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STAU1 selectively regulates the expression of inflammatory and immune response genes and alternative splicing of nerve growth factor receptor signaling genes

ABSTRACT: STAU1 selectively regulates the expression of inflammatory and immune response genes and alternative splicing of nerve growth factor receptor signaling genes

PROVIDER: PRJNA563927 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10069431_1.fastq.gz	Fastqsanger.gz
	SRR10069431_2.fastq.gz	Fastqsanger.gz
	SRR10069432_1.fastq.gz	Fastqsanger.gz
	SRR10069432_2.fastq.gz	Fastqsanger.gz
	SRR10069433_1.fastq.gz	Fastqsanger.gz

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STAU1 selectively regulates the expression of inflammatory and immune response genes and alternative splicing of nerve growth factor receptor signaling genes

Project description:To study the potential targets and functions of STAU1 which might be related to neuropathic pain, we obtained STAU1-regulated transcriptome in HeLa cells. High-throughput RNA sequencing(RNA-seq) were performed for HeLa cells and control cells to define the comprehensive gene expression profiles and identify the genome-wide alternative splicing events regulated by STAU1.

2020-10-20 | GSE136890 | GEO

3'READS+RIP defines differential Staufen1 binding to alternative 3'UTR isoforms and reveals structures and sequence motifs influencing binding and polysome association

Project description:Using 3ʹ region extraction and deep sequencing coupled to ribonucleoprotein immunoprecipitation (3’READS+RIP), together with reanalyzing previous STAU1 binding and RNA structure data, we delineate STAU1 interactions transcriptome-wide, including binding differences between alternative polyadenylation (APA) isoforms. Consistent with previous reports, RNA structures are dominant features for STAU1 binding to CDSs and 3ʹUTRs. Overall, relative to short 3ʹUTR counterparts, longer 3ʹUTR isoforms of genes have stronger STAU1 binding, most likely due to a higher frequency of RNA structures, including specialized IRAlus. However, a sizable fraction of genes express transcripts showing the opposite trend, attributable to AU-rich sequences in their alternative 3'UTRs, possibly recruiting antagonistic RBPs and/or destabilizing STAU1-binding RNA structures. Using STAU1-knockout cells, we show that strong STAU1 binding to mRNA 3'UTRs generally enhances polysome association. However, IRAlus have little impact on STAU1-mediated polysome association despite having strong interactions with the protein.

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RALY selectively regulates the alternative splicing of transcription factors and the expression of immune/ inflammatory response genes in HeLa cells

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STAU1 selectively regulates the expression of inflammatory and immune response genes and alternative splicing of the nerve growth factor receptor signaling pathway.

Project description:Double‑stranded RNA‑binding protein Staufen homolog 1 (STAU1) is a highly conserved multifunctional double‑stranded RNA‑binding protein, and is a key factor in neuronal differentiation. RNA sequencing was used to analyze the overall transcriptional levels of the upregulated cells by STAU1 and control cells, and select alternative splicing (AS). It was determined that the high expression of STAU1 led to changes in the expression levels of a variety of inflammatory and immune response genes, including IFIT2, IFIT3, OASL, and CCL2. Furthermore, STAU1 was revealed to exert a significant regulatory effect on the AS of genes related to the 'nerve growth factor receptor signaling pathway'. This is of significant importance for neuronal survival, differentiation, growth, post‑damage repair, and regeneration. In conclusion, overexpression of STAU1 was associated with immune response and regulated AS of pathways related to neuronal growth and repair. In the present study, the whole transcriptome of STAU1 expression was first analyzed, which laid a foundation for further understanding the key functions of STAU1.

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Viral-Induced Alternative Splicing of Host Genes Promotes Influenza Replication

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CCAR-1 regulates the alternative splicing of multiple genes in Caenorhabditis elegans

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APEX1-regulated alternative splicing of genes involve in lung cancer progression

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Splicing factor PRPF31 retinitis pigmentosa (RP11) is caused by disrupted alternative splicing programmes for genes implicated in pre-mRNA splicing, cellular adhesion and ciliogenesis

Project description:Mutations in pre-mRNA processing factors (PRPFs) cause autosomal dominant retinitis pigmentosa (RP), but it is unclear why mutations in ubiquitously expressed genes cause retinal disease. We have generated transcriptome profiles from RP11 (PRPF31-mutated) patient-derived retinal organoids and retinal pigment epithelium (RPE), as well as Prpf31+/- mouse tissues, which revealed that disrupted alternative splicing occurred for specific splicing programmes. Mis-splicing of genes encoding pre-mRNA splicing proteins was limited to patient-specific retinal cells and Prpf31+/- mouse retinae and RPE. Mis-splicing of genes implicated in ciliogenesis and cellular adhesion was associated with severe RPE defects that include disrupted apical-basal polarity, reduced trans-epithelial resistance and phagocytic capacity, and decreased cilia length and incidence. Disrupted cilia morphology also occurred in patient-derived photoreceptors, associated with progressive degeneration and cellular stress. In situ gene-editing of a pathogenic mutation rescued protein expression and key cellular phenotypes in RPE and photoreceptors, providing proof-of-concept for future therapeutic strategies.

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Widespread regulated alternative splicing of single codons accelerates proteome evolution

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