Ontology highlight
ABSTRACT:
PROVIDER: PRJNA577229 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10270572_subreads.fastq.gz | Fastqsanger.gz |
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Project description:Heat shock-induced ribosomal intergenic spacer RNA
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Project description:The combination of Chromatin Immunoprecipitation and Massively Parallel Sequencing, or ChIP-Seq, has greatly advanced our genome-wide understanding of chromatin and enhancer structures. However, its resolution at any given genetic locus is limited by several factors. In applying ChIP-Seq to study the ribosomal RNA genes we found that a major limitation to resolution was imposed by the often dominant variability in sequence coverage provided by the massively parallel sequencing technology. Here we describe a simple numerical deconvolution approach that in large part corrects for this variability and significantly improves both the resolution and quantitation of protein-DNA interaction maps deduced from ChIP-Seq data. This approach has allowed us to study the in vivo organization of the RNA Polymerase I pre-initiation complexes that form at the promoters of the mouse and human ribosomal RNA genes. The data identify and map a Spacer Promoter and associated stalled polymerase in the intergenic spacer of the human ribosomal genes and show that a very similar Enhancer structure and organization to that found in rodents and even in lower vertebrates also exists in human.
2017-12-31 | E-MTAB-6032 | biostudies-arrayexpress
Project description:Cells adapt to environmental stressors such as heat shock and extracellular acidosis through formation of nuclear membrane-less compartments called Amyloid bodies (A-bodies). Stressors activate formation of Amyloid bodies (A-bodies) via induction of ribosomal intergenic spacer RNA (rIGSRNA). RNA-seq on non-ribosome depleted RNA from human MCF7 cells exposed to heat shock (43C, 30 minutes) revealed the heat shock-specific expression profile of rIGSRNA.
2018-08-02 | GSE115731 | GEO
Project description:In eukaryotes, the synthesis of ribosomal subunits, which involves the maturation of the ribosomal (r)RNAs and assembly of ribosomal proteins, requires the co-ordinated action of a plethora of ribosome biogenesis factors. Many of these cofactors remain to be characterized in human cells. Here, we demonstrate that the human G-patch protein NF-κB-repressing factor (NKRF) forms a pre-ribosomal subcomplex with the DEAH-box helicase DHX15 and the 5’-3’ exonuclease XRN2. Using UV crosslinking and analysis of cDNA (CRAC), we reveal that NKRF binds to the transcribed spacer regions of the pre-rRNA transcript. Consistent with this, we find that depletion of NKRF, XRN2 or DHX15 impairs an early pre-rRNA cleavage step (A’). The catalytic activity of DHX15, which we demonstrate is stimulated by NKRF functioning as a cofactor, is required for efficient A’ cleavage, suggesting that a structural remodelling event may facilitate processing at this site. In addition, we show that depletion of NKRF or XRN2 also leads to the accumulation of excised pre-rRNA spacer fragments and that NKRF is essential for recruitment of the exonuclease to nucleolar pre-ribosomal complexes. Our findings therefore reveal a novel pre-ribosomal subcomplex that plays distinct roles in the processing of pre-rRNAs and the turnover of excised spacer fragments.
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Project description:Neurodegeneration in the human population is often associated with loss of protein homeostasis that is driven by accumulation of specific aggregated proteins. Here we investigate whether deficiency in Senataxin, an RNA-DNA helicase associated with cerebellar ataxia and ALS, induces destabilization of intrinsically disordered proteins as we previously found with Ataxia-telangiectasia (A-T) cells and tissue. We find that Senataxin loss does generate protein aggregates but, unlike in A-T, these are associated with the nucleolus and are independent of oxidative stress and PARP activity. Non-coding RNA expression from the intergenic spacer region of ribosomal DNA is induced in the absence of Senataxin and drives the association and aggregation of many proteins known to be prone to aggregation in neurodegenerative disease. Both non-coding RNAs and protein aggregates are eliminated by overexpression of RNaseH1, implicating RNA-DNA hybrids as the key driver of these outcomes. We find that hybrids are high in the absence of Senataxin at intergenic sites, not at annotated protein-coding genes; these include sites of Senataxin binding in the genome, ribosomal DNA, and peri-centromeric regions. These findings suggest that destabilization of the proteome is driven by Senataxin loss and that RNA-DNA hybrids and non-coding RNAs play a critical role in this process.
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