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Genome-wide identification of genes differentially expressed between wild-type and Prdm14-deficient ES cells grown in 2i culture conditions.

ABSTRACT: Analysis of Prdm14 function in mouse embryonic stem cells. Prdm14 null and overexpressing ES cells were generated and analyzed by microarray, immunoflurescence, flow cytometry, ELISA, qPCR in different culture conditions. 2 samples (wild-type control and knockout) were analyzed in biological triplicates

ORGANISM(S): Mus musculus

SUBMITTER: Charles Bradshaw

PROVIDER: E-GEOD-45507 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Prdm14

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

2013-04-01 | E-GEOD-45509 | biostudies-arrayexpress

Genome-wide identification of genes differentially expressed between control and Prdm14 overexpressing ES cells grown in serum conditions.

Project description:Analysis of Prdm14 function in mouse embryonic stem cells. Prdm14 null and overexpressing ES cells were generated and analyzed by microarray, immunoflurescence, flow cytometry, ELISA, qPCR in different culture conditions. 2 samples (control and overexpression) were analyzed in biological triplicates

2013-04-01 | E-GEOD-45508 | biostudies-arrayexpress

ETO Family Protein Mtgr1 Mediates Prdm14 Functions in Stem Cell Maintenance

Project description:Prdm14 is a sequence-specific transcriptional regulator of embryonic stem cell (ESC) pluripotency and primordial germ cell (PGC) formation. It exerts its function, at least in part, through repressing genes associated with epigenetic modification and cell differentiation. Here, we show that this repressive function is mediated through an ETO-family co-repressor Mtgr1, which tightly binds to the pre-SET/SET domains of Prdm14 and co-occupies its genomic targets in mouse ESCs. Structure-guided point mutants abrogated the Prdm14-Mtgr1 association and disrupted Prdm14's function in mESC gene expression and PGC formation in vitro. Altogether, our work uncovers the molecular mechanism underlying Prdm14-mediated repression. Examination of Prdm14 and Mtgr1 occupancy by ChIP-seq and effects on gene expression in mouse embryonic stem cells

2016-07-03 | E-GEOD-74547 | biostudies-arrayexpress

Genome-wide identification of genes differentially expressed between wild-type and Prdm14-deficient ES cells grown in 2i culture conditions.

2013-04-01 | GSE45507 | GEO

PRDM14 Knockdown in human embryonic stem cells

Project description:To identify the gene changes after PRDM14 knockdown 6 samples were collected in total. Each sample is done in triplicate and samples were collected at 3 days after transfection. Luciferase knockdown serves as negative control and PRDM14 knockdown is the experimental sample.

2010-10-20 | E-GEOD-22795 | biostudies-arrayexpress

Genome-wide mapping of PRDM14 binding sites in human embryonic stem cells

Project description:PRDM14 belongs to the PR (PRDI-BF1 and RIZ) domain proteins (PRDM) family which is a subclass of the SET domain proteins, a common domain found in histone modifying enzymes. PRDM14 has been previously implicated to regulate self-renewal of hESCs as knock-down of PRDM14 induced expression of differentiation marker genes and altered the cellular morphology. We showed that PRDM14 directly regulates the expression of key pluripotency gene POU5F1. Genome-wide location profiling experiments revealed that PRDM14 co-localized extensively with other key transcription factors such as OCT4, NANOG and SOX2. More importantly, in a gain-of-function assay, we showed that PRDM14 is able to enhance the efficiency of reprogramming of human fibroblasts in conjunction with OCT4, SOX2 and KLF4. Hence, PRDM14 exemplifies a key transcription factor that is required for the maintenance of human ESC identity and the reacquisition of pluripotency in human somatic cells. ChIP-seq of PRDM14 in human ESCs

2010-10-20 | E-GEOD-22767 | biostudies-arrayexpress

Genome-wide identification of genes differentially expressed between control and Prdm14 overexpressing ES cells grown in serum conditions.

2013-04-01 | GSE45508 | GEO

PRDM14 Ensures a Naïve Pluripotency by a Dual Mechanism Involving Signaling and Epigenetic Pathways in Mouse Embryonic Stem Cells

Project description:Mouse embryonic stem cells (mESCs) fluctuate between a naïve inner cell mass (ICM)-like state and a primed epiblast-like state of pluripotency in serum, but are harnessed exclusively in a distinctive, apparently more naïve state of pluripotency (the ground state) with inhibitors for mitogen-activated protein kinase (MAPK) and glycogen synthase kinase 3 pathways (2i). Understanding the mechanism ensuring a naïve state of pluripotency would be critical in realizing a full potential of ESCs. We show here that PRDM14, a PR domain-containing transcriptional regulator, ensures a naïve pluripotency by a dual mechanism: Antagonizing fibroblast growth factor receptor (FGFR) signaling that is activated paradoxically by the core transcriptional circuitry for pluripotency and directs a primed state and repressing de novo DNA methyltransferases that create a primed epiblast-like epigenome. PRDM14 exerts these functions by recruiting polycomb repressive complex 2 (PRC2) specifically to key targets and repressing their expression. Mouse Embryonic Stem Cells (mESCs) or mESC-like cells with different Prdm14 genotypes {Prdm14(+/+), Prdm14(-/-), and Prdm14(-/-) rescued with Avitag-EGFP-Prdm14 transgene [Prdm14(-/-)+AGP14]} are cultured on MEF in different medium [2i, Serum(day 2), Serum+MEK inhibitor (PD0325901) (day 2), Serum without LIF (day2)].

2013-01-18 | E-GEOD-42580 | biostudies-arrayexpress

Functional and Molecular Single-Cell Analyses Implicate PRDM14 in the Initiation of a Novel B-1 Cell Malignancy - Cut and Run experiments

Project description:Molecular mechanisms underlying high-risk subtypes of leukemia remain elusive. PR domain-containing 14 (Prdm14) is a potent oncogene implicated in the initiation of many cancers, including leukemia. Here, we interrogate the heterogeneity of Prdm14-expressing cell types in a mouse model of T-cell acute lymphoblastic leukemia (T-ALL). We identified an abnormal B-1 cell-like population in pre-leukemic bone marrow. B-1 cells are a self-renewing population of unconventional B cells established during embryonic development. This dataset contains genome-wide profiling of PRDM14, H3K4me1, and H3K4me3 to understand the genome-wide binding of the key TF in the abnormal B1 population and their B-cell conserved and B-1 cell-type specific enhancer and promoter regions. Cut-and-run experiments for each antibody were completed in triplicate, with IgG included as an extra experimental control.

2024-06-26 | E-MTAB-13159 | biostudies-arrayexpress

Transcriptional profiling by array of Klf2 wild-type and Klf2-Null mESCs cultured under 2i

Project description:The self-renewing pluripotent state was first captured in mouse embryonic stem cells (mESCs) over two decades ago. The standard condition requires the presence of serum and LIF, which provide growth promoting signals for cell expansion. However, there are pro-differentiation signals which destabilize the undifferentiated state of mESCs. The dual inhibition (2i) of the pro-differentiation Mek/Erk and Gsk3/Tcf3 pathways in mESCs is sufficient to establish an enhanced pluripotent “ground state” which bears features resembling the pre-implantation mouse epiblast. Gsk3 inhibition alleviates the repression of Esrrb, a transcription factor that can substitute for Nanog function in mESCs. The molecular mechanism that is mediated by Mek inhibition is however not clear. In this study, we investigate the pathway through which Mek inhibition operates to maintain ground state pluripotency. We have found that in mESCs, Kruppel-like factor 2 (Klf2) is a protein target of the Mek/Erk pathway; and that Klf2 protein is phosphorylated by Erk2 and subsequently degraded through the proteosome. It is therefore by Mek-inhibition through PD0325901 or 2i that enables the stabilization and accumulation of Klf2 to sustain ground state pluripotency. Importantly, we found that Klf2-null mESCs, while viable under LIF/Serum conditions, cannot be maintained and eventually gradually die within a few passages. Our result thus demonstrates that Klf2 is an essential factor of ground state pluripotency. Collectively, our study defines the Mek/Klf2 axis that cooperates with the Gsk3/Esrrb pathway in mediating ground state pluripotency.

2014-06-04 | E-MTAB-2366 | biostudies-arrayexpress

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