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PROVIDER: PRJNA909051 | ENA |
REPOSITORIES: ENA
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Project description:Transcription of the several hundred of mouse and human Ribosomal RNA (rRNA) genes accounts for the majority of RNA synthesis in the cell nucleus and is the determinant of cytoplasmic ribosome abundance, a key factor in regulating gene expression. The rRNA genes, referred to globally as the rDNA, are clustered as direct repeats at the Nucleolar Organiser Regions, NORs, of several chromosomes, and in many cells the active repeats are transcribed at near saturation levels. The rDNA is also a hotspot of recombination and chromosome breakage, and hence understanding its control has broad importance. Despite the need for a high level of rDNA transcription, typically only a fraction of the rDNA is transcriptionally active, and some NORs are permanently silenced by CpG methylation. Various chromatin-remodelling complexes have been implicated in counteracting silencing to maintain rDNA activity. However, the chromatin structure of the active rDNA fraction is still far from clear. Here we have combined a high-resolution ChIP-Seq protocol with conditional inactivation of key basal factors to better understand what determines active rDNA chromatin. The data resolve questions concerning the interdependence of the basal transcription factors, show that preinitiation complex formation is driven by the architectural factor UBF (UBTF) independently of transcription, and exclude a significant role for termination by a torpedomechanism. They further reveal the existence of an asymmetric Boundary Complex formed by CTCF, Cohesin and three phased nucleosomes lying adjacent to the rDNA Enhancer and an arrested RNA Polymerase I complex. We find that this complex is the only site of active histone modification in the whole 45kbp rDNA repeat. Strikingly, the Enhancer Boundary Complex not only delimits each functional rRNA gene, but also is stably maintained after gene inactivation and the re-establishment of surrounding repressive chromatin. Our data define the poised state of rDNA chromatin and place the Enhancer Boundary Complex as the likely entry point for the chromatin remodelling complexes.
2017-07-08 | E-MTAB-5839 | biostudies-arrayexpress
Project description:We used phylogenetic low-density microarrays targeting the 16S rRNA gene to characterize the gingival flora of acute noma and acute necrotizing gingivitis lesions, and compared them to healthy control subjects of the same geographical and social background. Various types of samples were collected (column characteristics); patients from the same hospital without mouth infection (H), matched control populations (T), patients suffering gengivitis (Gengivitis), patient suffering NOMA (noma), patient suffering NOMA receiving antimicrobials (N-ATB). Sampled from patients were retrieved from both sides (column Description); healthy- or lesion-side of the mouth. All controls are matched with specific patients (see column patient category and number) We designed low-density 16S rDNA arrays representing 339 different phylotypes. We used an arbitrary cutoff of 1% of overall abundance to select from this dataset the most abundant sequences for probe design. Using this cutoff, the 132 most abundant 16S rRNA gene sequences were scanned for probes respecting defined physico-chemical properties (Tm = 65M-BM-15M-BM-0C; probe length = 23M-bM-^@M-^S50 nt; < -5.0 kcal/mol for hairpins; < -8.0 kcal/mol for self-dimers; and dinucleotide repeats shorter than 5 bp) using a commercial software (Array Designer TM 2.0 by Premier Biosoft). The 335 oligonucleotide probes were synthesized with a C6-linker with free primary amine (Sigma-Aldrich) and spotted on ArrayStrips microarrays (Clondiag GmbH, Jena, Germany).
2013-12-27 | E-GEOD-43612 | biostudies-arrayexpress
Project description:In this study we perform ATAC-seq of budding yeast strains with variable copy number of the rRNA genes (rDNA CN). We aim to better understand the relationship between DNA accessibility and replicative lifespan in strains with variable rDNA CN.
2022-04-05 | GSE193598 | GEO
Project description:Eukaryotic genomes harbor hundreds of rRNA genes, many of which are transcriptionally silent. However, little is known about selective regulation of individual rDNA units. In Drosophila melanogaster, some rDNA repeats contain insertions of the R2 retrotransposon, which is capable to be transcribed only as part of pre-rRNA molecules. rDNA units with R2 insertions are usually inactivated, although R2 expression may be beneficial in cells with decreased rDNA copy number. Here we found that R2-inserted rDNA units are enriched with HP1a and H3K9me3 repressive mark, whereas disruption of the heterochromatin components slightly affects their silencing in ovarian germ cells. Surprisingly, we observed a dramatic upregulation of R2-inserted rRNA genes in ovaries lacking Udd (Under-developed) or other subunits (TAF1b and ТAF1c-like) of the SL1-like complex, which is homologues to mammalian Selective factor 1 (SL1) involved in rDNA transcription initiation. Derepression of rRNA genes with R2 insertions was accompanied by a reduction of H3K9me3 and HP1a enrichment. We suggest that the impairment of the SL1-like complex affects a mechanism of selective activation of intact rDNA units which competes with heterochromatin formation. We also propose that R2 derepression may serve as an adaptive response to compromised rRNA synthesis.
2021-10-09 | GSE183035 | GEO
Project description:16S rRNA gene sequencing of colonic feces from mice fed regular chow, regular chow+nobiletin, high-fat diet or high-fat diet+nobiletin.
2022-05-06 | E-MTAB-11551 | biostudies-arrayexpress
Project description:Ribosomal RNAs (rRNAs) are essential components of the ribosome and are among the most abundant macromolecules in the cell. To ensure high rRNA level, eukaryotic genomes contain dozens to hundreds of rDNA genes, however, only a fraction of the rRNA genes seems to be active, while others are transcriptionally silent. In Drosophila rDNA units damaged by insertions of retrotransposons are repressed by an unknown mechanism. Here, we established a new model to study regulation of rDNA expression using molecularly marked rDNA transgenes. Using this model, we show that insertion of any heterologous sequence into rDNA leads to transcriptional repression. We found that SUMO (Small Ubiquitin-like Modifier) is required for efficient repression of damaged rDNA units. Surprisingly, SUMO also controls expression of intact rDNA, demonstrating that a single pathway is responsible for both selective repression of damaged units and silencing of surplus rDNA.
2020-02-01 | GSE141068 | GEO
Project description:In this study we perform RNA-seq of budding yeast strains with variable copy number of the rRNA genes (rDNA CN) to assess the relationship between rDNA CN and gene expression. RNA-seq was performed on samples both with and without polyA selection (for all transcripts and for rRNA transcripts, respectively).
2022-04-05 | GSE193599 | GEO
Project description:Transcription of the >200 rRNA genes (rDNA) by RNA Polymerase I (RPI) determines as much as 35% of total nuclear RNA synthesis and is a major determinant of cell growth implicated in a range of hypertrophic and developmental disorders. Activation of the rDNA involves the formation of an extended nucleosome free region (NFR) by the multi-HMGbox factor UBTF, which is also implicated with the RPI specific TBP-TAFI factor SL1 in preinitiation complex formation. However, neither factor alone displays significant DNA sequence binding specificity. Here we show that in cell cooperation between SL1 and the UBTF1 splice variant creates the sequence specificity required for promoter recognition. While both UBTF1 and UBTF2 splice variants bind throughout the rDNA NFR, only UBTF1 binds at the rDNA promoters. Conditional deletion of the Taf1b subunit of SL1 depleted UBTF1 from the rDNA promoters but not from elsewhere across the rDNA NFR. We show RPI promoters are particularly poor binding sites for UBTF and suggest an induced-fit model in which promoter-specific remodelling by UBTF1 creates high affinity sites for SL1 binding. A mouse model of the UBTF-E210K pediatric neurodegeneration syndrome suggests this mutation affects cooperativity of UBTF-SL1 promoter recruitment and further supports the induced-fit model.
2022-02-03 | E-MTAB-11385 | biostudies-arrayexpress