Stimulation of nuclear RNA polymerase I activity by a soluble factor isolated from young rat liver nuclei

AGE ◽  
1983 ◽  
Vol 6 (4) ◽  
pp. 106-112 ◽  
Author(s):  
Patricia Fitzpatrick-Dimond ◽  
John A. Todhunter ◽  
Sameeh S. Elridi
Keyword(s):  
Rna Polymerase ◽  
Rat Liver ◽  
Rna Polymerase I ◽  
Soluble Factor ◽  
Nuclear Rna ◽  
Liver Nuclei ◽  
Young Rat ◽  
Polymerase I ◽  
Nuclear Rna Polymerase ◽  
Stimulation Of

scholarly journals Effects of glucocorticoid and cycloheximide on the activity and amount of RNA polymerase I in nuclei of rat liver

1986 ◽  
Vol 235 (3) ◽  
pp. 699-705 ◽  
Author(s):  
H Matsui ◽  
H Yazawa ◽  
N Suzuki ◽  
T Hosoya
Keyword(s):  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Rat Liver ◽  
Protein S ◽  
Rna Polymerase I ◽  
Free Form ◽  
Precursor Synthesis ◽  
Liver Nuclei ◽  
Polymerase I ◽  
Adrenalectomized Rats

The activity of the template-engaged form of RNA polymerase I from livers of adrenalectomized rats was about 50-60% of that of normal control rats, and increased about 2-fold at 6 h after the administration of dexamethasone. However, no change was found in the activity of the ‘free’ form of RNA polymerase I or the template-engaged form of RNA polymerase II. Immunochemical studies using guinea-pig anti-(RNA polymerase I) serum disclosed that the total number of RNA polymerase I molecules did not vary during the treatment with dexamethasone. Cycloheximide caused a rapid decrease in the template-engaged form of RNA polymerase I activity in normal rats and in dexamethasone-treated (6 h) adrenalectomized rats, to the value in adrenalectomized rats, but affected it only slightly in adrenalectomized rats. The elongation rate of rRNA-precursor synthesis in liver nuclei was not affected by a change in the concentration of circulating dexamethasone. From these results, it is concluded that about half the rRNA-precursor synthesis in rat liver is regulated by glucocorticoids, probably through the synthesis of short-lived protein(s) which may play a role in conversion of the ‘dormant’ form of RNA polymerase I into the ‘engaged’ form.

scholarly journals Control of activation of liver RNA polymerase I occurring after re-feeding of protein-depleted mice

1983 ◽  
Vol 210 (3) ◽  
pp. 837-844 ◽  
Author(s):  
L Haim ◽  
S Iapalucci-Espinoza ◽  
R Conde ◽  
M T Franze-Fernández
Keyword(s):  
Rna Polymerase ◽  
Fold Increase ◽  
Inhibitory Effect ◽  
Rna Polymerase I ◽  
Activated State ◽  
Solubilized Enzyme ◽  
Liver Nuclei ◽  
Inhibitor Of Protein Synthesis ◽  
Polymerase I ◽  
Stimulation Of

Shortly after feeding protein-depleted mice with a meal containing protein, the RNA polymerase I activity in isolated liver nuclei shows a 2-fold increase over the values in the nuclei of either normal or protein-depleted mice. The activity of the RNA polymerase I solubilized from nuclei of re-fed mice was slightly enhanced, probably reflecting an increase in enzyme amount. However, this increase only accounts for about 30% of the stimulation of transcription in the intact nuclei. Administration of pactamycin, an inhibitor of protein synthesis, to normal or protein-depleted mice has almost no inhibitory effect on the RNA polymerase I activity in the isolated nuclei. On the contrary, within 15 min after treatment with the drug, the stimulated activity in nuclei from re-fed mice declines towards the values in normal or protein-depleted mice and then remains constant. The activity of the solubilized enzyme remains slightly elevated for at least 2 1/2 h after re-fed mice are treated with pactamycin. These observations indicate that the stimulation of the RNA polymerase I activity in the intact nuclei after re-feeding is controlled by mechanisms other than an increase in the enzyme amount and suggest the presence of short-lived proteins required for inducing an activated state of transcription.

scholarly journals Relationship between RNA polymerase I activity and ornithine decarboxylase in rat liver tissues

1987 ◽  
Vol 241 (1) ◽  
pp. 169-174 ◽  
Author(s):  
M Urata ◽  
N Suzuki ◽  
T Hosoya
Keyword(s):  
Rna Polymerase ◽  
Ornithine Decarboxylase ◽  
Rat Liver ◽  
Protein Sequence ◽  
Rna Polymerase I ◽  
Rat Liver Nuclei ◽  
Liver Nuclei ◽  
Polymerase I ◽  
The Relationship ◽  
Liver Tissues

In order to examine the relationship between RNA polymerase I and ornithine decarboxylase (ODC), three lines of experiments were performed, with the following results. The glucocorticoid-induced increase of RNA polymerase I in rat liver nuclei was not abolished by administration of inhibitors of ODC synthesis and activity, namely 1,3-diaminopropane and 2-difluoromethylornithine respectively. Anti-ODC antibody did not cross-react with RNA polymerase I solubilized from rat liver nucleoli, indicating the absence of a common protein sequence in these enzymes. The ODC preparation which was treated with transglutaminase in the presence of putrescine could not stimulate the activity of RNA polymerase I in nuclei of liver and prostate. All these results suggest that the increases in ODC protein or activity are not a prerequisite to the increase in RNA polymerase I after hormonal or physiological stimuli, but rather that the increases in both enzymes are separate responses to the primary stimuli.

REGULATION OF DNA-DEPENDENT: RNA POLYMERASE I ACTIVITY IN RAT LIVER NUCLEI

1978 ◽  
pp. 525
Author(s):  
John A. Todhunter ◽  
Michael Tainsky ◽  
Herbert Weissbach ◽  
Nathan Brot
Keyword(s):  
Rna Polymerase ◽  
Rat Liver ◽  
Rna Polymerase I ◽  
Rat Liver Nuclei ◽  
Liver Nuclei ◽  
Polymerase I

scholarly journals Stimulation of the mouse rRNA gene promoter by a distal spacer promoter.

1995 ◽  
Vol 15 (8) ◽  
pp. 4648-4656 ◽  
Author(s):  
M H Paalman ◽  
S L Henderson ◽  
B Sollner-Webb
Keyword(s):  
Rna Polymerase ◽  
Gene Promoter ◽  
Rna Polymerase I ◽  
Rrna Gene ◽  
Transcriptional Terminator ◽  
Wide Range ◽  
Polymerase I ◽  
Enhancer Sequences ◽  
Stimulation Of

We show that the mouse ribosomal DNA (rDNA) spacer promoter acts in vivo to stimulate transcription from a downstream rRNA gene promoter. This augmentation of mammalian RNA polymerase I transcription is observed in transient-transfection experiments with three different rodent cell lines, under noncompetitive as well as competitive transcription conditions, over a wide range of template concentrations, whether or not the enhancer repeats alone stimulate or repress expression from the downstream gene promoter. Stimulation of gene promoter transcription by the spacer promoter requires the rDNA enhancer sequences to be present between the spacer promoter and gene promoter and to be oriented as in native rDNA. Stimulation also requires that the spacer promoter be oriented toward the enhancer and gene promoter. However, stimulation does not correlate with transcription from the spacer promoter because the level of stimulation is not altered by either insertion of a functional mouse RNA polymerase I transcriptional terminator between the spacer promoter and enhancer or replacement with a much more active heterologous polymerase I promoter. Further analysis with a series of mutated spacer promoters indicates that the stimulatory activity does not reside in the major promoter domains but requires the central region of the promoter that has been correlated with enhancer responsiveness in vivo.

Alterations in DNA-dependent RNA polymerase I from rat liver accompanying ethionine administration

1982 ◽  
Vol 105 (3) ◽  
pp. 799-805 ◽  
Author(s):  
Haruko Yamano ◽  
Yasuko Sawai ◽  
Wen Long Thung ◽  
Fumiyasu Sato ◽  
Kinji Tsukada
Keyword(s):  
Rna Polymerase ◽  
Rat Liver ◽  
Rna Polymerase I ◽  
Polymerase I
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