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PRPF8 controls alternative splicing of PIRH2 to modulate the p53 pathway and survival of human embryonic stem cells

ABSTRACT: To investigate the function of PRPF8 in survial in hESCs, we established hESC cell lines H9 in which PRPF8 has been knocked down by siRNA.We then performed gene expression profiling analysis and alternative splicing analysis using data obtained from RNA-seq of 4 different cells at two time points.

ORGANISM(S): Homo sapiens

PROVIDER: GSE213559 | GEO | 2023/12/31

REPOSITORIES: GEO

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PRPF8 controls alternative splicing of PIRH2 to modulate the p53 pathway and survival of human embryonic stem cells

Project description:PRPF8 controls alternative splicing of PIRH2 to modulate the p53 pathway and survival of human embryonic stem cells

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Assay for Transposase Accessible Chromatin with high-throughput sequencing (ATAC-seq) revealed genomic chromatin accessibilities change induced by loss of ARID1A in differentiated (day 4) H9 hESCs

Project description:We reported loss of ARID1A promoted neurogenesis and inhibited cardiogenesis. Under microscopy, we observed that spontaneously differentiated cells were induced in ARID1A KO H9 hESCs cultured in mTesR medium. We did not know what cells types were. Here ATAC-seq were used to investigate chromatin accessibilities change in differentiated (day 4) WT H9 hESCs and ARID1A KO hESC cells.

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Regulation of constitutive and alternative messenger RNA splicing across the human transcriptome by PRPF8 is determined by 5' splice site strength

Project description:RNA-sequencing experiments performed on control siRNA treated and PRPF8 depleted cells

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OGA-mediated protein glycosylation regulates pluripotency states in human embryonic stem cells

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PRPF8-mediated dysregulation of hBrr2 helicase disrupts human spliceosome kinetics and 5'-splice-site selection causing tissue-specific defects

Project description:The carboxy-terminus of the spliceosomal protein PRPF8, which regulates the RNA helicase Brr2, is a hotspot for mutations causing retinitis pigmentosa-type 13, with unclear role in human splicing and tissue-specificity mechanism. We used patient induced pluripotent stem cells-derived cells, carrying the heterozygous PRPF8 c.6926A>C (p.H2309P) mutation to demonstrate retinal-specific endophenotypes comprising photoreceptor loss, apical-basal polarity and ciliary defects. Comprehensive molecular, transcriptomic, and proteomic analyses revealed a role of the PRPF8/Brr2 regulation in 5’-splice site (5’SS) selection by spliceosomes, for which disruption impaired alternative splicing and weak/suboptimal 5’SS selection, and enhanced cryptic splicing, predominantly in ciliary and retinal-specific transcripts. Altered splicing efficiency, nuclear speckles organisation, and PRPF8 interaction with U6 snRNA, caused accumulation of active spliceosomes and poly(A)+ mRNAs in unique splicing clusters located at the nuclear periphery of photoreceptors. Collectively these elucidate the role of PRPF8/Brr2 regulatory mechanisms in splicing and the molecular basis of retinal disease, informing therapeutic approaches.

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PRPF8-mediated dysregulation of hBrr2 helicase disrupts human spliceosome kinetics and 5´-splice-site selection causing tissue-specific defects

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PRPF8 iCLIP on HeLa cells in response to eIF4A3 Knockdown

Project description:This experiment uses iCLIP to identify the binding pattern of the spliceosomal protein PRPF8 on RNA. The data shows that PRPF8 binds strongly and specifically in the region 12 to 14nt upstream of 5' splice sites (5ss). Due to PRPF8's role in the formation of the catalytically active spliceosome, this data can be used as a readout of 5ss selection. Here, we performed iCLIP on HeLa cells treated with control or EIF4A3 siRNA, with 4 replicate samples per condition and eIF4A3 protein levels reduced ~50% in knockdown. We investigated the role of the exon junction complex (EJC) in suppressing 5ss that are reconstituted at the junction of two canonical exons (RS-5ss) - selection of these splice sites would result in recursive splicing of canonical exons. We plotted the crosslink sites of reads that span an exon-exon junction, seperating reads that span RS-5ss from those that do not. We found that reads that span an RS-5ss are enriched at the 12-14nt window associated with 5ss selection, while reads that span other exon-exon junctions are not enriched. This effect is magnified greatly by knockdown of eIF4A3. The results indicate that RS-5ss can be used by the spliceosome, but that this process is usually repressed by the EJC. This data is evidence of recursive splicing of canonical exons and the role of the EJC in repressing recursive splicing.

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PRPF8-mediated dysregulation of hBrr2 helicase disrupts human spliceosome kinetics and 5´-splice-site selection causing tissue-specific defects

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