HNSCs siRNA NOVA2, PQBP1, BRPF1 and DYRK1A
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA577099 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10267209_1.fastq.gz | Fastqsanger.gz | |||
| SRR10267209_2.fastq.gz | Fastqsanger.gz | |||
| SRR10267210_1.fastq.gz | Fastqsanger.gz | |||
| SRR10267210_2.fastq.gz | Fastqsanger.gz | |||
| SRR10267211_1.fastq.gz | Fastqsanger.gz |
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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.
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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.
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Project description:DYRK1A is a protein kinase with several roles in brain development. This kinase is involved in two intellectual disability syndromes: Down syndrome and DYRK1A haploinsufficiency syndrome. The Dyrk1a+/- mouse is a model for DYRK1A haploinsufficiency syndrome. We used microarray to evaluate the impact of DYRK1A haploinsufficiency in the development of the cerebral cortex.
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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).
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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.
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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.
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Project description:Transcription profiling of transgenic down syndrome mouse model to show the role of DYRK1A gene. The molecular mechanisms that lead to the cognitive defects characteristic of Down syndrome (DS), the most frequent cause of mental retardation, have remained elusive. Here we use a transgenic DS mouse model to show that DYRK1A gene dosage imbalance deregulates chromosomal clusters of genes located near neuron-restrictive silencer factor (REST/NRSF) binding sites. We found that DYRK1A binds the SWI/SNF-complex known to interact with REST/NRSF. Mutation of a REST/NRSF binding site in the promoter of the REST/NRSF target gene L1cam modifies the transcriptional effect of Dyrk1Adosage imbalance on L1cam. DyrkA dosage imbalance perturbs Rest/Nrsf levels with decreased Rest/Nrsf expression in embryonic neurons and increased expression in adult neurons. We identified a coordinated deregulation of multiple genes that are responsible for the cellular phenotypic traits present in DS such as dendritic growth impairment and microcephaly during prenatal cortex development. Dyrk1a overexpression in primary mouse cortical neurons reduced the neuritic complexity. In the postnatal hippocampus, DYRK1A overexpression suppresses a form of synaptic plasticity that may be sufficient to cause DS cognitive defects. We propose that DYRK1A overexpression-related neuronal gene deregulation generates the brain phenotypic changes that characterize DS, with an accessory role for the gene dosage imbalance of other chromosome 21 genes. Transgenic embrionic brain regions versus wild type mice were analysed. The log2 values represent Cy5/Cy3 ratio (transgenic Cy5/wild type Cy3). Each array was scanned under a green laser (543 nm for Cy3 labeling) or a red laser (633 nm for Cy5 labeling) using a ScanArray Lite scanning confocal fuorescent scanner with 10 u resolution (laser power: 85% for Cy5 and 90% for Cy3, gain: 75% for Cy5 and 70% for Cy3). Scanned output files were analyzed using the GenePix Pro 3.0 software. Each spot was defined by automatic positioning of a grid of circles over the image. The average and median pixel intensity ratios calculated from both channels and the local background of each spot were determined. Local background corrected intensity ratios was determined for each spot. The background-corrected expression data were filtered for flagged spots and weak signal. Normalization was performed by the global Lowess method. Studentâs t-test was applied to determine the p value.
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