Gene expression analysis of E2A forced homodimer overexpression in mouse embryonic stem cells.
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ABSTRACT:
PROVIDER: PRJNA638369 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11966431_1.fastq.gz | Fastqsanger.gz | |||
| SRR11966431_2.fastq.gz | Fastqsanger.gz | |||
| SRR11966432_1.fastq.gz | Fastqsanger.gz | |||
| SRR11966432_2.fastq.gz | Fastqsanger.gz | |||
| SRR11966433_1.fastq.gz | Fastqsanger.gz |
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Project description: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.
2020-06-10 | GSE152118 | GEO
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
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 | GSE154482 | GEO
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 | GSE154479 | GEO
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. The E2A-deficient Sézary cell line Seax was transiently transfected with the E2A-expression constructs E47myc (a myc-tagged E47 construct) or E47-forced dimer (a construct coding for two covalently linked E47 molecules), respectively. Every experiment was performed as two replicates accompanied by control transfections with a Mock plasmid.
2011-07-07 | E-GEOD-21730 | biostudies-arrayexpress
Project description:Transcriptome profiling of wildtype and E2A knockout embryonic stem cells
| PRJNA646463 | ENA
Project description:E2A regulates neural ectoderm fate specification in human embryonic stem cells
| PRJNA646882 | ENA
Project description:Conjugation of small ubiquitin-like modifiers (SUMOs) to substrate proteins is a posttranslational protein modification that affects a diverse range of physiological processes. Global inhibition of SUMO conjugation in mice results in embryonic lethality, reflecting the importance of the SUMO pathways for embryonic development. Here, we demonstrated that SUMO1 overexpression was not well tolerated in murine embryonic carcinoma and embryonic stem (ES) cells and that only a few clones were recovered after transduction with vectors delivering SUMO1 expression constructs. Differentiated NIH/3T3 cells overexpress SUMO1 without deleterious effects and maintain high levels of both conjugated and free forms of SUMO1. The few embryonic cells surviving after forced overexpression retained all their SUMO1 in the form of a few high-molecular-weight conjugates and maintained undetectable levels of free SUMO1. The absence of free SUMO in embryonic cells was seen specifically upon overexpression of SUMO1, but not SUMO2. Moreover, blocking SUMO1 conjugation to endogenous substrates by C-terminal mutations of SUMO1 or by overexpression of a SUMO1 substrate "sponge" or by overexpression of the deSUMOylating enzyme SUMO-specific peptidase 1 (SENP1) dramatically restored free SUMO1 overexpression. The data suggest that overexpression of SUMO1 protein leading to an excess accumulation of critical SUMO1-conjugated substrates is not tolerated in embryonic cells. Surviving embryonic cells exhibit SUMO1 conjugation to allowed substrates but a complete absence of free SUMO1.IMPORTANCE Embryonic stem (ES) cells exhibit unusual transcriptional, proteomic, and signal response profiles, reflecting their unusual needs for rapid differentiation and replication. The work reported here demonstrated that mouse embryonic cell lines did not tolerate the overexpression of SUMO1, the small ubiquitin-like modifier protein that is covalently attached to many substrates to alter their intracellular localization and functionality. Forced SUMO1 overexpression is toxic to ES cells, and surviving cell populations adapt by dramatically reducing the levels of free SUMO1. Such a response is not seen in differentiated cells or with SUMO2 or with nonconjugatable SUMO1 mutants or in the presence of a SUMO1 "sponge" substrate that accepts the modification. The findings suggest that excess SUMO1 modification of specific substrates is not tolerated by embryonic cells and highlight a distinctive need for these cells to control the levels of SUMO1 available for conjugation.
| S-EPMC6890988 | biostudies-literature
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