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C-Myc Transcriptionally Amplifies Sox2 Target Genes to Regulate Self-Renewal in Multipotent Otic Progenitor Cells [ChIP-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.

ORGANISM(S): Mus musculus

PROVIDER: GSE62513 | GEO | 2015/02/18

SECONDARY ACCESSION(S): PRJNA264315

REPOSITORIES: GEO

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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

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

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

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

Project description: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-seq and ChIP-seq analyses revealed that C-MYC and SOX2 occupy over 85% of the same promoters. C-MYC and SOX2 target genes include cyclin-dependent kinases that regulate cell-cycle progression. iMOP cells continually divide but retain the ability to differentiate into functional hair cells and neurons. We propose that SOX2 and C-MYC regulate cell-cycle progression of these cells and that downregulation of C-MYC expression after growth factor withdrawal serves as a molecular switch for differentiation.

| S-EPMC4297878 | biostudies-other

Mus musculus

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

| PRJNA264315 | 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

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

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

2015-02-18 | E-GEOD-62514 | biostudies-arrayexpress

Chromatin remodelers and lineage specific factors interact to target enhancers to establish pro-neurosensory fate within otic ectoderm

Project description:Specification of Sox2+ pro-neurosensory progenitors within otic ectoderm is a prerequisite for the production of sensory cells and neurons for hearing. However, the underlying molecular mechanisms driving this lineage specification remain unknown. Here, we show that Brg1-based SWI/SNF chromatin-remodeling complex interacts with the neurosensory-specific transcriptional regulators Eya1/Six1 to induce Sox2 expression and promote pro-neurosensory-lineage specification. Ablation of the ATPase-subunit Brg1 or both Eya1/Six1 results in loss of Sox2 expression and lack of neurosensory identity, leading to abnormal apoptosis within the otic ectoderm. Brg1 binds to two of three distal 3' Sox2 enhancers occupied by Six1, and Brg1-binding to these regions depends on Eya1-Six1 activity. We demonstrate that the activity of these Sox2 enhancers in otic neurosensory cells specifically depends on binding to Six1. Furthermore, genome-wide and transcriptome profiling indicate that Brg1 may suppress apoptotic factor Map3k5 to inhibit apoptosis. Together, our findings reveal an essential role for Brg1, its downstream pathways, and their interactions with Six1/Eya1, in promoting pro-neurosensory fate induction in the otic ectoderm and subsequent neuronal lineage commitment and survival of otic cells.

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Project description:This SuperSeries is composed of the SubSeries listed below.

2015-02-18 | GSE62514 | GEO