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C-Myc Transcriptionally Amplifies Sox2 Target Genes to Regulate Self-Renewal in Multipotent Otic Progenitor Cells [RNA-Seq]

ABSTRACT: An immortalized multipotent otic progenitor (iMOP) cell was generated by transient expression of c-Myc in Sox2-expressing otic progenitor cells. The procedure activated endogenous c-Myc expression in the cells and amplified existing Sox2-dependent transcripts to promote self-renewal. Downregulation of c-Myc expression following growth factor withdrawal resulted in a molecular switch from self-renewal to otic differentiation. Progenitor cells from embryonic inner ear that form otospheres were infected with a c-Myc retrovirus to promote self-renewal

ORGANISM(S): Mus musculus

SUBMITTER: David Corey

PROVIDER: E-GEOD-62512 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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C-MYC transcriptionally amplifies SOX2 target genes to regulate self-renewal in multipotent otic progenitor cells.

Kwan Kelvin Y KY Shen Jun J Corey David P DP

Stem cell reports 20141211 1

Sensorineural hearing loss is caused by the loss of sensory hair cells and neurons of the inner ear. Once lost, these cell types are not replaced. Two genes expressed in the developing inner ear are c-Myc and Sox2. We created immortalized multipotent otic progenitor (iMOP) cells, a fate-restricted cell type, by transient expression of C-MYC in SOX2-expressing otic progenitor cells. This activated the endogenous C-MYC and amplified existing SOX2-dependent transcripts to promote self-renewal. RNA- ...[more]

PMID: 25497456

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c-Myc Transcriptionally Amplifies Sox2 Target Genes to Regulate Self-Renewal in Multipotent Otic Progenitor Cells [ChIP-Seq]

Project description:An immortalized multipotent otic progenitor (iMOP) cell was generated by transient expression of c-Myc in Sox2-expressing otic progenitor cells. The procedure activated endogenous c-Myc expression in the cells and amplified existing Sox2-dependent transcripts to promote self-renewal. Downregulation of c-Myc expression following growth factor withdrawal resulted in a molecular switch from self-renewal to otic differentiation. ChIP-Seq was accomplished by immunoprecipitating endogenous RNA PolII, c-Myc and Sox2

2015-02-18 | E-GEOD-62513 | biostudies-arrayexpress

c-Myc Transcriptionally Amplifies Sox2 Target Genes to Regulate Self-Renewal in Multipotent Otic Progenitor Cells [ChIP-Seq]

2015-02-18 | GSE62513 | GEO

c-Myc Transcriptionally Amplifies Sox2 Target Genes to Regulate Self-Renewal in Multipotent Otic Progenitor Cells [RNA-Seq]

2015-02-18 | GSE62512 | GEO

Project description:c-Myc Transcriptionally Amplifies Sox2 Target Genes to Regulate Self-Renewal in Multipotent Otic Progenitor Cells

| PRJNA264313 | ENA

Mus musculus

Project description:c-Myc Transcriptionally Amplifies Sox2 Target Genes to Regulate Self-Renewal in Multipotent Otic Progenitor Cells [RNA-Seq]

| PRJNA264316 | ENA

Mus musculus

Project description:c-Myc Transcriptionally Amplifies Sox2 Target Genes to Regulate Self-Renewal in Multipotent Otic Progenitor Cells [ChIP-Seq]

| PRJNA264315 | ENA

Determination of the protein interactome of the transcription factor Sox2 in embryonic stem cells engineered for inducible expression of four reprogramming factors

Project description:Coordinate expression of the somatic cell reprogramming factors Oct4, Sox2, Klf4 and c-Myc within embryonic stem cells preserves the self-renewal of these cells, while allowing for the expression epitope tagged Sox2. Taking advantage of this observation, we engineered embryonic stem cells (i-OSKM-ESC) to inducibly express Oct4, Klf4, c-Myc and an epitope tagged form of Sox2 from a polycistronic element, in the presence of doxycycline. We isolated Sox2 and its associated protein complexes by co-immunoprecipitation. Subsequently, we identified the Sox2-protein interactome in self-renewing embryonic stem cells using an unbiased proteomic screen (Multidimensional Protein Identification Technology [MudPIT]). Affymetrix microarrays were used to characterize the gene expression profile of i-OSKM-ESC in the absence and presence of doxycycline. Mouse embryonic stem cells (KH2) were engineered to express Oct4, epitope tagged Sox2, Klf4 and c-Myc in the presence of doxycyline, to produce i-OSKM-ESC. The i-OSKM-ESC were cultured in the absence or presence of doxycyline (4 Âµg/mL) for 24 hours. RNA was extracted from each condition, and used for microarray analysis.

2012-02-20 | E-GEOD-34801 | biostudies-arrayexpress

CUT&RUN Targeting c-FOS, c-JUN and SOX2 in neurospheres derived from mouse brain cells

Project description:Other than in the development of the brain, SOX2 is essential for the long-term self-renewal of neural stem cells (NSCs). The mechanisms of how SOX2 maintains the stemness of NSCs is not yet understood. We have identified Fos as a downstream target of SOX2, and therefore used CUT&RUN to investigate where these transcription factors - and the c-FOS partner c-JUN - interact with the genome. By comparing binding patterns of c-FOS, c-JUN and SOX2, we find that they co-occupate the promoter of the SOCS3 locus, which we also have identified as a gene that rescues SOX2 deletion induced senescence when overexpressed in neurospheres grown from Sox2-deleted mouse NSCs. Taken together, our data provide a basis for elucidating a gene regulatory network necessary for the maintenance of self-renewal in post-embryonic neural stem cells.

2021-04-01 | E-MTAB-9897 | biostudies-arrayexpress

Determination of the protein interactome of the transcription factor Sox2 in embryonic stem cells engineered for inducible expression of four reprogramming factors

2012-02-20 | GSE34801 | GEO

p53 Enables Self Renewal of Nephron Progenitor Cells

Project description:p53 limits the self-renewing ability of a variety of stem cells. Here, contrary to its classical role in restraining cell proliferation, we demonstrate a divergent function of p53 in maintenance of self-renewal of the nephron progenitor population in the embryonic mouse kidney. p53-null nephron progenitor cells (NPC) exhibit progressive loss of the self-renewing progenitor niche in the cap mesenchyme, identified by Cited1 and Six2 expression, and loss of cap integrity. Nephron endowment is regulated by NPC availability and their differentiation to nephrons. Quantitatively, the Six2p53-/- cap has 30% fewer Six2GFP+ cells. While the apoptotic index is unchanged the proliferation index is significantly lower, in accordance with cell cycle analysis data showing less mutant Six2p53-/-;GFP+ cells in S and G2/M phases in comparison to Six2p53+/+;GFP+ cells. The mutant kidneys also show nephron deficit and decreased Fgf8 expression. To investigate the underlying changes in gene expression in the cap mesenchyme that contribute to the Six2p53-/- phenotype, we utilized RNA-Seq for transcriptome comparison. Top biological processes affected by p53 loss are development and morphogenesis, cell adhesion/migration, cell survival and metabolism. Cells from the mutant CM showed increased cellular ROS levels as well as deregulated expression of energy metabolism and mitochondrial genes suggesting metabolic dysfunction. Adhesion defects are visualized by decreased immunostaining of adhesion marker NCAM, and may possibly contribute to the differentiation defect as well. Altogether our data suggest a novel role for p53 in enabling self-renewal of the NPC and preservation of the progenitor niche, and thus regulating nephron endowment. mRNA profiles of wild-type (WT) and conditional p53 knockout (KO) of Six2+ mouse nephron progenitor cells (NPC) at embryonic day 15.5

2015-02-16 | E-GEOD-56253 | biostudies-arrayexpress

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