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A set of Sox2-dependent OSN enhancers mediates the immediate response to neural induction and default neural differentiation of embryonic stem cells

ABSTRACT: A set of Sox2-dependent OSN enhancers mediates the immediate response to neural induction and default neural differentiation of embryonic stem cells

PROVIDER: PRJNA1003385 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25567700_1.fastq.gz	Fastqsanger.gz
	SRR25567700_2.fastq.gz	Fastqsanger.gz
	SRR25567701_1.fastq.gz	Fastqsanger.gz
	SRR25567701_2.fastq.gz	Fastqsanger.gz
	SRR25567702_1.fastq.gz	Fastqsanger.gz

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A set of Sox2-dependent OSN enhancers mediates the immediate response to neural induction and default neural differentiation of embryonic stem cells

Project description:Sox2 is a transcription factor involved in the regulatory network maintaining the pluripotency of embryonic stem cells in culture as well as in early embryos. In addition, Sox2 plays a pivotal role in neural stem cell formation and neurogenesis. How Sox2 can serve both processes has remained elusive. Here we identified a set of Sox2-dependent neural associated enhancers (SONAE) activated immediately following neural induction and required in neural gene activation. SONAE are a distinct subgroup (1898) of 8531 Oct4/Sox2/Nanog (OSN) bound enhancers, characterized by enhanced Sox2 binding and chromatin accessibility. SONAE activation is triggered by neural induction via Retinoic Acid treatment of wild type cells and is antagonized by mesodermal transcription factors repressing Sox2 following mesoderm induction. Neural differentiation is also set off by default in Smad4 ablated cells resistant to mesodermal induction. Our data provide mechanistic insight into the regulation of early neural versus mesodermal induction in ESCs and embryos.

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Project description:The transcription factors OCT4 and SOX2 play an essential role in the establishment and maintenance of pluripotent embryonic stem cells (ESCs). Yet, their function in specialized stem cell populations is still poorly understood. Here, we show that the OCT4 and SOX2 work as dimers to regulate the epigenomic landscape of neural crest cells. By isolating primary neural crest cells at a range of developmental stages, we characterized the transcriptomic and epigenomic changes that take place during specification, migration, and early differentiation. Analysis of these datasets revealed that the OCT4/SOX2 dimer promotes an epigenomic signature inherent to the multipotent neural crest. We found that the emergence of this epigenomic state requires the translocation of OCT4/SOX2 to tissue-specific cis-regulatory regions. By examining genome organization during the induction of hESCs into neural crest cells, we observed that the patterns of genomic occupancy of the dimer are modified during cell fate commitment. Dimer translocation is guided by neural crest-specific pioneer transcription factors, which physically interact with the OCT4/SOX to modify their genomic targets. Our results demonstrate how the ESC pluripotency program is repurposed in specialized stem cells to control chromatin organization and define the developmental potential of embryonic progenitors.

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OCT4-SOX2 dimers reshape the epigenome to promote neural crest multipotency [ATAC-Seq]

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OCT4-SOX2 dimers reshape the epigenome to promote neural crest multipotency [RNA-Seq]

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