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A global regulatory mechanism for activating an exon network required for neurogenesis

ABSTRACT: A global regulatory mechanism for activating an exon network required for neurogenesis

OTHER RELATED OMICS DATASETS IN: MSV000078609

PROVIDER: PRJNA246157 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1269750_1.fastq.gz	Fastqsanger.gz
	SRR1269750_2.fastq.gz	Fastqsanger.gz
	SRR1269760.fastq.gz	Fastqsanger.gz
	SRR1269751_1.fastq.gz	Fastqsanger.gz
	SRR1269751_2.fastq.gz	Fastqsanger.gz

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A global regulatory mechanism for activating an exon network required for neurogenesis

Project description:The vertebrate and neural-specific SR-related protein nSR100/SRRM4 regulates an extensive program of alternative splicing with critical roles in nervous system development. However, the mechanism by which nSR100 controls its target exons is poorly understood. We demonstrate that nSR100-dependent neural exons are associated with a unique configuration of intronic cis-elements that promote rapid switch-like regulation during neurogenesis. A key feature of this configuration is the insertion of specialized intronic enhancers between polypyrimidine tracts and acceptor sites that bind nSR100 to potently activate exon inclusion in neural cells, while weakening 3' splice site recognition and contributing to exon skipping in non-neural cells. nSR100 further operates by forming multiple interactions with early spliceosome components bound proximal to 3' splice sites. These multifaceted interactions achieve dominance over neural exon silencing mediated by the splicing regulator PTBP1. The results thus illuminate a widespread mechanism by which a critical neural exon network is activated during neurogenesis. RNA-Seq was used to obtain mRNA profiles of various N2A and 293T cell lines from human and mouse, respectively, to investigate the roles of nSR100, Ptbp1 and U2af65 in alternative splicing regulation. PAR-iCLIP and iCLIP experiments followed by high throughput sequencing were conducted to obtain RNA binding profiles of nSR100, PTBP1 and U2af65.

2014-09-11 | E-GEOD-57278 | biostudies-arrayexpress

A global regulatory mechanism for activating an exon network required for neurogenesis

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A global regulatory mechanism for activating an exon network required for neurogenesis.

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CHD5 is required for neurogenesis and has a dual role in facilitating gene expression and Polycomb gene repression

Project description:The chromatin remodeler CHD5 is expressed in neural tissue and is frequently deleted in aggressive neuroblastoma. Very little is known about the function of CHD5 in the nervous system or its mechanism of action. Here we report that depletion of Chd5 in the developing murine neocortex blocks neuronal differentiation and leads to an accumulation of undifferentiated progenitors. CHD5 binds a large cohort of genes and is required for facilitating the activation of neuronal genes. It also binds a cohort of Polycomb targets and is required for the maintenance of H3K27me3 on these genes. Interestingly, the chromodomains of CHD5 directly bind H3K27me3 and are required for neuronal differentiation. In the absence of CHD5, a subgroup of Polycomb-repressed genes becomes aberrantly expressed. These findings provide new insights into the regulatory role of CHD5 during neurogenesis and suggest how inactivation of this candidate tumor suppressor might contribute to neuroblastoma. Examination of genome-wide binding/occupancy of CHD5 in the SH-SY5Y cell line

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Ptbp1 is not required for retinal neurogenesis and cell fate specification [RNA-seq]

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