scholarly journals The fission yeast RPA21 subunit of RNA polymerase I: an evolutionarily conserved subunit interacting with ribosomal DNA (rDNA) transcription factor Rrn3p for recruitment to rDNA promoter

2002 ◽  
Vol 77 (3) ◽  
pp. 147-147 ◽  
Author(s):  
Yukiko Imazawa ◽  
Koji Hisatake ◽  
Kaori Nakagawa ◽  
Masami Muramatsu ◽  
Yasuhisa Nogi
Keyword(s):  
Transcription Factor ◽  
Rna Polymerase ◽  
Fission Yeast ◽  
Ribosomal Dna ◽  
Rna Polymerase I ◽  
Rdna Transcription ◽  
Evolutionarily Conserved ◽  
Polymerase I

scholarly journals The fission yeast RPA51 is a functional homolog of the budding yeast A49 subunit of RNA polymerase I and required for maximizing transcription of ribosomal DNA

2003 ◽  
Vol 78 (3) ◽  
pp. 199-209 ◽  
Author(s):  
Kaori Nakagawa ◽  
Koji Hisatake ◽  
Yukiko Imazawa ◽  
Akira Ishiguro ◽  
Masahito Matsumoto ◽  
...  
Keyword(s):  
Rna Polymerase ◽  
Fission Yeast ◽  
Ribosomal Dna ◽  
Budding Yeast ◽  
Rna Polymerase I ◽  
Functional Homolog ◽  
Polymerase I

scholarly journals Recruitment of the Nucleolar Remodeling Complex NoRC Establishes Ribosomal DNA Silencing in Chromatin

2004 ◽  
Vol 24 (4) ◽  
pp. 1791-1798 ◽  
Author(s):  
Ralf Strohner ◽  
Attila Németh ◽  
Karl P. Nightingale ◽  
Ingrid Grummt ◽  
Peter B. Becker ◽  
...  
Keyword(s):  
Rna Polymerase ◽  
Ribosomal Dna ◽  
Active Role ◽  
Rna Polymerase I ◽  
In Vivo Studies ◽  
Rrna Gene ◽  
Rdna Transcription ◽  
Transcription Terminator ◽  
Polymerase I

ABSTRACT The rRNA gene cluster consists of multiple transcription units. Half of these are active, while the other half are transcriptionally inactive. Previously, in vivo studies have demonstrated that silencing of ribosomal DNA (rDNA) is mediated by the chromatin remodeling NoRC (nucleolar remodeling complex). To explore the mechanisms underlying NoRC-directed silencing of rDNA transcription, we investigated the effect of recombinant NoRC on RNA polymerase I transcription on reconstituted chromatin templates. We show that NoRC interacts with the transcription terminator factor (TTF-I), and this interaction is required both for the binding of TTF-I to its promoter-proximal target site and for the recruitment of NoRC to the promoter. After association with the rDNA promoter, NoRC alters the position of the promoter-bound nucleosome, thereby repressing RNA polymerase I transcription. This NoRC-directed rDNA repression requires the N terminus of histone H4. Repression is effective before preinitiation complex formation and as such is unable to exert an effect upon activated rDNA genes. Furthermore, the early steps of rDNA repression do not depend on DNA and histone modifications. These results reveal an important role for TTF-I in recruiting NoRC to rDNA and an active role for NoRC in the establishment of rDNA silencing.

The absence of a human-specific ribosomal DNA transcription factor leads to nucleolar dominance in mouse greater than human hybrid cells

1984 ◽  
Vol 4 (7) ◽  
pp. 1306-1312
Author(s):  
R Miesfeld ◽  
B Sollner-Webb ◽  
C Croce ◽  
N Arnheim
Keyword(s):  
Transcription Factor ◽  
Rna Polymerase ◽  
Hybrid Cell ◽  
Rna Polymerase I ◽  
Hybrid Cells ◽  
Rdna Transcription ◽  
Nucleolar Dominance ◽  
Cell Extracts ◽  
Polymerase I ◽  
Human Specific

The basis for nucleolar dominance in mouse-human cell hybrids which contained all of the mouse chromosomes but an incomplete set of human chromosomes (M greater than H) was examined at the molecular level. S1 mapping data showed that these cells had the expected levels of steady-state rRNA transcribed from mouse ribosomal gene (rDNA) transcription units but undetectable levels of rRNA derived from the human rDNA transcription templates that are also present. RNA polymerase I-dependent, cell-free transcription extracts were made from three hybrid lines and were found to be capable of transcribing cloned rDNA templates of mouse but not human origin. Partially purified human factors required for rDNA transcription in vitro were added to the M greater than H extracts. One fraction with almost no RNA polymerase I activity conferred on these hybrid cell extracts the ability to transcribe a human rDNA template. These rescue experiments suggested that this required human-specific rDNA transcription factor(s) was effectively absent from the lines we examined and could account for nucleolar dominance in M greater than H hybrid cells.

scholarly journals The absence of a human-specific ribosomal DNA transcription factor leads to nucleolar dominance in mouse greater than human hybrid cells.

1984 ◽  
Vol 4 (7) ◽  
pp. 1306-1312 ◽  
Author(s):  
R Miesfeld ◽  
B Sollner-Webb ◽  
C Croce ◽  
N Arnheim
Keyword(s):  
Transcription Factor ◽  
Rna Polymerase ◽  
Hybrid Cell ◽  
Rna Polymerase I ◽  
Hybrid Cells ◽  
Rdna Transcription ◽  
Nucleolar Dominance ◽  
Cell Extracts ◽  
Polymerase I ◽  
Human Specific

The basis for nucleolar dominance in mouse-human cell hybrids which contained all of the mouse chromosomes but an incomplete set of human chromosomes (M greater than H) was examined at the molecular level. S1 mapping data showed that these cells had the expected levels of steady-state rRNA transcribed from mouse ribosomal gene (rDNA) transcription units but undetectable levels of rRNA derived from the human rDNA transcription templates that are also present. RNA polymerase I-dependent, cell-free transcription extracts were made from three hybrid lines and were found to be capable of transcribing cloned rDNA templates of mouse but not human origin. Partially purified human factors required for rDNA transcription in vitro were added to the M greater than H extracts. One fraction with almost no RNA polymerase I activity conferred on these hybrid cell extracts the ability to transcribe a human rDNA template. These rescue experiments suggested that this required human-specific rDNA transcription factor(s) was effectively absent from the lines we examined and could account for nucleolar dominance in M greater than H hybrid cells.

scholarly journals Species-specific rDNA transcription is due to promoter-specific binding factors.

1984 ◽  
Vol 4 (2) ◽  
pp. 221-227 ◽  
Author(s):  
R Miesfeld ◽  
N Arnheim
Keyword(s):  
Rna Polymerase ◽  
Transcriptional Control ◽  
Specific Binding ◽  
Rna Polymerase I ◽  
Rdna Transcription ◽  
Nucleolar Dominance ◽  
Cell Extracts ◽  
Species Specific ◽  
Polymerase I

RNA polymerase I transcription factors were purified from HeLa and mouse L cell extracts by phosphocellulose chromatography. Three fractions from each species were found to be required for transcription. One of these fractions, virtually devoid of RNA polymerase I activity, was found to form a stable preinitiation complex with small DNA fragments containing promoter sequences from the homologous but not the heterologous species. These species-specific DNA-binding factors can explain nucleolar dominance in vivo in mouse-human hybrid somatic cells and species specificity in cell-free, RNA polymerase I-dependent transcription systems. The evolution of species-specific transcriptional control signals may be the natural outcome of a special relationship that exists between the RNA polymerase I transcription machinery and the multigene family coding for rRNA.

Abstract A46: Wnt5a signals through DVL1 to repress ribosomal DNA transcription by RNA polymerase I

2017 ◽  
Author(s):  
Randall Dass ◽  
Aishe Sarshad ◽  
Brittany Carson ◽  
Jennifer Feenstra ◽  
Amanpreet Kaur ◽  
...  
Keyword(s):  
Rna Polymerase ◽  
Ribosomal Dna ◽  
Rna Polymerase I ◽  
Dna Transcription ◽  
Polymerase I

scholarly journals Regulation of ribosomal DNA transcription by insulin

1998 ◽  
Vol 275 (1) ◽  
pp. C130-C138 ◽  
Author(s):  
Katherine M. Hannan ◽  
Lawrence I. Rothblum ◽  
Leonard S. Jefferson
Keyword(s):  
Rna Polymerase ◽  
Cell Types ◽  
Rna Polymerase I ◽  
Model Systems ◽  
Serum Starvation ◽  
Swiss Albino Mouse ◽  
Rdna Transcription ◽  
Cellular Content ◽  
Upstream Binding Factor ◽  
Polymerase I

The experiments reported here used 3T6-Swiss albino mouse fibroblasts and H4-II-E-C3 rat hepatoma cells as model systems to examine the mechanism(s) through which insulin regulates rDNA transcription. Serum starvation of 3T6 cells for 72 h resulted in a marked reduction in rDNA transcription. Treatment of serum-deprived cells with insulin was sufficient to restore rDNA transcription to control values. In addition, treatment of exponentially growing H4-II-E-C3 with insulin stimulated rDNA transcription. However, for both cell types, the stimulation of rDNA transcription in response to insulin was not associated with a change in the cellular content of RNA polymerase I. Thus we conclude that insulin must cause alterations in formation of the active RNA polymerase I initiation complex and/or the activities of auxiliary rDNA transcription factors. In support of this conclusion, insulin treatment of both cell types was found to increase the nuclear content of upstream binding factor (UBF) and RNA polymerase I-associated factor 53. Both of these factors are thought to be involved in recruitment of RNA polymerase I to the rDNA promoter. Nuclear run-on experiments demonstrated that the increase in cellular content of UBF was due to elevated transcription of the UBF gene. In addition, overexpression of UBF was sufficient to directly stimulate rDNA transcription from a reporter construct. The results demonstrate that insulin is capable of stimulating rDNA transcription in both 3T6 and H4-II-E-C3 cells, at least in part by increasing the cellular content of components required for assembly of RNA polymerase I into an active complex.

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