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Gene expression analysis of E2A forced homodimer overexpression in mouse embryonic stem cells.

ABSTRACT: We set out to investigate whether overexpression of the bHLH transcription factor, E2A, is sufficient to drive neural differentiation in mouse embryonic stem cells under non-permissive culture conditions. Having identified that overexpression of specifically E2A homodimers, but not E2A monomers, was sufficient to drive neural differentiation, we sought to identify early downstream targets of E2A during the process of neural commitment using RNA-sequencing.

ORGANISM(S): Mus musculus

PROVIDER: GSE152118 | GEO | 2020/06/10

REPOSITORIES: GEO

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Gene expression analysis of E2A forced homodimer overexpression in mouse embryonic stem cells.

Project description:Gene expression analysis of E2A forced homodimer overexpression in mouse embryonic stem cells.

| PRJNA638369 | ENA

Genome-wide maps of chromatin state in wild type and E2A knockout neural progenitor cells

Project description:Background: E2A, encoded by the TCF3 gene locus, belongs to the E protein transcription factor family, which also includes HEB (TCF12) and E2-2 (TCF4), has been suggested to play an important role in leukemogenesis. However, far less is known about the function of E2A in cell-fate regulation of hESCs. Therefore, further understanding of E2A in self-renewal and differentiation of embryonic stem cells may be influenced. In the study, we demonstrated E2A knockout exhibited blocked neural differentiation, which is tightly related to histone modification H3K4me3 and H3K27me3. Methods: The genomic DNA of H3K4me3 and H3K27me3 binding peaks in wild type and E2A knockout neural progenitor cells were generated by ChIP-seq technique using IIIumina Hiseq 2500. Results: A comprehensive human chromatin state of H3K4me3 and H3K27me3 in wild type and E2A knockout neural progenitor cells was provided. Function enrichment, network characteristics and disease association of the binding peaks were analyzed. Conclusion: The dataset could serve as a baseline resource for investigating the potential effects and mechanism of H3K4me3/H3K27me3/E2A complex in neural differentiation period of embryonic stem cells

2020-07-16 | GSE154480 | GEO

RNA-sequencing of E2a-deficient or E2a and Lef1-deficient leukemia cell lines

Project description:We compared the transcriptome of leukemia cell lines generated from 7 E2a-/- and 8 E2a-/-Lef1f/fLckCre+ mice

2021-10-25 | GSE186420 | GEO

Loss of thymocyte competition underlies the tumor suppressive functions of the E2a transcription factor in T-ALL

Project description:T lymphocyte acute lymphoblastic leukemia (T-ALL) is frequently associated with increased expression of the E protein transcription factor inhibitors TAL1 and LYL1. In mouse models, ectopic expression of Tal1 or Lyl1 in T cell progenitors, or inactivation of E2a, is sufficient to predispose mice to develop T-ALL. How E2a suppresses thymocyte transformation is currently unknown. Here, we show that early deletion of E2a, prior to the DN3 stage, was required for robust leukemogenesis and was associated with alterations in thymus cellularity, T cell differentiation, and gene expression in immature CD4+CD8+ thymocytes. Introduction of wild-type thymocytes into mice with early deletion of E2a prevented leukemogenesis, or delayed disease onset, and impacted the expression of multiple genes associated with transformation and genome instability. Our data indicate that E2a suppresses leukemogenesis by promoting T cell development and enforcing inter-thymocyte competition, a mechanism that is emerging as a safeguard against thymocyte transformation. These studies have implications for understanding how multiple essential regulators of T cell development suppress T-ALL and support the hypothesis that thymus cellularity is a determinant of leukemogenesis

2023-12-12 | GSE234609 | GEO

Transcriptome profiling of wildtype and E2A knockout embryonic stem cells

Project description:Background: E2A, encoded by the TCF3 gene locus, belongs to the E protein transcription factor family, which also includes HEB (TCF12) and E2-2 (TCF4), has been suggested to play an important role in leukemogenesis. However, far less is known about the function of E2A in cell-fate regulation of hESCs. Therefore, further understanding of E2A in self-renewal and differentiation of embryonic stem cells may be influenced. Methods: The mRNA profiles of wildtype and E2A knockout embryonic stem cells were generated by RNA-seq technique, in triplicate for each group, using IIIumina Hiseq 2500. Results: A comprehensive human transcriptome map of wild type and E2A knockout embryonic stem cells was provided. Function enrichment, network characteristics and disease association of the differentially expressed genes were analyzed. Conclusion: The dataset could serve as a baseline resource for investigating the potential effects and mechanism of E2A in embryonic stem cells.

2020-07-16 | GSE154481 | GEO

Gene expression profiling of the Se-Ax cell line following E2A reconstitution

Project description:The transcription factor E2A is essential for lymphocyte development. In this study, we describe a recurrent E2A gene deletion in at least 70% of patients with Sézary syndrome (SS), a subtype of T cell lymphoma. Loss of E2A results in enhanced proliferation and cell cycle progression via derepression of the proto-oncogene MYC and the cell cycle regulator CDK6. Furthermore, by examining the gene expression profile of SS cells following restoration of E2A expression, we identify a number of E2A-regulated genes that interfere with oncogenic signaling pathways including the Ras pathway. Several of these genes are down-regulated or lost in primary SS tumor cells. These data demonstrate a tumor suppressor function of E2A in human lymphoid cells and could help to develop new treatment strategies for human lymphomas with altered E2A activity.

2011-07-07 | GSE21730 | GEO

Allosaccharopolyspora coralli strain:E2A

Project description:Allosaccharopolyspora coralli strain:E2A Genome sequencing

| PRJNA588104 | ENA

HEB and E2A function as SMAD/FOXH1 cofactors

Project description:Nodal signaling, mediated through SMAD transcription factors, is necessary for pluripotency maintenance and endoderm commitment. We have identified a new motif, termed SMAD Complex Associated (SCA) that is bound by SMAD2/3/4 and FOXH1 in human embryonic stem cells (hESCs) and derived endoderm. We demonstrate that two bHLH proteins - HEB and E2A - bind the SCA motif at regions overlapping SMAD2/3 and FOXH1. Further, we show that HEB and E2A associate with SMAD2/3 and FOXH1, suggesting they form a complex at critical target regions. This association is biologically important, as E2A is critical for mesendoderm specification, gastrulation, and Nodal signal transduction in Xenopus tropicalis embryos. Taken together, E2A is a novel Nodal signaling cofactor that associates with SMAD2/3 and FOXH1 and is necessary for mesendoderm differentiation.

2011-08-23 | GSE30146 | GEO

Expression data from WT and E2A-deficient murine DN2 cells

Project description:The E2A transcription factors promote the development of thymus-seeding cells but it remains unknown whether these proteins play a role in T lymphocyte lineage specification or commitment. By examining E2A-dependent genes in developing T cells, we will address whether these proteins are involved in these processes. DN2 cells from WT and E2A-deficient murine fetal thymi were FACS sorted. Subsequently RNA was extracted, labelled and hybridized to Affymetrix microarrays. The goal of this study is to investigate E2A-dependent genes in developing T cells

2013-02-01 | E-GEOD-43224 | biostudies-arrayexpress

Gene expression profiling of the Se-Ax cell line following E2A reconstitution

2011-07-07 | E-GEOD-21730 | biostudies-arrayexpress

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