Genomic occurrence analysis of PRMT6-dependent H3R2me2a
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA420759 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6338620.fastq.gz | Fastqsanger.gz | |||
| SRR6338630.fastq.gz | Fastqsanger.gz | |||
| SRR6338640.fastq.gz | Fastqsanger.gz | |||
| SRR6338650.fastq.gz | Fastqsanger.gz | |||
| SRR6338660.fastq.gz | Fastqsanger.gz |
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Project description:Protein arginine methyltransferase 6 (PRMT6) is an epigenetic regulator of fundamental cellular processes, such as gene expression and DNA repair. Asymmetric dimethylation of histone H3 at arginine 2 (H3R2me2a) is the major histone modification catalyzed by PRMT6. To identify the genome-wide deposition and transcriptional impact of H3R2me2a, we established PRMT6 deletion in a human cell model of neural differentiation. These knockout cells show severe neural differentiation defects. ChIP-seq profiling reveals that H3R2me2a is present at promoter as well as non-promoter sites in a PRMT6-dependent manner. Loss of H3R2me2a causes enhanced H3K4me3 deposition and target gene transcription supporting a genome-wide repressive nature of H3R2me2a. Intriguingly, the non-promoter H3R2me2a peaks co-localize with active enhancer marks, such as H3K4me1 and H3K27ac.
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Project description:Protein arginine methyltransferase 6 (PRMT6) is an epigenetic regulator of fundamental cellular processes, such as gene expression and DNA repair. Asymmetric dimethylation of histone H3 at arginine 2 (H3R2me2a) is the major histone modification catalyzed by PRMT6. To identify the genome-wide deposition and transcriptional impact of H3R2me2a, we established PRMT6 deletion in a human cell model of neural differentiation. These knockout cells show severe neural differentiation defects. ChIP-seq profiling reveals that H3R2me2a is present at promoter as well as non-promoter sites in a PRMT6-dependent manner. Loss of H3R2me2a causes enhanced H3K4me3 deposition and target gene transcription supporting a genome-wide repressive nature of H3R2me2a. Intriguingly, the non-promoter H3R2me2a peaks co-localize with active enhancer marks, such as H3K4me1 and H3K27ac.
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Project description:To identify transcription factors of PRMT6 which could recruit PRMT6 to target genes, we used affinity purification of avi-tagged PRMT6 in combination with stable isotope labeling of amino acids in cell culture (SILAC) based mass spectrometry. For this, K562 cells were transduced with a lentiviral co expression vector for the BirA-ligase and avi-PRMT6 with a 21 amino acid taq, which is biotinylated in the cells. Cells expressing the BirA-ligase only served as a control. Avi-PRMT6 cells were grown in heavy SILAC medium and control cells in light SILAC medium for seven passages. Nuclear extracts were prepared from 1x108 cells and subjected to avi-PRMT6 affinity purification using magnetic streptavidin beads. Subsequently, the proteins were eluted from the beads. The eluates from the avi-PRMT6 and the control were mixed in a one to one ratio. Subsequently, we performed quantitative mass spectrometry (MS)-based analysis of the PRMT6 interactome.
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Project description:Protein arginine methyltransferase 6 (PRMT6) is an epigenetic regulator of fundamental cellular processes, such as gene expression and DNA repair. Asymmetric dimethylation of histone H3 at arginine 2 (H3R2me2a) is the major histone modification catalyzed by PRMT6. To identify the genome-wide deposition and transcriptional impact of H3R2me2a, we established PRMT6 deletion in a human cell model of neural differentiation. These knockout cells show severe neural differentiation defects. ChIP-seq profiling reveals that H3R2me2a is present at promoter as well as non-promoter sites in a PRMT6-dependent manner. Loss of H3R2me2a causes enhanced H3K4me3 deposition and target gene transcription supporting a genome-wide repressive nature of H3R2me2a. Intriguingly, the non-promoter H3R2me2a peaks co-localize with active enhancer marks, such as H3K4me1 and H3K27ac.
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Project description:Genomic location of PRMT6-dependent H3R2 methylation is decisive for the transcriptional outcome of associated genes
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Project description:PRMT6, a type I arginine methyltransferase, di-methylates the arginine residues of both histones and non-histones asymmetrically. Increasing evidence indicates that PRMT6 plays a tumor mediator involved in human malignancies. Here, we aim to uncover the essential role and underlying mechanisms of PRMT6 in promoting glioblastoma (GBM) proliferation. Investigation of PRMT6 expression in glioma tissues demonstrated that PRMT6 is overexpressed, and elevated expression of PRMT6 is negatively correlated with poor prognosis in glioma/GBM patients. Silencing PRMT6 inhibited GBM cell proliferation and induced cell cycle arrest at the G0/G1 phase, while overexpressing PRMT6 had opposite results. Further, we found that PRMT6 attenuates the protein stability of CDKN1B by promoting its degradation. Subsequent mechanistic investigations showed that PRMT6 maintains the transcription of CDC20 by activating histone methylation mark (H3R2me2a), and CDC20 interacts with and destabilizes CDKN1B. Rescue experimental results confirmed that PRMT6 promotes the ubiquitinated degradation of CDKN1B and cell proliferation via CDC20. We also verified that the PRMT6 inhibitor (EPZ020411) could attenuate the proliferative effect of GBM cells. Our findings illustrate that PRMT6, an epigenetic mediator, promotes CDC20 transcription via H3R2me2a to mediate the degradation of CDKN1B to facilitate GBM progression. Targeting PRMT6-CDC20-CDKN1B axis might be a promising therapeutic strategy for GBM.
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