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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE44402 | GEO | 2013/03/15

SECONDARY ACCESSION(S): PRJNA189776

REPOSITORIES: GEO

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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

PQBP1-associated proteins spectrums in HEK-293 cells

Project description:Our study shows that deletion of the alternative splicing regulator PQBP1 in striatal progenitors resulted in defective striatal development due to impaired neurogenesis of spiny projection neurons (SPNs). Therefore, we further reveal that PQBP1 associated with components in splicing machinery by LC-MS/MS. These findings identify PQBP1 as a novel regulator in balancing striatal progenitor proliferation and differentiation.

2023-03-16 | PXD040439 | Pride

PQBP1 regulates striatum development through balancing striatal progenitor proliferation and differentiation

Project description:The balance between cell proliferation and differentiation is essential for maintaining the neural progenitor pool and brain development. Although the mechanisms underlying cell proliferation and differentiation at the transcriptional level have been studied intensively, post-transcriptional regulation of cell proliferation and differentiation remains largely unclear. Here, we show that deletion of the alternative splicing regulator PQBP1 in striatal progenitors resulted in defective striatal development due to impaired neurogenesis of spiny projection neurons (SPNs). Pqbp1 deficiency striatal progenitors exhibit declined proliferation and increased differentiation, resulting in a reduced striatal progenitor pool. We further reveal that PQBP1 associates with components in splicing machinery. The alternative splicing profiles identify that PQBP1 promotes the exon 9 inclusion of Numb, a variant that mediates progenitor proliferation. These findings identify PQBP1 as a novel regulator in balancing striatal progenitor proliferation and differentiation and provide alternative insights into the pathogenic mechanisms underlying Renpenning syndrome.

2023-02-21 | GSE225486 | GEO

SpyTag-based CLIP (SpyCLIP) sequencing of PQBP1 in ovarian cancer cells

Project description:Dysregulated expression of splicing factors has important roles in cancer development and progression. However, it remains a major challenge to identify the cancer-specific splicing variants. Here we demonstrated that splicing factor PQBP1 is commonly overexpressed in high-grade serous ovarian carcinoma (HGSOC) and high level of PQBP1 is associated with poor prognosis. To gain global insights into PQBP1-RNA binding property, RNA immunoprecipitation sequencing (RIP-seq) and SpyTag-based CLIP (SpyCLIP) were performed to analysis the interaction between PQBP1 and the target RNA.

2024-05-01 | GSE223196 | GEO

RNA immunoprecipitation sequencing (RIP-seq) of PQBP1 in ovarian cancer cells

2024-05-01 | GSE223090 | GEO

RNA sequencing (RNA-seq) of PQBP1 knockdown in ovarian cancer cells

Project description:To investigate the comprehensive function of PQBP1 in the regulation of RNA splicing, we established Dox-inducible PQBP1 knockdown HEY cell line. We then performed gene expression profiling analysis using data obtained from RNA-seq of PQBP1 knockdown and control HEY cells (three biological replications of each sample).

2024-05-01 | GSE223091 | GEO

Axonogenesis is coordinated by 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 axongeneisis-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.

2019-02-04 | GSE124554 | GEO

Long-read nanopore sequencing (Nanopore-seq) of PQBP1 knockdown in ovarian cancer cells

Project description:To investigate the comprehensive function of PQBP1 in the regulation of RNA splicing, we established Dox-inducible PQBP1 knockdown HEY cell line. We then performed transcript expression profiling analysis using data obtained from long-read nanopore-seq of PQBP1 knockdown and control HEY cells (three biological replications of each sample).

2024-05-01 | GSE223088 | GEO

Gene expression profiling of Golabi-Ito-Hall derived lymphoblast cells compared to a matched healthy person

Project description:A point mutation in the WW domain of PQBP1 that mediates its interaction with SIPP1 causes the Golabi-Ito-Hall (GIH) syndrome, which is associated with severe mental retardation and physical deformations. In this project we compared lymphoblast cell lines from a healthy person and a patient with the GIH syndrome and we found that the interaction between SIPP1 and the PQBP1-Y65C mutant is strongly impaired and is associated with significant differences in the expression of numerous genes. Furthermore, our data show that the Y65C mutation in PQBP1 results in a deficiency of (alternative) splicing and in major effects on several epigenetic markers. Thus, we suggest that GIH syndrome is a splicing disease€™ and that both PQBP1 and SIPP1 play an important role in its etiology. Four replicates were obtained from one lymphoblast cell line derived from a patient with Golabi-Ito-Hall syndrome, labeled as GIH. Four replicates were obtained from one lymphoblast cell line derived from a matched healthy person and is indicated as control.

2011-01-01 | E-GEOD-19724 | biostudies-arrayexpress