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Role of Pou3f1 during mouse pluripotent stem cell neural fate commitment

ABSTRACT: Role of Pou3f1 during mouse pluripotent stem cell neural fate commitment

PROVIDER: PRJNA286995 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1151400.fastq.gz	Fastqsanger.gz
	SRR1151401.fastq.gz	Fastqsanger.gz
	SRR1151402.fastq.gz	Fastqsanger.gz
	SRR1151395.fastq.gz	Fastqsanger.gz
	SRR1151396.fastq.gz	Fastqsanger.gz

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Genome-wide ChIP-seq analysis of Pou3f1 during mouse pluripotent stem cell neural fate commitment

Project description:Appropriate neural initiation of the pluripotent stem cells in the early embryos is critical for the development of the central nervous system. This process is regulated by the coordination of extrinsic signals and intrinsic programs. However, how the coordination is achieved to ensure proper neural fate commitment is largely unknown. Here, taking advantage of genome-wide ChIP-sequencing (ChIP-seq) and RNA-sequencing (RNA-seq) analyses, we demonstrate that the transcriptional factor Pou3f1 is an upstream activator of neural-promoting genes, and it is able to repress neural-inhibitory signals as well. Further studies revealed that Pou3f1 could directly bind neural lineage genes like Sox2 and downstream targets of neural inhibition signaling such as BMP and Wnt. Our results thus identify Pou3f1 as a critical dual-regulator of the intrinsic transcription factors and the extrinsic cellular signals during neural fate commitment. ChIP-seq assay was ultilized to characterize the targets of Pou3f1 on ESC differentiation day 2.

2015-11-23 | E-GEOD-69778 | biostudies-arrayexpress

Genome-wide ChIP-seq analysis of Pou3f1 during mouse pluripotent stem cell neural fate commitment

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The transcription factor Pou3f1 promotes neural fate commitment via activation of neural lineage genes and inhibition of external signaling pathways

Project description:The neural fate commitment of pluripotent stem cells requires repression of extrinsic inhibitory signals and activation of intrinsic positive transcription factors. However, it remains elusive how these two events are integrated to ensure appropriate neural conversion. Here, we show that Oct6 functions as an essential positive factor for neural differentiation of mouse embryonic stem cells (ESCs), specifically during the transition from epiblast stem cells (EpiSCs) to neural progenitor cells (NPCs). Chimera analysis showed that Oct6 knockdown leads to markedly decreased incorporation of ESC in neuroectoderm. By contrast, Oct6-overexpressing ESC derivatives preferentially contribute to neuroectoderm. Genome-wide ChIP-seq and RNA-seq analyses indicate that Oct6 is an upstream activator of neural lineage genes, and also a repressor of BMP and Wnt signalings. Our results establish Oct6 as a critical regulator that promotes neural commitment of pluripotent stem cells through a dual role: activating internal neural induction programs and antagonizing extrinsic neural inhibitory signals.

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Oct6 promotes neural commitment via activation of neural lineage genes and inhibition of BMP/Wnt signals

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Genome-wide ChIP-seq and RNA-seq analyses of Pou3f1 during mouse pluripotent stem cell neural fate commitment.

Project description:Appropriate neural initiation of the pluripotent stem cells in the early embryos is critical for the development of the central nervous system. This process is regulated by the coordination of extrinsic signals and intrinsic programs. However, how the coordination is achieved to ensure proper neural fate commitment is largely unknown. Here, taking advantage of genome-wide ChIP-sequencing (ChIP-seq) and RNA-sequencing (RNA-seq) analyses, we demonstrate that the transcriptional factor Pou3f1 is an upstream activator of neural-promoting genes, and it is able to repress neural-inhibitory signals as well. Further studies revealed that Pou3f1 could directly bind neural lineage genes like Sox2 and downstream targets of neural inhibition signaling such as BMP and Wnt. Our results thus identify Pou3f1 as a critical dual-regulator of the intrinsic transcription factors and the extrinsic cellular signals during neural fate commitment. Data were deposited in Gene Expression Omnibus (GEO) datasets under reference number GSE69865.

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Role of Pou3f1 during mouse pluripotent stem cell neural fate commitment

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

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Project description:Nicotinamide promotes formation of retinal organoids from human pluripotent stem cells via enhanced neural cell fate commitment

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Nicotinamide promotes formation of retinal organoids from human pluripotent stem cells via enhanced neural cell fate commitment

Project description:Retinal organoids (ROs) derived from human pluripotent stem cells (hPSCs) recapitulate key features of human retinogenesis and thus provide a promising platform to study the mechanisms of retinal development and disease in a human context and to evaluate therapies. Although multiple differentiation protocols are currently in use, hPSCs exhibit tremendous variability in differentiation efficiency, with some cell lines consistently yielding few or even no ROs thus limiting their utility in research. To improve the efficiency and robustness of RO generation, we set out to identify factors that promote neural retina differentiation from hPSCs. We report here that nicotinamide (NAM) treatment at the early stage of differentiation significantly improved RO yield across 8 hPSC lines from different donors. Importantly, NAM treatment enabled efficient production of ROs from cell lines that would otherwise fail to generate meaningful number of ROs. Further analyses revealed that NAM treatment promotes neural commitment of hPSCs at the expense of non-neural ectodermal cell fate, which in turn increases eye field commitment and RO generation. This effect is mediated, at least in part, through inhibition of BMP signaling. Thus, our modified protocol with a simple NAM treatment improves the yield of ROs in all lines tested, and importantly greatly benefits to cell lines that previously proved to be intractable in retinal differentiation. Our data should facilitate the broader use of human ROs for disease modeling applications requiring the use of multiple cell lines or a larger scale of cell source such as therapy screening.

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Role of Pou3f1 during mouse pluripotent stem cell neural fate commitment

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2015-06-15 | GSE69865 | GEO

The transcription factor Pou3f1 promotes neural fate commitment via activation of neural lineage genes and inhibition of external signaling pathways.

Project description:The neural fate commitment of pluripotent stem cells requires the repression of extrinsic inhibitory signals and the activation of intrinsic positive transcription factors. However, how these two events are integrated to ensure appropriate neural conversion remains unclear. In this study, we showed that Pou3f1 is essential for the neural differentiation of mouse embryonic stem cells (ESCs), specifically during the transition from epiblast stem cells (EpiSCs) to neural progenitor cells (NPCs). Chimeric analysis showed that Pou3f1 knockdown leads to a markedly decreased incorporation of ESCs in the neuroectoderm. By contrast, Pou3f1-overexpressing ESC derivatives preferentially contribute to the neuroectoderm. Genome-wide ChIP-seq and RNA-seq analyses indicated that Pou3f1 is an upstream activator of neural lineage genes, and also is a repressor of BMP and Wnt signaling. Our results established that Pou3f1 promotes the neural fate commitment of pluripotent stem cells through a dual role, activating internal neural induction programs and antagonizing extrinsic neural inhibitory signals.

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