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Mus musculus

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

PROVIDER: PRJNA361557 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5180513_1.fastq.gz	Fastqsanger.gz
	SRR5180513_2.fastq.gz	Fastqsanger.gz
	SRR5180514_1.fastq.gz	Fastqsanger.gz
	SRR5180514_2.fastq.gz	Fastqsanger.gz
	SRR5180515_1.fastq.gz	Fastqsanger.gz

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

Project description: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.

2017-03-16 | GSE93682 | GEO

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

Mus musculus

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

| PRJNA380202 | ENA

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

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

2013-03-15 | GSE44402 | GEO

Nuclear Paxillin Modulates Alternative Splicing Programs in Neurons during Sensitive Periods of Brain Development

Project description:During sensitive postnatal periods, brain neural circuits undergo significant refinement coincident with widespread neuronal alternative splicing events in which hundreds of genes alter their splice site selection to generate isoforms essential for synaptic plasticity. Here, we reveal that neuronal activity-dependent serine119 phosphorylation of paxillin (p-paxillin S119) acts as a molecular switch in the nucleus to modulate alternative splicing during this period. We report that following NMDA receptor activation, nuclear p-paxillin S119 is recruited to nuclear speckles, where it interacts with U2AFs and splicing factors. Neuronal paxillin expression is required for timely alternative splicing of synaptic factors, including Snap25. Consequently, young mice lacking paxillin S119 phosphorylation exhibit significantly reduced levels of Snap25-5b isoforms, impaired presynaptic function at hippocampal Schaffer collateral-CA1 synapses, and deficits in short-term learning and memory. These findings support the idea that nuclear p-paxillin S119 is a critical mediator of alternative splicing programs in postnatal neurons during a sensitive period essential for neural plasticity.

2025-08-08 | PXD060131 | Pride

Neuronal activity regulates alternative exon usage

Project description:Neuronal activity regulates alternative exon usage

| PRJNA622919 | ENA

Mus musculus

Project description:Control of Neuronal Synapse Specification by a Highly Dedicated Alternative Splicing program

| PRJNA317347 | ENA

Early establishment of neuronal transcriptome signatures is critical for nervous system differentiation

Project description:Cell-type-specific gene regulatory programs are crucial for cell differentiation and function. In animal neurons, the highly conserved ELAV/Hu family of proteins promotes alternative splicing and alternative polyadenylation of mRNA precursors to create unique neuronal transcript isoforms. Here, we show in Drosophila that the ELAV-mediated establishment of neuron-specific mRNA isoforms at the onset of neuronal differentiation constitutes a developmental bottleneck. While ELAV loss during a critical developmental time window is lethal and cannot be rescued later by the activation of the ELAV-like paralogue FNE, loss of ELAV function outside of that window results in neurological defects of differing nature and degree. FNE can effectively perform all molecular functions of ELAV, and, when activated early enough, fully rescue neuronal development. Our findings demonstrate the essential role of robust ELAV activity and intact neuronal signatures in the differentiation and function of the nervous system.

2022-11-15 | GSE199714 | GEO

Efficacy of longevity interventions in C. elegans is determined by early life activity of RNA splicing factors II

Project description:Geroscience aims to target the aging process to extend healthspan. However, even isogenic individuals show heterogeneity in natural aging rate and responsiveness to pro-longevity interventions, limiting translational potential. Using in vivo mini gene reporters in isogenic C. elegans, we show that alternative splicing of mRNAs related to lipid metabolism in young animals is coupled to subsequent life expectancy. Further, activity of RNA splicing factors REPO-1 and SFA-1 early in life modulates effectiveness of specific longevity interventions via POD-2/ACC1 and regulation of lipid utilization. In addition, early inhibition of REPO-1 renders animals refractory to late onset suppression of the TORC1 pathway. Together these data suggest that activity of RNA splicing factors and the metabolic landscape early in life can modulate responsiveness to longevity interventions and may explain variance in efficacy between individuals.

2025-11-07 | GSE293218 | GEO

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