Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA237042 | ENA |
REPOSITORIES: ENA
Dataset's files
| 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 |
Items per page: 5 1 - 5 of 8 |
Similar Datasets
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
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.
2015-11-23 | GSE69778 | GEO
Project description:Role of Pou3f1 during mouse pluripotent stem cell neural fate commitment
| PRJNA286995 | ENA
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. RNA-seq was performed to examine Oct6 function in ESC neural differentiation at Day2, Day4 and Day6 after dox induction. On Day4 EB, ChIP-seq assay was ultilized to characterize the targets of Oct6.
2014-01-31 | E-GEOD-54569 | biostudies-arrayexpress
Project description:We show that lysosomes are antagonistically controlled by TFEB and MYC to balance catabolic and anabolic processes required for activating LT-HSC and guiding their lineage fate. TFEB-mediated induction of the endolysosomal pathway for membrane receptor degradation limits LT-HSC metabolic and mitogenic activation; this promotes quiescence and self-renewal and governs erythroid-myeloid commitment. By contrast, MYC engages biosynthetic processes while repressing lysosomal catabolism to drive LT-HSC activation. Collectively, our study identifies lysosomes as a central regulatory hub for proper and coordinated stem cell fate determination.
| EGAD00001006884 | EGA
Project description:Genome-wide ChIP-seq analysis of Pou3f1 during mouse pluripotent stem cell neural fate commitment
| PRJNA286774 | ENA
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.
2014-01-31 | GSE54569 | GEO
Project description:We have determined that sustained expression of EBF suppresses alternate lineage genes independently of Pax5. Keywords: Transcription factor EBF restricts alternate lineage options and promotes B cell fate commitment independently of Pax5.
2007-12-15 | GSE9878 | GEO
Project description:The process of cell fate commitment requires sequential changes in the gene expression profiles of embryonic progenitors. This is exemplified in the development of the neural crest, a migratory stem cell population derived from the ectoderm of vertebrate embryos. Neural crest formation involves a series of regulatory changes, in which cells adopt distinct transcriptional states in a stepwise manner. The mechanisms underpinning these shifts in cell identity are still poorly understood. Here we employ enhancer analysis to identify a genetic sub-circuit that controls developmental transitions in neural crest development. This sub-circuit links Wnt target genes in an incoherent forward loop that controls the sequential activation of genes in the neural crest lineage. By examining the cis-regulatory apparatus of Wnt effector gene AXUD1, we found that multipotency factor SP5 directly promotes neural plate border identity, while inhibiting premature specification by interacting with tissue specific enhancers.
2020-12-17 | GSE152599 | GEO
Project description:Geminin cooperates with Polycomb to restrain multi-lineage commitment in the early embryo: Transient maintenance of a pluripotent embryonic cell population followed by the onset of multi-lineage commitment is a fundamental aspect of development. However, molecular regulation of this transition is not well characterized in vivo. Here we demonstrate that the nuclear protein Geminin is required to restrain commitment and spatially restrict mesoderm, endoderm, and non-neural ectoderm to their proper locations in the Xenopus embryo. We used microarray analyses to demonstrate that Geminin overexpression represses many genes associated with cell commitment and differentiation, while elevating expression levels of genes that maintain pluripotent early and immature neurectodermal cell states. We characterized Geminin’s relationship to cell signaling and found that Geminin broadly represses Activin-, FGF-, and BMP-mediated cell commitment. Conversely, Geminin knockdown enhances commitment responses to growth factor signaling and causes ectopic mesodermal, endodermal, and epidermal fate commitment in the embryo. We also characterized Geminin’s functional relationship with transcription factors that had similar activities and found that Geminin represses commitment independent of Oct4 ortholog (Oct25/60) activities, but depends upon intact Polycomb repressor function. Consistent with this, chromatin immunoprecipitation assays directed at mesodermal genes demonstrate that Geminin promotes Polycomb binding and Polycomb-mediated repressive histone modifications, while inhibiting modifications associated with gene activation. This work defines Geminin as an essential regulator of the embryonic transition from pluripotency through early multi-lineage commitment, and demonstrates that functional cooperativity between Geminin and Polycomb contributes to this process.
2010-12-06 | GSE25158 | GEO