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

PROVIDER: PRJNA264313 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1616830.fastq.gz	Fastqsanger.gz
	SRR1616840.fastq.gz	Fastqsanger.gz
	SRR1616831.fastq.gz	Fastqsanger.gz
	SRR1616841.fastq.gz	Fastqsanger.gz
	SRR1616832.fastq.gz	Fastqsanger.gz

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c-Myc Transcriptionally Amplifies Sox2 Target Genes to Regulate Self-Renewal in Multipotent Otic Progenitor Cells [RNA-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. Progenitor cells from embryonic inner ear that form otospheres were infected with a c-Myc retrovirus to promote self-renewal

2015-02-18 | E-GEOD-62512 | biostudies-arrayexpress

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

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

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

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

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

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Lineage reprogramming of adult mouse liver cells and B-lymphocytes to neural stem-like cells using defined factors

Project description:The overexpression of transcription factors Oct4, Sox2, Klf4, and c-Myc reprograms a somatic nucleus to one that is transcriptionally and epigenetically indistinguishable from an embryonic stem (ES) cell. However, it is still unclear if transcription factors can completely convert the nucleus of a differentiated cell into that of a distantly related cell type such that it maintains complete transcriptional and epigenetic reprogramming in the absence of exogenous factor expression. To test this idea, we screened a library of doxycycline-inducible vectors encoding neural stem cell (NSC)-expressed genes and found that stable, self-maintaining NSC-like cells could be induced under defined growth conditions after transduction of transcription factors. These induced NSCs (iNSCs) were characterized in the absence of exogenous factor induction and were shown to be transcriptionally, epigenetically, and functionally similar to endogenous embryonic cortical NSCs. Importantly, iNSCs could be generated from multiple adult cell types including liver cells and B-cells with genetic rearrangements. Our results show that self-maintaining proliferative neural cells can be induced from non-ectodermal cells by expressing specific combinations of transcription factors. ChIP-seq data from primary neural progenitor cells (Sox2-GFP) and induced neural progenitor cells were generated by deep sequencing using Illumina Hi-Seq 2000.

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CD47 Inhibits Self-renewal and Reprogramming by Regulating c-Myc and Other Stem Cell Transcription Factors

Project description:Signaling through the thrombospondin-1 receptor CD47 broadly limits cell and tissue survival of stress, but the molecular mechanisms are incompletely understood. We now show that loss of CD47 permits sustained proliferation of primary murine endothelial cells and enables these cells to spontaneously reprogram to form multipotent embryoid bodies. c-Myc, Klf4, Oct4, and Sox2 expression is elevated in CD47-null endothelial cells, in several tissues of CD47- or thrombospondin-1-null mice, and in a human T cell line lacking CD47. CD47 knockdown acutely increases mRNA levels of c-Myc and other stem cell transcription factors in cells and in vivo, whereas CD47 ligation by thrombospondin-1 suppresses c-Myc expression. The inhibitory effects of increasing CD47 levels can be overcome by maintaining c-Myc expression and are absent in cells with dysregulated c-Myc. Thus, CD47 antagonists enable cell self-renewal and reprogramming by overcoming negative regulation of c-Myc and other stem cell transcription factors. To identify gene expression changes associated with CD47 null cells, we compared the gene expression profile of these cells with WT endothelial cell, CD47 null Embryoid bodies cells and an established Embryonic Stem cell line.

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