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CPEB3 regulates neuron-specific alternative splicing and involves neurogenesis gene expression [RNA-seq]

ABSTRACT: CPEB3 regulates neuron-specific alternative splicing and involves neurogenesis gene expression [RNA-seq]

PROVIDER: PRJNA641660 | ENA |

REPOSITORIES: ENA

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CPEB3 regulates neuron-specific alternative splicing and involves neurogenesis gene expression

Project description:CPEB3 regulates neuron-specific alternative splicing and involves neurogenesis gene expression

| PRJNA641657 | ENA

CPEB3 regulates neuron-specific alternative splicing and involves neurogenesis gene expression [RIP-seq]

Project description:In the mammalian brain, alternative pre-mRNA splicing is a fundamental mechanism that modifies neuronal function dynamically where secretion of different splice variants regulates neurogenesis, development, pathfinding, maintenance, migration, and synaptogenesis. Sequence-specific RNA Binding Protein CPEB3 has distinctive isoform-distinct biochemical interactions and neuronal development assembly roles. Nonetheless, the mechanisms moderating splice isoform options remain unclear. To establish the modulatory trend of CPEB3, we cloned and excessively expressed CPEB3 in HT22 cells. We used RNA-seq to analyze CPEB3-regulated alternative splicing on control and CPEB3-overexpressing cells. Moreover, we used iRIP-seq to identify CPEB-binding targets. We additionally validated CPEB3-modulated genes using RT-qPCR. CPEB3 overexpression had insignificant effects on gene expression in HT22 cells. Notably, CPEB3 partially modulated differential gene splicing enhanced in the modulation of transcription, cell cycle, Wnt signaling cascade, neurotrophin, synapse, and specific development pathway. qRT‑PCR verified the CPEB3‑modulated transcription of neurogenesis genes LCN2 and NAV2, synaptogenesis gene CYLD, as well as development gene JADE1. Herein, we established that CPEB3 is a critical modulator of alternative splicing in neurogenesis, which remarkably enhances the current understanding of the CPEB3 mediated alternative pre-mRNA splicing.

2021-02-17 | GSE153167 | GEO

CPEB3 regulates neuron-specific alternative splicing and involves neurogenesis gene expression [RNA-seq]

2021-02-17 | GSE153166 | GEO

CPEB3 regulates neuron-specific alternative splicing and involves neurogenesis gene expression [RIP-seq]

Project description:CPEB3 regulates neuron-specific alternative splicing and involves neurogenesis gene expression [RIP-seq]

| PRJNA641661 | ENA

CPEB3 regulates neuron-specific alternative splicing and involves neurogenesis gene expression.

Project description: Not available

| S-EPMC7880327 | biostudies-literature

CPEB3 regulates neuron-specific alternative splicing and involves neurogenesis gene expression

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-02-17 | GSE153168 | GEO

m6A modification involves in enriched environment-induced neurogenesis and cognition enhancement

Project description:m6A modification involves in enriched environment-induced neurogenesis and cognition enhancement

| PRJNA811978 | ENA

Single-cell alternative splicing analysis with Expedition reveals splicing dynamics during neuron differentiation

Project description:Alternative splicing (AS) generates isoform diversity critical for cellular identity and homeostasis, yet characterization of this diversity in single cells remains limited. We developed Expedition, a computational framework to categorize and visualize the heterogeneity of AS from single-cell transcriptomes. Expedition consists of (i) outrigger, a de novo splice graph transversal algorithm to detect AS from single cell RNA-seq; (ii) anchor, a Bayesian approach to assign splicing modalities and (iii) bonvoyage, using non-negative matrix factorization to visualize modality changes. By applying Expedition to single iPSCs undergoing neuron differentiation, we discover that 25% of AS exons exhibit bimodality and are flanked by longer and more conserved introns harboring distinct cis-regulatory motifs. Bimodal exons are highly dynamic during cellular transitions, preserve translatability, enriched in recently emerged genes and have conserved AS in mammals. Applying Expedition (http://github.com/YeoLab/Expedition) in single cells redefines our estimates and understanding of AS in evolution and biology.

2017-07-12 | GSE85908 | GEO

Regulation of alternative splicing by histone modifications

Project description:Alternative splicing of pre-mRNA is a prominent mechanism to generate protein diversity, yet its regulation is poorly understood. Here, we demonstrate a direct role for histone modifications in alternative splicing. We find distinctive histone modification signatures which correlate with splicing outcome in a set of human genes. Modulation of histone modifications causes splice site switching. The mechanism for histone-mediated splice site selection involves a histone mark which is read by a chromatin protein, which in turn recruits a splicing regulator. These results outline an adaptor system for reading of histone marks by the pre-mRNA splicing machinery. To obtain an estimate of how many PTB-dependent alternative splicing events are regulated by SET2/MRG15-mediated recruitment of PTB, we carried out a genomewide comparative analysis of alternative splicing in hMSC cells depleted of either SETD2, MRG15 or PTB using specific siRNAs, or mock-depleted using a control siRNA.

2010-02-10 | E-GEOD-19373 | biostudies-arrayexpress

Attenuation of PTBP2 facilitates fibroblast to neuron conversion by promoting alternative splicing of neuronal genes

Project description:The direct conversion of human skin fibroblasts to neurons has a low efficiency and unclear mechanism. Here, we show that the knockdown of PTBP2 (nPTB) significantly enhanced the transdifferentiation induced by ASCL1, MiR124-9/9* and p53 shRNA to generate mostly GABAergic neurons. Longitudinal RNAseq analyses identified the continuous induction of many RNA Splicing Regulators (RSRs). Among these, the knockdown of RBFOX3, which encodes the mature neuronal marker NeuN, significantly abrogated the transdifferentiation. Overexpression of RBFOX3 significantly enhanced the conversion induced by AMp; the enhancement was occluded by PTBP2 knockdown. We found that PTBP2 attenuation significantly favored neuron-specific alternative splicing (AS) of many genes involved in synaptic transmission, signal transduction, and axon formation. RBFOX3 knockdown significantly reversed the effect, while RBFOX3 overexpression enhanced it. The study reveals the critical role of neuron-specific AS in the direct conversion of human skin fibroblasts to neurons by showing that PTBP2 attenuation enhances this mechanism in concert with RBFOX3.

2023-10-12 | GSE210131 | GEO

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