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The proneural transcription factor ASCL1 regulates cell proliferation and primes for differentiation in neuroblastoma

ABSTRACT: The proneural transcription factor ASCL1 regulates cell proliferation and primes for differentiation in neuroblastoma

PROVIDER: PRJNA836855 | ENA |

REPOSITORIES: ENA

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The proneural transcription factor ASCL1 regulates cell proliferation and primes for differentiation in neuroblastoma [ATAC-seq]

Project description:The proneural transcription factor ASCL1 regulates cell proliferation and primes for differentiation in neuroblastoma [ATAC-seq]

| PRJNA836849 | ENA

The proneural transcription factor ASCL1 regulates cell proliferation and primes for differentiation in neuroblastoma [RNA-Seq]

Project description:The proneural transcription factor ASCL1 regulates cell proliferation and primes for differentiation in neuroblastoma [RNA-Seq]

| PRJNA836861 | ENA

The proneural transcription factor ASCL1 regulates cell proliferation and primes for differentiation in neuroblastoma [RNA-Seq]

Project description:To compare the function of endogenous ASCL1 in different neuroblastoma cell contexts, we have used CRISPR-mediated deletion to compare the effects of ASCL1 deletion in a MYCN-amplified and an ALK-driven neuroblastoma line and assessed the transcriptome wide impact of ASCL1 knockout using RNA-seq

2022-08-31 | GSE202634 | GEO

The proneural transcription factor ASCL1 regulates cell proliferation and primes for differentiation in neuroblastoma [ATAC-seq]

Project description:To compare the function of endogenous ASCL1 in different neuroblastoma cell contexts, we have used CRISPR-mediated deletion to compare the effects of ASCL1 deletion in a MYCN-amplified and an ALK-driven neuroblastoma line and assessed the impact of ASCL1 knockout on chromatin accessiblity genome-wide using ATAC-seq

2022-08-31 | GSE202629 | GEO

ASCL1: a pioneer factor that induces subtype switching and characterizes adrenergic neuroblastoma

Project description:Neuroblastoma is an embryonic malignancy originating from early nerve cells. Neuroblastoma retains plasticity, interconverting between the mesenchymal (MES) and adrenergic (ADRN) states, which are controlled by different sets of transcription factors forming the core regulatory circuit (CRC). However, their functional roles and cooperative mechanisms in neuroblastoma pathogenesis are poorly understood. Here, we demonstrate that overexpression of ASCL1 in MES neuroblastoma cells opens closed chromatin at the promoters of key ADRN genes, accompanied by epigenetic activation and establishment of enhancer-promoter interactions, thereby initiating subtype switching. ASCL1 inhibits the TGFb-SMAD2/3 pathway but activates the BMP-SMAD1-ID3/4 pathway, serving as negative feedback to balance the function of ASCL1-TCF12 dimers. ASCL1 and other ADRN CRC members potentiate each other’s activity, increasing the expression of the original targets and inducing a new set of genes, thereby promoting conversion to ADRN neuroblastoma. Thus, via its pioneer factor function, ASCL1 serves as a master regulator that characterizes ADRN neuroblastoma.

2023-12-08 | PXD037670 | Pride

Molecular basis of neuronal subtype bias introduced by proneural factors Ascl1 and Neurog2 (ChIP-seq)

Project description:Basic helix-loop-helix (bHLH) proneural transcription factors (TFs) Ascl1 and Neurog2 are integral to the development of the nervous system. Here, we investigated the molecular mechanisms by which Ascl1 and Neurog2 control the acquisition of generic neuronal fate and impose neuronal subtype identity. Using direct neuronal programming of embryonic stem cells, we found that Ascl1 and Neurog2 regulate distinct targets by binding to largely different sets of sites. Their divergent binding pattern is not determined by the previous chromatin state but distinguished by specific E-box enrichments which reflect the DNA sequence preference of the bHLH domain. The divergent Ascl1 and Neurog2 binding patterns result in distinct chromatin accessibility and enhancer activity landscapes that shape the binding and activity of downstream TFs during neuronal specification. Our findings suggest that proneural factors contribute to neuronal diversity by differentially altering the chromatin landscapes that shape the binding of neuronally expressed TFs.

2019-02-27 | GSE114172 | GEO

Molecular basis of neuronal subtype bias introduced by proneural factors Ascl1 and Neurog2 (ATAC-seq)

2019-02-27 | GSE114171 | GEO

Molecular basis of neuronal subtype bias introduced by proneural factors Ascl1 and Neurog2 (RNA-seq)

2019-02-27 | GSE114173 | GEO

ChIP NS5 Ascl1-ERT2

Project description:Here we performed a ChIP-seq experiment on a sample of adherent cultures of mouse neural stem cells (NS5 cell line) under normal growth conditions and upon short term activation (30 minutes) of an inducible version of the proneural factor Mash1/Ascl1 (Ascl1-ERT2). This resulted in the generation of a genome-wide map of Ascl1 binding to chromatin.

2015-02-16 | E-MTAB-2384 | biostudies-arrayexpress

Molecular basis of neuronal subtype bias introduced by proneural factors Ascl1 and Neurog2 (single-cell RNA-seq)

2019-02-27 | GSE125620 | GEO