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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE153168 | GEO | 2021/02/17

REPOSITORIES: GEO

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

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. Consequently, 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 neural development, neuron cycle, neurotrophin, synapse, and specific development pathway, implying an alternative splicing regulatory mechanism associated with neurogenesis. Moreover, qRT-PCR verified the CPEB3-modulated transcription of neurogenesis genes LCN2 and NAV2, synaptogenesis gene CYLD, as well as neural 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.

| S-EPMC7880327 | biostudies-literature

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]

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 | GSE153166 | GEO

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

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

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

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

| PRJNA641660 | ENA

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

SRRM4-dependent neuron-specific alternative splicing of protrudin transcripts regulates neurite outgrowth.

Project description:Alternative splicing gives rise to diversity of the proteome, and it is especially prevalent in the mammalian nervous system. Indeed, many factors that control the splicing process govern nervous system development. Among such factors, SRRM4 is an important regulator of aspects of neural differentiation including neurite outgrowth. The mechanism by which SRRM4 regulates neurite outgrowth has remained poorly understood, however. We now show that SRRM4 regulates the splicing of protrudin gene (Zfyve27) transcripts in neuronal cells. SRRM4 was found to promote splicing of protrudin pre-mRNA so as to include a microexon (exon L) encoding seven amino acids in a neuron-specific manner. The resulting protein (protrudin-L) promotes neurite outgrowth during neurogenesis. Depletion of SRRM4 in Neuro2A cells impaired inclusion of exon L in protrudin mRNA, resulting in the generation of a shorter protein isoform (protrudin-S) that is less effective at promoting neurite extension. SRRM4 was found to recognize a UGC motif that is located immediately upstream of exon L and is necessary for inclusion of exon L in the mature transcript. Deletion of exon L in Neuro2A or embryonic stem cells inhibited neurite outgrowth. Our results suggest that SRRM4 controls neurite outgrowth through regulation of alternative splicing of protrudin transcripts.

| S-EPMC5247714 | biostudies-literature

Axonogenesis Is Coordinated by Neuron-Specific Alternative Splicing Programming and Splicing Regulator PTBP2.

Project description:How a neuron acquires an axon is a fundamental question. Piecemeal identification of many axonogenesis-related genes has been done, but coordinated regulation is unknown. Through unbiased transcriptome profiling of immature primary cortical neurons during early axon formation, we discovered an association between axonogenesis and neuron-specific alternative splicing. Known axonogenesis genes exhibit little expression alternation but widespread splicing changes. Axonogenesis-associated splicing is governed by RNA binding protein PTBP2, which is enriched in neurons and peaks around axonogenesis in the brain. Cortical depletion of PTBP2 prematurely induces axonogenesis-associated splicing, causes imbalanced expression of axonogenesis-associated isoforms, and specifically affects axon formation in vitro and in vivo. PTBP2-controlled axonogenesis-associated Shtn1 splicing determines SHTN1's capacity to regulate actin interaction, polymerization, and axon growth. Precocious Shtn1 isoform switch contributes to disorganized axon formation of Ptbp2-/- neurons. We conclude that PTBP2-orchestrated alternative splicing programming is required for robust generation of a single axon in mammals.

| S-EPMC6474845 | biostudies-literature

Muscleblind-like proteins regulate embryonic stem cell-specific alternative splicing and reprogramming

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-06-26 | E-GEOD-45505 | biostudies-arrayexpress

Quaking is a global regulator of muscle-specific alternative splicing in vertebrates

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-06-05 | E-GEOD-40962 | biostudies-arrayexpress