Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Neuronal activity-induced late-onset alternative splicing and H3K9me3 modification

ABSTRACT: Activity-induced alternative splicing has emerged as an important mechanism for the dynamic modification of neuronal function. To examine whether activity could cause transcriptional programs alteration in alternative splicing and associative H3K9me3 in the specific genomic loci, we performed whole genome RNA-sequencing (RNA-seq) in cultured cortical neurons at 24 hours after membrane depolarization by exposure to high extracellular KCl (50mM, 10min). A transient neuronal activation could induce alternation of splice isoform choice in many genes at 24hrs after stimuli. To detect the correlation of activity-induced H3K9me3 accumulation with the splicing events, we performed ChIP-seq in hippocmapus of mice, which were subjected to enriched environment for 24 hours and kept in homecage for 1 week.

ORGANISM(S): Mus musculus

PROVIDER: GSE93682 | GEO | 2017/03/16

SECONDARY ACCESSION(S): PRJNA361557

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Mus musculus

Project description:Neuronal activity-induced late-onset alternative splicing and H3K9me3 modification

| PRJNA361557 | ENA

HDAC3-mediated regulation of the circadian gene Per1 contributes to age-related impairments in hippocampal memory and synaptic plasticity

Project description:We performed an RNA Sequencing experiment on dorsal hippocampal tissue from six groups of animals: Aging (18-20-month-old) HDAC3flox/flox homecage (H3F-HC); Aging (18-20-month-old) HDAC3flox/flox 60min post training (H3F-BV); Aging (18-20-month-old) wildtype homecage (OWT-HC); Aging (18-20-month-old) wildtype 60min post training (OWT-BV); Young (2-4-month-old) wildtype homecage (YWT-HC); Young (2-4-month-old) wildtype 60min post training (YWT-BV). Homecage animals were sacrificed directly from the animal's cage. Behavior animals were sacrificed sixty minutes following a 10min Object Location Memory training session.

2018-07-16 | GSE94832 | GEO

Neuronal activity regulates alternative exon usage

Project description:Neuronal activity regulates alternative exon usage

| PRJNA622919 | ENA

Position-dependent alternative splicing activity revealed by global profiling of alternative splicing events regulated by PTB

Project description:This SuperSeries is composed of the following subset Series: GSE23513: Position-dependent alternative splicing activity revealed by global profiling of alternative splicing events regulated by PTB (HJAY) GSE23514: Position-dependent alternative splicing activity revealed by global profiling of alternative splicing events regulated by PTB (Exon array) Refer to individual Series

2010-09-01 | E-GEOD-23522 | biostudies-arrayexpress

SAM68-specific splicing is required for proper selection of alternative 3'UTR isoforms in the nervous system

Project description:Neuronal alternative splicing is dynamically regulated in a spatiotemporal fashion. We previously found that STAR family proteins (SAM68, SLM1, SLM2) regulate spatiotemporal alternative splicing in the nervous system. However, the whole aspect of alternative splicing programs governed by STARs remains unclear. We deciphered the alternative splicing programs of SAM68 and SLM1 proteins using transcriptomics. We reveal that SAM68 and SLM1 encode distinct alternative splicing programs; SAM68 preferentially controls alternative last exon (ALE) splicing. Interleukin 1-receptor accessory protein (Il1rap) is a novel target for SAM68. The usage of Il1rap ALEs results in mainly two variants encoding two functionally different isoforms, a membrane-bound (mIL1RAcP) and a soluble (sIL1RAcP) type. The brain exclusively expresses mIL1RAcP. SAM68 knockout results in remarkable conversion into sIL1RAcP in the brain, which significantly disturbs IL1RAcP neuronal function. Thus, we uncover the critical role of proper neuronal isoform selection through ALE choice by the SAM68-specific splicing program.

2019-12-29 | GSE110258 | GEO

Chromatin-mediated alternative splicing regulates cocaine reward behavior

Project description:Neuronal alternative splicing is a key gene regulatory mechanism in brain. Yet the spliceosome machinery is insufficient to fully specify splicing complexity. In considering the role of the epigenome in activity-dependent alternative splicing, we and others find the histone modification, H3K36me3, to be a putative splicing regulator. In the current study, we found that mouse cocaine self-administration caused widespread differential alternative splicing, concomitant with enrichment of H3K36me3 at differentially spliced junctions. Importantly, only targeted epigenetic editing can distinguish between a direct role of H3K36me3 in splicing and an indirect role via regulation of splice factor expression elsewhere on the genome. We targeted Srsf11, which was both alternatively spliced and H3K36me3 enriched in brain following cocaine self-administration. Results: Epigenetic editing of H3K36me3 at Srsf11 was sufficient to drive its alternative splicing and enhanced cocaine self-administration, establishing the direct causal relevance of H3K36me3 to alternative splicing of Srsf11 and to reward behavior.

2021-07-31 | GSE180988 | GEO

The Neuron-specific chromatin regulatory subunit BAF53b is necessary for synaptic plasticity and memory.

Project description:We performed an RNA Sequencing experiment on dorsal hippocampal tissue from four groups of animals: Baf53b+/- homecage (Baf53b+/- HC); Baf53b+/- behavior (Baf53b+/- Beh); wildtype homecage (WT HC); and wildtype behavior (WT Beh). Homecage animals were sacrificed directly from the animal's cage. Behavior animals were sacrificed thirty minutes following Object Location Memory training. The objective of this study was to examine activity regulated gene expression following a learning event (HC vs Beh) in wildtype and Baf53b+/- mutant mice. Examination of gene expression following a learning event in wildtype and Baf53b+/- mutant mice in dorsal hippocampus.

2013-03-24 | E-GEOD-44229 | biostudies-arrayexpress

Next-generation sequencing identifies mRNAs targets that experience significant changes in alternative splicing upon PQBP1 knockdown in mouse embryonic cortical neurons

Project description:PQBP1 is a highly conserved protein closely related to neurodegenerative disorders. We identified PQBP1 as an important alternative splicing effector necessary for maintaining normal neuron functions in the brain. In order to explore PQBP1's functions in alternative splicing regulation and neuronal activities, we systematically profiled the alternative splicing targets of PQBP1 in mouse embryonic cortical neurons by RNA-seq. The mRNAs whose alternative splicing are affected by PQBP1 showed tissue-specific functional enrichment especially in neurite outgrowth, with strong Gene Ontology (GO) enrichments for neuron projection development/morphogenesis, dendrite development and axonogenesis. PQBP1's alternative splicing targets are also functionally enriched in RNA splicing, chromatin modification, and ARF signal transduction. We applied RNA-seq to compare the transcriptomes of mock and PQBP1 knockdown mouse embryonic cortical neuron samples.

2013-03-15 | E-GEOD-44402 | biostudies-arrayexpress

Splicing analyses of mESCs, mNPCs, and mMNs

Project description:PTBP1 and PTBP2 control alternative splicing programs during neuronal development, but the cellular functions of most PTBP1/2-regulated isoforms remain unknown. We show that PTBP1 guides developmental gene expression by regulating the transcription factor Pbx1. We identify exons that are differentially spliced when mouse embryonic stem cells (ESCs) differentiate into neuronal progenitor cells (NPCs) and neurons, and transition from PTBP1 to PTBP2 expression. We define those exons controlled by PTBP1 in ESCs and NPCs by RNA-seq analysis after PTBP1 depletion and PTBP1 crosslinking-immunoprecipitation. We find that PTBP1 represses Pbx1 exon 7 and the expression of its neuronal isoform Pbx1a in ESC. Using CRISPR-Cas9 to delete regulatory elements for exon 7, we induce Pbx1a expression in ESCs, finding that this activates transcription of specific neuronal genes including known Pbx1 targets. Thus PTBP1 controls the activity of Pbx1 and suppresses its neuronal transcriptional program prior to differentiation. HB9-GFP mESCs were differentiated into mNPCs and mMNs. Poly-A RNA was isolated from isolated populations of mESCs, mNPCs, and mMNs for RNA-sequencing and splicing analyses.

2016-07-03 | E-GEOD-71079 | biostudies-arrayexpress

Mus musculus

Project description:Cell type-specific alternative splicing during mammalian neuronal differentiation

| PRJNA380202 | ENA