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Genome-wide map of MAZ transcription factor in primary human erythroid cells

ABSTRACT: We report the distribution of binding sites of Myc-associated zinc finger (MAZ) transcription factor in primary human erythroid cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE139281 | GEO | 2021/06/30

REPOSITORIES: GEO

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MAZ induces MYB expression during the exit from quiescence via the E2F site in the MYB promoter

Project description:Most E2F-binding sites repress transcription through the recruitment of Retinoblasoma (RB) family members until the end of the G1 cell-cycle phase. Although the MYB promoter contains an E2F-binding site, its transcription is activated shortly after the exit from quiescence, before RB family members inactivation, by unknown mechanisms. We had previously uncovered a nuclear factor distinct from E2F, Myb-sp, whose DNA-binding site overlapped the E2F element and had hypothesized that this factor might overcome the transcriptional repression of MYB by E2F-RB family members. We have purified Myb-sp and discovered that Myc-associated zinc finger proteins (MAZ) are major components. We show that various MAZ isoforms are present in Myb-sp and activate transcription via the MYB-E2F element. Moreover, while forced RB or p130 expression repressed the activity of a luciferase reporter driven by the MYB-E2F element, co-expression of MAZ proteins not only reverted repression, but also activated transcription. Finally, we show that MAZ binds the MYB promoter in vivo, that its binding site is critical for MYB transactivation, and that MAZ knockdown inhibits MYB expression during the exit from quiescence. Together, these data indicate that MAZ is essential to bypass MYB promoter repression by RB family members and to induce MYB expression.

2017-10-04 | PXD006857 | Pride

Genome-wide map of MAZ transcription factor in primary human erythroid cells

Project description:Genome-wide map of MAZ transcription factor in primary human erythroid cells

| PRJNA579097 | ENA

CRISPR and biochemical screens Identify MAZ as a co-factor in CTCF-mediated insulation at Hox Clusters

Project description:In this experiment, we sought to identify how the distribution of MAZ change in WT, MAZ HoxA(Δ5|6), and MAZ HoxD(Δ4|8) cells during differentiation of mouse embryonic stem cells (ESCs) into cervical motor neurons (MNs)

2022-02-06 | GSE190991 | GEO

CRISPR and biochemical screens Identify MAZ as a co-factor in CTCF-mediated insulation at Hox Clusters [ChIP-seq_set6]

Project description:In this experiment, we sought to identify how the distribution of CTCF and MAZ change in WT and MAZ knock-out (KO) cells during differentiation of mouse embryonic stem cells (ESCs) into cervical motor neurons (MNs)

2022-02-06 | GSE192426 | GEO

CRISPR and biochemical screens Identify MAZ as a co-factor in CTCF-mediated insulation at Hox Clusters [ChIP-seq_set3]

Project description:In this experiment, we sought to identify how the distribution of CTCF change in WT, MAZ HoxA(Δ5|6), MAZ HoxD(Δ4|8), and CTCF (Δ5|6:6|7) cells during differentiation of mouse embryonic stem cells (ESCs) into cervical motor neurons (MNs).

2022-02-06 | GSE190989 | GEO

CRISPR and biochemical screens Identify MAZ as a co-factor in CTCF-mediated insulation at Hox Clusters [ChIP-seq_set4]

Project description:In this experiment, we sought to identify how the distribution of H3K27me3 and H3K4me3 change in WT, MAZ HoxA(delta5|6), MAZ HoxD(delta4|8), and CTCF (delta5|6:6|7) cells during differentiation of mouse embryonic stem cells (ESCs) into cervical motor neurons (MNs)

2022-02-06 | GSE190990 | GEO

CRISPR and biochemical screens Identify MAZ as a co-factor in CTCF-mediated insulation at Hox Clusters [CUT&RUN_set1]

Project description:In this experiment, we sought to identify how the distribution of CTCF, RAD21, H3K27me3 and H3K4me3 change in WT and double-positive MAZ HoxA(Δ5|6) cervical motor neurons (MNs).

2022-02-06 | GSE190987 | GEO

The Myc-Associated Zinc Finger Protein (MAZ) Works Both Independently and Together with CTCF to Control Cohesin Positioning and Genome Organization

Project description:The Myc-Associated Zinc Finger Protein (MAZ) Works Both Independently and Together with CTCF to Control Cohesin Positioning and Genome Organization

| PRJNA602294 | ENA

Downregulation of Myc is essential for terminal erythroid maturation

Project description:Terminal differentiation of mammalian erythroid progenitors involves 4-5 cell divisions and induction of many erythroid important genes, followed by chromatin and nuclear condensation and enucleation. The protein levels of c-myc (Myc) are reduced dramatically during late stage erythroid maturation, coinciding with cell cycle arrest in G1-phase and enucleation, suggesting possible roles for c-myc in either or both of these processes. Here we demonstrate that ectopic Myc expression affects terminal erythroid maturation in a dose-dependent manner. Expression of Myc at physiological levels did not affect erythroid differentiation or cell cycle shutdown, but specifically blocked erythroid nuclear condensation and enucleation. Myc prevented deacetylation of several lysine residues in histones H3 and H4 that are normally deacetylated during erythroid maturation. When over-expressed at levels higher than the physiological range, Myc blocked erythroid differentiation and the cells continued to proliferate in cytokine-free, serum-containing culture medium with an early erythroblast morphology. These studies reveal an important dose-dependent function of Myc in regulating terminal maturation in mammalian erythroid cells. Our findings further support the emerging notion that Myc regulates chromatin structure by regulating global histone acetylation states. Five groups with three biological replicates in each.

2010-10-13 | E-GEOD-18558 | biostudies-arrayexpress

Downregulation of Myc is essential for terminal erythroid maturation

2010-10-13 | GSE18558 | GEO

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