Regulation of rDNA Transcription in Spinach Plastids by Transcription Factor CDF2

2001 ◽  
pp. 279-285
Author(s):  
Silva Lerbs-Mache
Keyword(s):  
Transcription Factor ◽  
Rdna Transcription

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 mTOR-Dependent Regulation of Ribosomal Gene Transcription Requires S6K1 and Is Mediated by Phosphorylation of the Carboxy-Terminal Activation Domain of the Nucleolar Transcription Factor UBF†

2003 ◽  
Vol 23 (23) ◽  
pp. 8862-8877 ◽  
Author(s):  
Katherine M. Hannan ◽  
Yves Brandenburger ◽  
Anna Jenkins ◽  
Kerith Sharkey ◽  
Alice Cavanaugh ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cell Growth ◽  
Gene Transcription ◽  
Ribosome Biogenesis ◽  
Ribosomal Gene ◽  
3T3 Cells ◽  
Rdna Transcription ◽  
Activation Domain ◽  
Carboxy Terminal ◽  
Nih 3T3

ABSTRACT Mammalian target of rapamycin (mTOR) is a key regulator of cell growth acting via two independent targets, ribosomal protein S6 kinase 1 (S6K1) and 4EBP1. While each is known to regulate translational efficiency, the mechanism by which they control cell growth remains unclear. In addition to increased initiation of translation, the accelerated synthesis and accumulation of ribosomes are fundamental for efficient cell growth and proliferation. Using the mTOR inhibitor rapamycin, we show that mTOR is required for the rapid and sustained serum-induced activation of 45S ribosomal gene transcription (rDNA transcription), a major rate-limiting step in ribosome biogenesis and cellular growth. Expression of a constitutively active, rapamycin-insensitive mutant of S6K1 stimulated rDNA transcription in the absence of serum and rescued rapamycin repression of rDNA transcription. Moreover, overexpression of a dominant-negative S6K1 mutant repressed transcription in exponentially growing NIH 3T3 cells. Rapamycin treatment led to a rapid dephosphorylation of the carboxy-terminal activation domain of the rDNA transcription factor, UBF, which significantly reduced its ability to associate with the basal rDNA transcription factor SL-1. Rapamycin-mediated repression of rDNA transcription was rescued by purified recombinant phosphorylated UBF and endogenous UBF from exponentially growing NIH 3T3 cells but not by hypophosphorylated UBF from cells treated with rapamycin or dephosphorylated recombinant UBF. Thus, mTOR plays a critical role in the regulation of ribosome biogenesis via a mechanism that requires S6K1 activation and phosphorylation of UBF.

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 Structural determinant of the species-specific transcription of the mouse rRNA gene promoter.

1989 ◽  
Vol 9 (1) ◽  
pp. 349-353 ◽  
Author(s):  
G Safrany ◽  
N Tanaka ◽  
T Kishimoto ◽  
Y Ishikawa ◽  
H Kato ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Core Promoter ◽  
Wild Type Mouse ◽  
Basic Structure ◽  
Chimeric Gene ◽  
Rrna Gene ◽  
Rdna Transcription ◽  
Mouse Promoter

Mammalian ribosomal DNA (rDNA) transcription has a certain species specificity such that, both in vivo and in vitro, human rDNA cannot be transcribed by mouse machinery and vice versa. This is due to a species-dependent transcription factor, TFID (Y. Mishima, I. Financsek, R. Kominami, and M. Muramatsu, Nucleic Acids Res. 10:6659-6670, 1982). On the basis of the information obtained from 5' and 3' substitution mutants, we prepared a chimeric gene in which the mouse sequence from positions -32 to -14 was inserted into the corresponding location of the human rDNA promoter. The chimeric gene could be transcribed by mouse extracts nearly as efficiently as the wild-type mouse promoter. The chimeric gene could also sequester transcription factor TFID at an efficiency similar to that for the mouse promoter. Partially purified mouse TFID that could not protect the human rDNA promoter against DNase I produced a clear footprint on this chimeric gene that was similar to that on mouse rDNA promoter. The basic structure of the mouse rDNA core promoter is discussed in relation to the interaction with TFID.

scholarly journals Factors and nucleotide sequences that direct ribosomal DNA transcription and their relationship to the stable transcription complex.

1986 ◽  
Vol 6 (10) ◽  
pp. 3451-3462 ◽  
Author(s):  
J Tower ◽  
V C Culotta ◽  
B Sollner-Webb
Keyword(s):  
Transcription Factor ◽  
Ribosomal Dna ◽  
Core Region ◽  
Rrna Genes ◽  
Stable Complex ◽  
Rdna Transcription ◽  
Essential Region ◽  
Protein Components ◽  
Factor C ◽  
Polymerase I

We have studied the protein components and nucleic acid sequences involved in stably activating the ribosomal DNA (rDNA) template and in directing accurate transcription of mammalian rRNA genes. Two protein components are necessary to catalyze rDNA transcription, and these have been extensively purified. The first, factor D, can stably associate by itself with the rDNA promoter region and is responsible for template commitment. The second component, factor C, which appears to be an activated subset of polymerase I, can stably bind to the factor D-rDNA complex but not to the rDNA in the absence of factor D. A third component which had been previously identified as a rDNA transcription factor is shown to be a RNase inhibitor. Extending our earlier observation that the approximately 150-base-pair mouse rDNA promoter consists of a minimal essential region (residues approximately -35 to approximately +9) and additional upstream stimulatory domains, we now report that each of these promoter domains acts to augment the binding of the polymerase I transcription factors. A minimum core region (residues approximately -35 to approximately -15) is capable of stable complex formation and of binding transcription factor D. Factor C can also bind to this D-core region complex.

Structural determinant of the species-specific transcription of the mouse rRNA gene promoter

1989 ◽  
Vol 9 (1) ◽  
pp. 349-353
Author(s):  
G Safrany ◽  
N Tanaka ◽  
T Kishimoto ◽  
Y Ishikawa ◽  
H Kato ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Core Promoter ◽  
Wild Type Mouse ◽  
Basic Structure ◽  
Chimeric Gene ◽  
Rrna Gene ◽  
Rdna Transcription ◽  
Mouse Promoter

Mammalian ribosomal DNA (rDNA) transcription has a certain species specificity such that, both in vivo and in vitro, human rDNA cannot be transcribed by mouse machinery and vice versa. This is due to a species-dependent transcription factor, TFID (Y. Mishima, I. Financsek, R. Kominami, and M. Muramatsu, Nucleic Acids Res. 10:6659-6670, 1982). On the basis of the information obtained from 5' and 3' substitution mutants, we prepared a chimeric gene in which the mouse sequence from positions -32 to -14 was inserted into the corresponding location of the human rDNA promoter. The chimeric gene could be transcribed by mouse extracts nearly as efficiently as the wild-type mouse promoter. The chimeric gene could also sequester transcription factor TFID at an efficiency similar to that for the mouse promoter. Partially purified mouse TFID that could not protect the human rDNA promoter against DNase I produced a clear footprint on this chimeric gene that was similar to that on mouse rDNA promoter. The basic structure of the mouse rDNA core promoter is discussed in relation to the interaction with TFID.

scholarly journals Transcription Factor UAF, Expansion and Contraction of Ribosomal DNA (rDNA) Repeats, and RNA Polymerase Switch in Transcription of Yeast rDNA

1999 ◽  
Vol 19 (12) ◽  
pp. 8559-8569 ◽  
Author(s):  
Melanie Oakes ◽  
Imran Siddiqi ◽  
Loan Vu ◽  
John Aris ◽  
Masayasu Nomura
Keyword(s):  
Transcription Factor ◽  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Ribosomal Dna ◽  
Tandem Repeats ◽  
Single Mutation ◽  
Rdna Transcription ◽  
Pol Ii ◽  
Pol I

ABSTRACT Strains of the yeast Saccharomyces cerevisiae defective in transcription factor UAF give rise to variants able to grow by transcribing endogenous ribosomal DNA (rDNA) by RNA polymerase II (Pol II). We have demonstrated that the switch to growth using the Pol II system consists of two steps: a mutational alteration in UAF and an expansion of chromosomal rDNA repeats. The first step, a single mutation in UAF, is sufficient to allow Pol II transcription of rDNA. In contrast to UAF mutations, mutations in Pol I or other Pol I transcription factors can not independently lead to Pol II transcription of rDNA, suggesting a specific role of UAF in preventing polymerase switch. The second step, expansion of chromosomal rDNA repeats to levels severalfold higher than the wild type, is required for efficient cell growth. Mutations in genes that affect recombination within the rDNA repeats, fob1 and sir2, decrease and increase, respectively, the frequency of switching to growth using Pol II, indicating that increased rDNA copy number is a cause rather than a consequence of the switch. Finally, we show that the switch to the Pol II system is accompanied by a striking alteration in the localization and morphology of the nucleolus. The altered state that uses Pol II for rDNA transcription is semistable and heritable through mitosis and meiosis. We discuss the significance of these observations in relation to the plasticity of rDNA tandem repeats and nucleolar structures as well as evolution of the Pol I machinery.

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