ATAC-seq of IMR90 cells during OIS under TPR depletion
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ABSTRACT:
PROVIDER: PRJNA1102328 | ENA |
REPOSITORIES: ENA
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Project description:RNA-seq of IMR90 cells during OIS under TPR depletion
| PRJNA1102322 | ENA
Project description:During oncogene-induced senescence there are striking changes in the structure of the nucleus and the organisation of heterochromatin. This is accompanied by activation of a pro-inflammatory gene expression programme – the senescence associated secretory phenotype (SASP) – driven by transcription factors such as NF-κB. Here we show that TPR, a protein of the nuclear pore complex basket, is required for the very early activation of NF- κB signalling during the stress-response phase of oncogene-induced senescence. This is prior to activation of the SASP and occurs without affecting NF-κB nuclear import. We show that TPR is required for the activation of TBK1 signalling at these early stages of senescence and we link this to the formation of heterochromatin-enriched cytoplasmic chromatin fragments thought to bleb off from the nuclear periphery. These cytoplasmic chromatin fragments appear to lack nuclear pore components. Our data suggest that TPR at the nuclear pore is involved in the loss of structural integrity of the nuclear periphery during senescence. We propose that this acts as a trigger for activation of cytoplasmic nucleic acid sensing, NF-κB signalling, and activation of the SASP, during senescence.
2024-12-19 | GSE264390 | GEO
Project description:During oncogene-induced senescence there are striking changes in the structure of the nucleus and the organisation of heterochromatin. This is accompanied by activation of a pro-inflammatory gene expression programme – the senescence associated secretory phenotype (SASP) – driven by transcription factors such as NF-κB. Here we show that TPR, a protein of the nuclear pore complex basket, is required for the very early activation of NF- κB signalling during the stress-response phase of oncogene-induced senescence. This is prior to activation of the SASP and occurs without affecting NF-κB nuclear import. We show that TPR is required for the activation of TBK1 signalling at these early stages of senescence and we link this to the formation of heterochromatin-enriched cytoplasmic chromatin fragments thought to bleb off from the nuclear periphery. These cytoplasmic chromatin fragments appear to lack nuclear pore components. Our data suggest that TPR at the nuclear pore is involved in the loss of structural integrity of the nuclear periphery during senescence. We propose that this acts as a trigger for activation of cytoplasmic nucleic acid sensing, NF-κB signalling, and activation of the SASP, during senescence.
2024-12-19 | GSE264387 | GEO
Project description:We used SLAM-seq approach to define a contribution of RNA synthesis into RNA abundance changes after Tpr loss. Basket nucleoporin Tpr was AID-tagged and depleted through Auxin Induced Degradation system. Loss of Tpr led to rapid changes in rates of RNA synthesis. The majority of transcripts were downregulated. Analysis of RNA-seq and SLAM-seq indicated that the changes in RNA abundance of most of Tpr-dependent up- and downregulated genes resulted from increased or decreased rates of RNA synthesis, respectively.
2020-06-15 | GSE149890 | GEO
Project description:Background: The nuclear basket is a ‘fishtrap’-like structure on the nucleoplasmic face of the nuclear pore complex which has been implicated in diverse functions including RNA export, heterochromatin organisation, and mitosis. Recently, a novel component of the nuclear basket, ZC3HC1, has been described. The localisation of ZC3HC1 to nuclear pores has been reported to occur reciprocally with TPR, a major structural component of the nuclear basket. Methods and Results: Using immunofluorescence and RNA sequencing, here we show that in human fibroblasts, although ZC3HC1 localisation to nuclear pores is TPR-dependent, TPR localises to pores regardless of the presence of ZC3HC1. We demonstrate that knockdown of TPR and ZC3HC1 produce distinct transcriptional profiles. Conclusions: Our results suggest that there is little overlap in function between these two nuclear basket proteins
2025-02-18 | GSE286436 | GEO
Project description:How splicing regulates the nuclear export of mRNAs has been a source of much debate. While splicing has been shown to enhance nuclear export, it has remained unclear whether mRNAs generated from intronless genes use specific machinery to promote their export. Here we investigate the role of the major nuclear pore basket protein, TPR, in regulating mRNA and lncRNA nuclear export. We provide evidence that TPR is required for the nuclear export of mRNAs and lncRNAs that are generated from intronless or intron-poor genes. In contrast, TPR is not required for the nuclear retention of mRNAs that have retained introns, or unused 5’ splice site motifs. In summary, our study provides one of the first examples of a factor that is specifically required for the nuclear export of intronless mRNAs.
2020-10-02 | GSE135537 | GEO
Project description:Gene expression data from IMR90 Control, IMR90 HRAS-G12V, IMR90 HRAS-G12V+shDOT1L, IMR90 DOT1L Overexpression
| PRJNA658579 | ENA
Project description:To identify changes in splicing patterns following WTAP and TPR knockdown, RNA-sequencing was performed on breast cancer cells transfected with siRNAs targeting WTAP or TPR.
2019-12-26 | GSE130873 | GEO
Project description:Segregation errors of chromosomes into daughter cells lead to aneuploidy that is considered a major feature of solid tumors. How diploid cells face chromosome mal-segregation and the mechanisms driving aneuploidy tolerance in tumor cells are not yet completely defined. Thus, an important goal in cancer genetics is to identify gene networks leading to aneuploidy as well involved in its tolerance. To this aim we induced aneuploidy in IMR90 human primary cells and analyzed their gene expression profiles by DNA microarrays. Bioinformatics analysis revealed the presence of shared differentially expressed genes, up or down regulated in IMR90 cells after depletion of pRb, DNMT1 and MAD2 all inducing aneuploidy. Normalized data were also analyzed with the Gene Set Enrichment Analysis (GSEA) software to detect deregulated gene-sets associated with the aneuploidy phenotype. GSEA analysis suggested the existence of shared gene-sets/pathways characterizing aneuploidy cells that might be exploited for novel therapeutic approaches in cancer
2019-03-31 | GSE120641 | GEO