REST regulation of gene networks in adult neural stem cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA289389 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2095963.fastq.gz | Fastqsanger.gz | |||
| SRR2095964.fastq.gz | Fastqsanger.gz | |||
| SRR2095965.fastq.gz | Fastqsanger.gz | |||
| SRR2095966.fastq.gz | Fastqsanger.gz | |||
| SRR2095967.fastq.gz | Fastqsanger.gz |
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Project description:Cell epigenomics depends on the marks released by transcription factors operating via the assembly of complexes that induce focal changes of DNA and histone structure. Among these factors is REST, a repressor that, via its strong decrease, governs both neuronal and neural cell differentiation and specificity. REST operation on thousands of possible genes can occur directly or via indirect mechanisms including repression of other factors. In previous studies of gene down- and up-regulation, processes had been only partially investigated in neural cells. PC12 are well known neural cells sharing properties with neurons. In the widely used PC12 populations, low-REST cells coexist with few, spontaneous high-REST PC12 cells. High- and low-REST PC12 clones were employed to investigate the role and the mechanisms of the repressor action. Among 15,500 expressed genes we identified 1,770 target and non-target, RESTdependent genes. Functionally, these genes were found to operate in many pathways, from synaptic function to extracellular matrix. Mechanistically, downregulated genes were predominantly repressed directly by REST; up-regulated genes were mostly governed indirectly. Among other factors, Polycomb complexes cooperated with REST for down-regulation, Smad3 and Myod1 participated in up-regulation. In conclusion, we have highlighted that PC12 clones are a useful model to investigate REST, opening opportunities to development of epigenomic investigation. 4 samples have been analyzed: 2 replicates from wtPC12 clone and 2 replicates from the hrPC12 clones
2015-08-31 | E-GEOD-59946 | biostudies-arrayexpress
Project description:Neural differentiation of embryonic stem cells (ESCs) requires coordinated repression of the pluripotency regulatory programme and reciprocal activation of the neurogenic regulatory programme. Upon neural induction, ESCs rapidly repress expression of pluripotency genes followed by staged activation of neural progenitor and differentiated neuronal and glial genes. The transcriptional factors that underlie pluripotency are partially characterized, whereas those underlying neural induction are much less explored, and the factors that coordinate these two developmental programs are completely unknown. One transcription factor, REST (RE1 silencing transcription factor), has been linked with terminal differentiation of neural progenitors, and more recently and controversially, with control of pluripotency. Here, we show that in the absence of REST, coordination of pluripotency and neural induction is lost and there is a resultant delay in repression of pluripotency genes and a precocious activation of both neural progenitor and differentiated neuronal and glial genes. Further, we show that REST is not required for production of radial glia-like progenitors but is required for their subsequent maintenance and differentiation into neurons, oligodendrocytes and astrocytes. We propose that REST acts as a regulatory hub that coordinates timely repression of pluripotency with neural induction and neural differentiation. We have investigated the role of REST in the coupling of pluripotency and neural induction and neurogenesis using Rest-null mouse ESCs (mESCs) in conjunction with a novel mESC neural differentiation protocol. Differential expression between Rest-null ESCs and controls was tested using Illumina Mouse Ref-8 v2 BeadArray technology. Three replicates were used for Rest-null and three for control. Data analysis was performed using Bioconductor libraries beadarray and limma.
2011-12-08 | E-GEOD-34244 | biostudies-arrayexpress
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Project description:Neural differentiation of embryonic stem cells (ESCs) requires coordinated repression of the pluripotency regulatory programme and reciprocal activation of the neurogenic regulatory programme. Upon neural induction, ESCs rapidly repress expression of pluripotency genes followed by staged activation of neural progenitor and differentiated neuronal and glial genes. The transcriptional factors that underlie pluripotency are partially characterized, whereas those underlying neural induction are much less explored, and the factors that coordinate these two developmental programs are completely unknown. One transcription factor, REST (RE1 silencing transcription factor), has been linked with terminal differentiation of neural progenitors, and more recently and controversially, with control of pluripotency. Here, we show that in the absence of REST, coordination of pluripotency and neural induction is lost and there is a resultant delay in repression of pluripotency genes and a precocious activation of both neural progenitor and differentiated neuronal and glial genes. Further, we show that REST is not required for production of radial glia-like progenitors but is required for their subsequent maintenance and differentiation into neurons, oligodendrocytes and astrocytes. We propose that REST acts as a regulatory hub that coordinates timely repression of pluripotency with neural induction and neural differentiation.
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Project description:Neurodevelopmental changes and impaired stress resistance have been implicated in the pathogenesis of bipolar disorder (BD), but the underlying regulatory mechanisms are unresolved. Here we describe a cerebral organoid model of BD that exhibits altered early neural development, elevated neural network activity, and a major shift in the transcriptome. These phenotypic changes were reproduced in cerebral organoids generated from iPS cell lines derived in multiple different laboratories. The BD cerebral organoid transcriptome showed highly significant enrichment for gene targets of the transcriptional repressor REST. This was associated with reduced nuclear REST and REST binding to target gene recognition sites. Reducing the oxygen concentration in organoid cultures to a physiological range ameliorated the developmental phenotype and restored REST expression. These effects were mimicked by treatment with lithium. Reduced nuclear REST and derepression of REST targets genes was also observed in the prefrontal cortex of BD patients. Thus, an impaired cellular stress response in BD cerebral organoids leads to altered neural development and transcriptional dysregulation associated with downregulation of REST. These findings provide a new model and conceptual framework for exploring the molecular basis of BD
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