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Distal regulation of c-myb expression during IL-6 inudced differentiation in murine myeloid progenitor M1 cells [DHS-seq]

ABSTRACT: We report DNAase1 hypersensitive sites located upstream of the c-myb gene,associated with gene expression

ORGANISM(S): Mus musculus

PROVIDER: GSE81030 | GEO | 2017/02/21

SECONDARY ACCESSION(S): PRJNA320316

REPOSITORIES: GEO

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Distal regulation of c-myb expression during IL-6 induced differentiation in murine myeloid progenitor M1 cells [4C-seq]

Project description:We report genome-wide long-range interactions of the c-myb promoter in M1 cells.

2017-02-21 | GSE81029 | GEO

Distal regulation of c-myb expression during IL-6-induced differentiation in murine myeloid progenitor M1 cells.

Project description:The c-Myb transcription factor is a major regulator that controls differentiation and proliferation of hematopoietic progenitor cells, which is frequently deregulated in hematological diseases, such as lymphoma and leukemia. Understanding of the mechanisms regulating the transcription of c-myb gene is challenging as it lacks a typical promoter and multiple factors are involved. Our previous studies identified some distal regulatory elements in the upstream regions of c-myb gene in murine myeloid progenitor M1 cells, but the detailed mechanisms still remain unclear. In the present study, we found that a cell differentiation-related DNase1 hypersensitive site is located at a -28k region upstream of c-myb gene and that transcription factors Hoxa9, Meis1 and PU.1 bind to the -28k region. Circular chromosome conformation capture (4C) assay confirmed the interaction between the -28k region and the c-myb promoter, which is supported by the enrichment of CTCF and Cohesin. Our analysis also points to a critical role for Hoxa9 and PU.1 in distal regulation of c-myb expression in murine myeloid cells and cell differentiation. Overexpression of Hoxa9 disrupted the IL-6-induced differentiation of M1 cells and upregulated c-myb expression through binding of the -28k region. Taken together, our results provide an evidence for critical role of the -28k region in distal regulatory mechanism for c-myb gene expression during differentiation of myeloid progenitor M1 cells.

| S-EPMC5059869 | biostudies-literature

Distal regulation of c-myb expression in human myeloid leukemia cells

Project description:The transcription factor c-Myb a key regulator in proliferation and differentiation of hematopoietic progenitor cells, is precisely regulated during essential cellular processes. Overexpression and rearrangement of c-myb has been reported in human tumors including myeloid leukemia, but exact regulatory mechanisms have remained elusive. Here, we identified, using 4C assay with the c-myb promoter as an anchor, the interaction site at -34k region upstream of c-myb gene that are involved in c-myb expression. Furthermore, we found that the long-range interactions changed with c-myb being down-regulated on differentiation progress in human myeloid leukemia cell lines. Taken together, our date revealed that a potential c-myb enhancer-promoter interactions may be a particularly important regulatory mechanism for c-myb gene expression in human myeloid leukemia cells.

2020-11-13 | GSE140321 | GEO

Distal regulation of c-myb expression during IL-6 induced differentiation in murine myeloid progenitor M1 cells

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

2017-02-21 | GSE81031 | GEO

Genome-wide Myb chromatin occupancy in murine myeloid progenitor cells

Project description: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

2011-02-23 | E-GEOD-22095 | biostudies-arrayexpress

Distal regulation of c-myb expression during IL-6 induced differentiation in murine myeloid progenitor M1 cells

Project description:Distal regulation of c-myb expression during IL-6 induced differentiation in murine myeloid progenitor M1 cells

| PRJNA320313 | ENA

Genome-wide Myb chromatin occupancy in murine myeloid progenitor cells

Project description: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 - β-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.

2011-02-23 | GSE22095 | GEO

B-myb is Essential Regulator of Hematopoietic Stem Cell and Myeloid Progenitor Cell Development

Project description:The B-myb (MYBL2) gene is a member of the MYB family of transcription factors and is involved in cell cycle regulation, DNA replication and maintenance of genomic integrity. However, its function during adult development and hematopoiesis is unknown. We show here that conditional inactivation of B-myb in vivo results in depletion of the HSC pool, leading to profound reductions in mature lymphoid, erythroid and myeloid cells. This defect is autonomous to the bone marrow and is first evident in the HSCs, which accumulate in the S and G2/M phases. B-myb inactivation also causes defects in the myeloid progenitor compartment and results in an accumulation of GMPs. Microarray studies indicate that B-myb null LKS+ cells differentially express genes that direct myeloid lineage development and commitment, suggesting that B-myb is a key player in controlling cell fate. Collectively, these studies demonstrate that B-myb is essential for HSC and progenitor maintenance and survival during hematopoiesis. Total RNA was isolated from FACS purified LKS+ cells isolated from pIpC-treated control and B-myb floxed-MxCre mice. Each sample is derived from a pool of 3-5 mice. 2 samples were analyzed for each genotype.

2014-02-12 | E-GEOD-53875 | biostudies-arrayexpress

B-myb is Essential Regulator of Hematopoietic Stem Cell and Myeloid Progenitor Cell Development

2014-02-12 | GSE53875 | GEO

ChIP-on-chip from murine myeloid cell line M1 and virus-induced myeloid leukemia cell lines for H3K4me3, H3K9/14ac, H3K4me1, H3K27me3, H3K9me3 and CTCF

Project description:Histone modifcations and CTCF binding at the c-myb locus were compared in cell lines with c-myb expressing, which are myeloblatic M1 cells and leukemia cells with virus integration, VS. M1 cells without c-myb expression induced by IL-6. Distribution of active histone marks at the c-myb gene and the upstream regions are associated with active c-myb transcription. The enrichment of all of these active histone marks decreased with differentiation-induced down-regulation of c-myb, but increased and spread in tumor cells. ChIP-on-chip from murine myeloid cell line M1 and virus-induced myeloid leukemia cell lines for H3K4me3, H3K9/14ac, H3K4me1, H3K27me3, H3K9me3 and CTCF

2012-09-01 | E-GEOD-34770 | biostudies-arrayexpress

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