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PRMT5/WDR77 moonlights as an RNA-binding complex and shapes T cell function and anti-tumor immunity via post-transcriptional regulation of PDCD1

ABSTRACT: To reveal the potential RNA targets of PRMT5 in jurkat cells, we performed Flag Immunoprecipitation sequencing (RIP-seq) in PRMT5-Flag overexpression (OE) jurkat cells after stimulated with polyhydroxyalkanoates (PHA) for 48 hours.

ORGANISM(S): Homo sapiens

PROVIDER: GSE276385 | GEO | 2025/09/27

REPOSITORIES: GEO

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Genome-wide analysis of genes regulated by p44/wdr77 and PRMT5 in lung and prostate cancer cells

Project description:Analysis of gene expression in lung and prostate cancer cells expressing non-target (NT), p44/wdr77. or PRMT5 shRNA. Results provide important information on how p44/wdr77 and PRMT5 control cellular proliferation. Total RNA obtained from cells expressing NT, p44/wdr77, or PRMT5 shRNA.

2014-04-14 | E-GEOD-56757 | biostudies-arrayexpress

The role of PRMT5/WDR77 complex in promoting breast cancer oncogenesis [RNA-Seq_HPTB]

Project description:Comprehensive RNA-seq experiments in DMSO and HPTB (inhibitor of PRMT5) treated cells delineate the role of PRMT5 complex in promoting breast cancer oncogenesis

2017-12-31 | GSE75742 | GEO

Transcriptomic Analysis Reveals Co-Regulation by PRMT5 and WDR77 in HSC-5 Cells

Project description:CRISPR was utilized to deplete either PRMT5 or WDR77 in HSC-5 cells. Subsequently, RNA-seq was performed to identify changes in the transcriptome following the loss of PRMT5 or WDR77 in these cells. Critically, Gene Set Enrichment Analysis (GSEA) was conducted to screen and identify a list of genes co-regulated by PRMT5 and WDR77.

2024-09-19 | GSE272319 | GEO

The role of PRMT5/WDR77 complex in promoting breast cancer oncogenesis [RNA-Seq]

Project description:Comprehensive RNA-seq experiments in control and PRMT5 and WDR77 shRNA infected cells delineate the role of PRMT5/WDR77 complex in promoting breast cancer oncogenesis

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The role of PRMT5/WDR77 complex in promoting breast cancer oncogenesis [ChIP-Seq]

Project description:The PRMT5/WDR77 complex is known to regulate alternative splicing through the symmetric dimethylation of spliceosome proteins in the cytoplasm. Overexpression of this complex is observed in different types of cancer including breast cancer, where it shows increased nuclear accumulation.To understand the nuclear role and the chromatin binding properties of PRMT5 we performed genome-wide ChIP-Seq analysis in the breast cancer cell line MDA-MB-231.

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Genome-wide analysis of genes regulated by p44/wdr77 and PRMT5 in lung and prostate cancer cells

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The underlying mechanism by which DAZAP1 exerted carcinogenesis and its potential targets in MM

Project description:An RIP experiment was performed in CAG cells using FLAG antibody as bait. The position of peak summit around transcript start sites of genes can predict the interaction sites of protein and gene. We compared the peak summit of CAG EV and CAG DAZAP1 OE cells to find the differences between CAG EV cells and CAG DAZAP1 OE cells.

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The PRMT5/WDR77 complex restricts hepatitis E virus replication.

Project description:Hepatitis E virus (HEV) is one of the main pathogenic agents of acute hepatitis in the world. The mechanism of HEV replication, especially host factors governing HEV replication is still not clear. Here, using HEV ORF1 trans-complementation cell culture system and HEV replicon system, combining with stable isotope labelling with amino acids in cell culture (SILAC) and mass spectrometry (MS), we aimed to identify the host factors regulating HEV replication. We identified a diversity of host factors associated with HEV ORF1 protein, which were putatively responsible for viral genomic RNA replication, in these two cell culture models. Of note, the protein arginine methyltransferase 5 (PRMT5)/WDR77 complex was identified in both cell culture models as the top hit. Furthermore, we demonstrated that PRMT5 and WDR77 can specifically inhibit HEV replication, but not other viruses such as HCV or SARS-CoV-2, and this inhibition is conserved among different HEV strains and genotypes. Mechanistically, PRMT5/WDR77 can catalyse methylation of ORF1 on its R458, impairing its replicase activity, and virus bearing R458K mutation in ORF1 relieves the restriction of PRMT5/WDR77 accordingly. Taken together, our study promotes more comprehensive understanding of viral infections but also provides therapeutic targets for intervention.

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PRMT5 is essential for sustaining normal adlut hematopoiesis

Project description:Examining the effects of PRMT5 loss on the gene expression profile of hematopoietic stem and progenitor cells We established the PRMT5 conditional KO mice, and bred the mice with Mx1 cre transgenic mice to delete PRMT5 in hematopoietic cells. We isolated hematopoetic stem and progenitor cells 3 days after PRMT5 deletion, and examined the gene expression files using RNA-sequencing.

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The PRMT5/WDR77 complex regulates alternative splicing through ZNF326 in breast cancer.

Project description:We observed overexpression and increased intra-nuclear accumulation of the PRMT5/WDR77 in breast cancer cell lines relative to immortalized breast epithelial cells. Utilizing mass spectrometry and biochemistry approaches we identified the Zn-finger protein ZNF326, as a novel interaction partner and substrate of the nuclear PRMT5/WDR77 complex. ZNF326 is symmetrically dimethylated at arginine 175 (R175) and this modification is lost in a PRMT5 and WDR77-dependent manner. Loss of PRMT5 or WDR77 in MDA-MB-231 cells leads to defects in alternative splicing, including inclusion of A-T rich exons in target genes, a phenomenon that has previously been observed upon loss of ZNF326. We observed that the alternatively spliced transcripts of a subset of these genes, involved in proliferation and tumor cell migration like REPIN1/AP4, ST3GAL6, TRNAU1AP and PFKM are degraded upon loss of PRMT5. In summary, we have identified a novel mechanism through which the PRMT5/WDR77 complex maintains the balance between splicing and mRNA stability through methylation of ZNF326.

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