1 phase of the cell cycle at 24 hours post-nucleofection and subsequently were forced towards macrophage differentiation, as demonstrated by immunophenotypic and morphological analysis. Indeed, c-Myb-silenced CD14- cells differentiate to macrophage even after the treatment with ATRA 10-6 M, demonstrating that the c-Myb knockdown strongly impairs the ability of myeloblasts to differentiate to granulocytes. Gene expression profiling of c-Myb-silenced CD14- cells identified some potential c-Myb targets that can account for these effects. To maximize siRNA transfection efficiency, we utilized the NucleofectorTM technology (Amaxa). CD14- cells were transfected with a mixture of 3 siRNAs targeting c-Myb mRNA, with a non-targeting siRNA as a negative control (NegCTR) and without siRNA (MOCK). c-Myb siRNAs were transfected at days 1 to 3 after the CD14- myeloblasts purification based on the observation that this timing represented a phase of phisiological increase in c-Myb expression in myeloblasts. Western Blot analysis at 24 hours post-nucleofection demonstrated the c-Myb protein knockdown in MYBsiRNA CD14- cells as compared with control samples (MOCK, NegCTR).

2010-07-14 | E-GEOD-21943 | biostudies-arrayexpress

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2021-07-26 | E-MTAB-9959 | biostudies-arrayexpress

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2021-09-08 | PXD015126 | Pride

Amplicon-seq of an enhancer region targeted by CRISPR to assess the mutations introduced by different sgRNA guides

Project description:Following a CRISPR enhancer scan covering the GATA2 super-enhancer region, the top sgRNAs were selected for further inspection. MUTZ3 cells were thus treated with the selected sgRNAs and the region of interested was subjected to amplicons sequencing (amplicon-seq). To that end, we used the Illumina PCR-based custom amplicon sequencing method using the TruSeq Custom Amplicon index kit (Illumina). The same experiment was conducted in K562 cells, which do not harbor an inv(3)/t(3;3), to investigate the role of MYB in this enhancer in other leukemia settings

2021-07-26 | E-MTAB-9945 | biostudies-arrayexpress

Transcription profiling of human MCF7 cells infected with adenovirus expressing c-Myb, v-Myb or the hybrid construct, 3MutC

Project description:The transcriptional activities of c-Myb and its oncogenic variant v-Myb were compared by expressing them in human MCF7 cells using recombinant adenovirus vectors. A hybrid construct, 3Mutc, which is a variant of c-Myb harboring three v-Myb-derived DNA binding domain mutations was also analyzed. All the samples were compared to cells infected with a control adenovirus. The results showed that v-Myb, which differs from c-Myb only by N- and C-terminal deletions and eleven amino acid substitutions, has a qualitatively different transcriptional activity. Experiment Overall Design: 2 replicates of each type were analyzed. Replicates were performed independently, more than a week apart.

2007-12-12 | E-GEOD-2815 | biostudies-arrayexpress

Determination of HOXA1 and HOXA9 target genes with inducible HOX constructs

Project description:Target genes of HOXA1 and HOXA9 were determined with the help of inducible HOX-ER constructs. For this purpose bone marrow was harvested from C57BL/6 mice and c-Kit positive progenitors were enriched by magnetic sorting (MACS technology, Miltenyi, Germany). After retroviral infection by spinoculation the cells were plated for three rounds in methylcellulose. Subsequently cells were maintained in liquid culture in RPMI1640 supplemented with murine recombinant cytokines at 100ng/ml (stem cell factor) and 10ng/ml (IL-3, IL-6, granulocyte/macrophage-colony stimulating factor) as well as 100nM 4-hydroxy-tamoxifen (TAM) for HOX activation.<br><br>For microarray analysis 4 independent cell lines were created for each HOX construct. RNA was isolated from cells in the presence of TAM and 72h after withdrawal of the inductor. Pairs of RNA replicates were pooled and two +TAM as well as two -TAM duplicates per HOX gene were hybridized to Agilent44K mouse expression arrays. Array processing and evaluation was done commercially according to Agilent specifications by ImaGenes (now SourceBioScience), Berlin, Germany.

2012-11-02 | E-MEXP-3648 | biostudies-arrayexpress

MYB silencing in CD34+ progenitor cells

Project description:The c-Myb transcription factor is highly expressed in immature hematopoietic cells and down-regulated during differentiation. To define the role of c-Myb in human hematopoietic lineage commitment, we studied the effects of its silencing during the commitment of human CD34+ Hematopoietic stem/progenitor cells. In CD34+ cells c-Myb silencing determined a cell cycle arrest in G0/G1 phase which strongly decreased the clonogenic efficiency, togheter with a reduction of erythroid colonies coupled with an increase of the macrophage and megakaryocyte ones. Moreover, morphological and flow cytometry data supported the preferential macrophage and megakaryocyte differentiation of c-Myb-silenced CD34+ cells. Taken together our data indicate that c-Myb is essential for the commitment along the erythroid and granulocyte lineages but not for the macrophage and megakaryocyte differentiation. Gene expression profiling of c-Myb-silenced CD34+ cells identified some potential c-Myb targets which can account for these effects, to study by Chromatin Immunoprecipitation and Luciferase Reporter Assay. To maximize siRNA transfection efficiency, we utilized the NucleofectorTM technology (Amaxa). CD34+ cells were transfected with a mixture of 3 siRNAs targeting c-Myb mRNA and with a non-targeting siRNA as a negative control. The expression level of c-Myb protein on control cells (MOCK and negative control treated cells) and MYBsiRNA treated cells was assessed by Western Blot at 24 and 48h post-nucleofection.

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