Expression of the tumor-expressed protein MageB2 enhances rRNA transcription

2021 ◽  
Vol 1868 (7) ◽  
pp. 119015
Author(s):  
María Fátima Ladelfa ◽  
Leticia Yamila Peche ◽  
Gastón Ezequiel Amato ◽  
Micaela Carolina Escalada ◽  
Stefania Zampieri ◽  
...  
Keyword(s):  
Rrna Transcription

Co-localization of polar replication fork barriers and rRNA transcription terminators in mouse rDNA

1998 ◽  
Vol 277 (2) ◽  
pp. 249-256 ◽  
Author(s):  
Carlos López-Estraño ◽  
Jorge B Schvartzman ◽  
Dora B Krimer ◽  
Pablo Hernández
Keyword(s):  
Replication Fork ◽  
Rrna Transcription

Human rRNA transcription is modulated by the coordinate binding of two factors to an upstream control element

Cell ◽  
1986 ◽  
Vol 45 (6) ◽  
pp. 847-857 ◽  
Author(s):  
R.Marc Learned ◽  
Tammy K. Learned ◽  
Michelle M. Haltiner ◽  
Robert T. Tjian
Keyword(s):  
Control Element ◽  
Rrna Transcription ◽  
Two Factors ◽  
Upstream Control

Factor-independent activation of Escherichia coli rRNA transcription

1991 ◽  
Vol 220 (3) ◽  
pp. 555-568 ◽  
Author(s):  
Sigrid Leirmo ◽  
Richard L. Gourse
Keyword(s):  
Escherichia Coli ◽  
Rrna Transcription

scholarly journals The Splicing ATPase Prp43p Is a Component of Multiple Preribosomal Particles

2005 ◽  
Vol 25 (21) ◽  
pp. 9269-9282 ◽  
Author(s):  
Simon Lebaron ◽  
Carine Froment ◽  
Micheline Fromont-Racine ◽  
Jean-Christophe Rain ◽  
Bernard Monsarrat ◽  
...  
Keyword(s):  
Affinity Purification ◽  
Rna Polymerase I ◽  
Rrna Processing ◽  
Rrna Transcription ◽  
Pol I ◽  
Final Maturation ◽  
Steady State Levels ◽  
Splicing Defects ◽  
Polymerase I ◽  
Two Hybrid

ABSTRACT Prp43p is a putative helicase of the DEAH family which is required for the release of the lariat intron from the spliceosome. Prp43p could also play a role in ribosome synthesis, since it accumulates in the nucleolus. Consistent with this hypothesis, we find that depletion of Prp43p leads to accumulation of 35S pre-rRNA and strongly reduces levels of all downstream pre-rRNA processing intermediates. As a result, the steady-state levels of mature rRNAs are greatly diminished following Prp43p depletion. We present data arguing that such effects are unlikely to be solely due to splicing defects. Moreover, we demonstrate by a combination of a comprehensive two-hybrid screen, tandem-affinity purification followed by mass spectrometry, and Northern analyses that Prp43p is associated with 90S, pre-60S, and pre-40S ribosomal particles. Prp43p seems preferentially associated with Pfa1p, a novel specific component of pre-40S ribosomal particles. In addition, Prp43p interacts with components of the RNA polymerase I (Pol I) transcription machinery and with mature 18S and 25S rRNAs. Hence, Prp43p might be delivered to nascent 90S ribosomal particles during pre-rRNA transcription and remain associated with preribosomal particles until their final maturation steps in the cytoplasm. Our data also suggest that the ATPase activity of Prp43p is required for early steps of pre-rRNA processing and normal accumulation of mature rRNAs.

scholarly journals Epigenetic Programming of the rRNA Promoter by MBD3

2007 ◽  
Vol 27 (13) ◽  
pp. 4938-4952 ◽  
Author(s):  
Shelley E. Brown ◽  
Moshe Szyf
Keyword(s):  
Small Interfering Rna ◽  
Rna Polymerase I ◽  
Rrna Genes ◽  
Rrna Gene ◽  
Rrna Transcription ◽  
Epigenetic Programming ◽  
Binding Factor ◽  
Upstream Binding Factor ◽  
Polymerase I ◽  
Interfering Rna

ABSTRACT Within the human genome there are hundreds of copies of the rRNA gene, but only a fraction of these genes are active. Silencing through epigenetics has been extensively studied; however, it is essential to understand how active rRNA genes are maintained. Here, we propose a role for the methyl-CpG binding domain protein MBD3 in epigenetically maintaining active rRNA promoters. We show that MBD3 is localized to the nucleolus, colocalizes with upstream binding factor, and binds to unmethylated rRNA promoters. Knockdown of MBD3 by small interfering RNA results in increased methylation of the rRNA promoter coupled with a decrease in RNA polymerase I binding and pre-rRNA transcription. Conversely, overexpression of MBD3 results in decreased methylation of the rRNA promoter. Additionally, overexpression of MBD3 induces demethylation of nonreplicating plasmids containing the rRNA promoter. We demonstrate that this demethylation occurs following the overexpression of MBD3 and its increased interaction with the methylated rRNA promoter. This is the first demonstration that MBD3 is involved in inducing and maintaining the demethylated state of a specific promoter.

Making Ribosomes: Pre-rRNA Transcription and Processing

2014 ◽  
pp. 217-232 ◽  
Author(s):  
Kathleen L. McCann ◽  
Susan J. Baserga
Keyword(s):  
Rrna Transcription

scholarly journals Nucleolin loss-of-function leads to aberrant FGF signaling and craniofacial anomalies

2021 ◽  
Author(s):  
Soma Dash ◽  
Paul Trainor
Keyword(s):  
Ribosome Biogenesis ◽  
Craniofacial Development ◽  
Rrna Synthesis ◽  
Growth Factor Signaling ◽  
Craniofacial Anomalies ◽  
Fgf Signaling ◽  
Loss Of Function ◽  
Tissue Specific ◽  
Rrna Transcription ◽  
Exogenous Addition

rRNA transcription and ribosome biogenesis are global processes required for growth and proliferation of all cells, yet perturbation of these processes in vertebrates leads to tissue-specific defects termed ribosomopathies. Mutations in rRNA transcription and processing proteins often lead to craniofacial anomalies, however the cellular and molecular reasons for this are poorly understood. Therefore, we examined the function of the most abundant nucleolar phosphoprotein, Nucleolin (Ncl), in vertebrate development. We discovered that Nucleolin is dynamically expressed during embryonic development with high enrichment in the craniofacial tissues. Consistent with this pattern of expression, ncl homozygous mutant (ncl-/-) zebrafish present with craniofacial anomalies such as mandibulofacial hypoplasia. We observe that ncl-/- mutants exhibit decreased rRNA synthesis and p53-dependent neuroepithelial cell death. In addition, the half-life of fgf8a mRNA is reduced in ncl-/- mutants, which perturbs Fgf signaling, resulting in misregulation of Sox9a mediated chondrogenesis and Runx2 mediated osteogenesis. Exogenous addition of human recombinant FGF8 to the mutant zebrafish significantly rescues the cranioskeletal phenotype, suggesting that Nucleolin regulates osteochondroprogenitor differentiation during craniofacial development by post-transcriptionally regulating Fgf signaling. Our work has therefore uncovered a novel tissue-specific function for Nucleolin in rRNA transcription and growth factor signaling during embryonic craniofacial development.

scholarly journals Control of rRNA transcription in Escherichia coli.

1995 ◽  
Vol 59 (4) ◽  
pp. 623-645 ◽  
Author(s):  
C Condon ◽  
C Squires ◽  
C L Squires
Keyword(s):  
Escherichia Coli ◽  
Rrna Transcription
Sign in / Sign up

Export Citation Format

Share Document