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.

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 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.

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 MxA GTPase Blocks Reporter Gene Expression of Reconstituted Thogoto Virus Ribonucleoprotein Complexes

2000 ◽  
Vol 74 (1) ◽  
pp. 560-563 ◽  
Author(s):  
Friedemann Weber ◽  
Otto Haller ◽  
Georg Kochs
Keyword(s):  
Rna Polymerase ◽  
Inhibitory Effect ◽  
Polymerase Activity ◽  
Rna Polymerase I ◽  
Wild Type ◽  
Transfected Cells ◽  
Ribonucleoprotein Complexes ◽  
Polymerase I ◽  
Cellular Compartments ◽  
Antiviral Mechanism

ABSTRACT Human MxA protein accumulates in the cytoplasm of interferon-treated cells and inhibits the multiplication of several RNA viruses, including Thogoto virus (THOV), a tick-borne orthomyxovirus that transcribes and replicates its genome in the cell nucleus. The antiviral mechanism of MxA was investigated by using two alternative minireplicon systems in which recombinant viral ribonucleoprotein complexes (vRNPs) of THOV were reconstituted from cloned cDNAs. A chloramphenicol acetyltransferase reporter minigenome RNA was expressed either by T7 RNA polymerase in the cytoplasm of transfected cells or, alternatively, by RNA polymerase I in the nucleus. The inhibitory effect of MxA was studied in both cellular compartments by coexpressing wild-type MxA or TMxA, an artificial nuclear form of MxA. Our results indicate that both MxA proteins recognize the assembled vRNP rather than the newly synthesized unassembled components. The present findings are consistent with previous data which indicated that cytoplasmic MxA prevents transport of vRNPs into the nucleus, whereas nuclear MxA directly inhibits the viral polymerase activity in the nucleus.

Sequences within the spacer region of yeast rRNA cistrons that stimulate 35S rRNA synthesis in vivo mediate RNA polymerase I-dependent promoter and terminator activities

1989 ◽  
Vol 9 (3) ◽  
pp. 1243-1254
Author(s):  
R Mestel ◽  
M Yip ◽  
J P Holland ◽  
E Wang ◽  
J Kang ◽  
...  
Keyword(s):  
Rna Polymerase ◽  
Base Pair ◽  
Rna Polymerase I ◽  
Rrna Synthesis ◽  
Deletion Mapping ◽  
Gene Promoters ◽  
Transcriptional Terminator ◽  
Polymerase I ◽  
Stimulation Of

Sequences within the spacer region of yeast rRNA cistrons stimulate synthesis of the major 35S rRNA precursor in vivo 10- to 30-fold (E. A. Elion and J. R. Warner, Cell 39:663-673, 1984). Spacer sequences that mediate this stimulatory activity are located approximately 2.2 kilobases upstream from sequences that encode the 5' terminus of the 35S rRNA precursor. By utilizing a centromere-containing plasmid carrying a 35S rRNA minigene, a 160-base-pair region of spacer rDNA was identified by deletion mapping that is required for efficient stimulation of 35S rRNA synthesis in vivo. A 22-base-pair sequence, previously shown to support RNA polymerase I-dependent selective initiation of transcription in vitro, was located 15 base pairs upstream from the 3' boundary of the stimulatory region. A 77-base pair region of spacer DNA that mediates transcriptional terminator activity in vivo was identified immediately downstream from the 5' boundary of the stimulatory region. Deletion mutations extending downstream from the 5' boundary of the 160-base-pair stimulatory region simultaneously interfere with terminator activity and stimulation of 35S rRNA synthesis from the minigene. The terminator region supported termination of transcripts initiated by RNA polymerase I in vivo. The organization of sequences that support terminator and promoter activities within the 160-base-pair stimulatory region is similar to the organization of rDNA gene promoters in higher organisms. Possible mechanisms for spacer-sequence-dependent stimulation of yeast 35S rRNA synthesis in vivo are discussed.

scholarly journals NAD+, ADP-ribosylation and transcription in permeabilized mammalian cells

1981 ◽  
Vol 199 (3) ◽  
pp. 813-817 ◽  
Author(s):  
J Walker ◽  
C K Pearson
Keyword(s):  
Rna Polymerase ◽  
Mammalian Cells ◽  
Inhibitory Effect ◽  
Polymerase Activity ◽  
Rna Polymerase I ◽  
Permeabilized Cells ◽  
Adp Ribosylation ◽  
Deoxyribonuclease I ◽  
Rna Polymerase Activity ◽  
Polymerase I

When permeabilized hamster fibroblasts were incubated with 4 mM-NAD+, the substrate for poly(ADP-ribose) polymerase, RNA polymerase I activity was inhibited by about 85%. This inhibition was not relieved by prior incubation of cells with 3-aminobenzamide, a potent inhibitor of the poly(ADP-ribose) polymerase. Digestion of cells with pancreatic deoxyribonuclease I resulted in the inhibition of RNA polymerase I by 80% and the activation of poly(ADP-ribose) polymerase by up to 300%; prior incubation with 3-aminobenzamide did not prevent the inhibition of the RNA polymerase activity. No radioactivity was found associated with RNA polymerase I during later stages of purification of this enzyme from permeabilized cells previously incubated with [14C]NAD+. The inhibitory effect of NAD+ on RNA polymerase I was not specific for NAD+, as other small, negatively charged molecules with a nuclear location also inhibited the enzyme. The results do not support the concept of a role for ADP-ribosylation in transcription catalysed by RNA polymerase I.

scholarly journals Sequences within the spacer region of yeast rRNA cistrons that stimulate 35S rRNA synthesis in vivo mediate RNA polymerase I-dependent promoter and terminator activities.

1989 ◽  
Vol 9 (3) ◽  
pp. 1243-1254 ◽  
Author(s):  
R Mestel ◽  
M Yip ◽  
J P Holland ◽  
E Wang ◽  
J Kang ◽  
...  
Keyword(s):  
Rna Polymerase ◽  
Base Pair ◽  
Rna Polymerase I ◽  
Rrna Synthesis ◽  
Deletion Mapping ◽  
Gene Promoters ◽  
Transcriptional Terminator ◽  
Polymerase I ◽  
Stimulation Of

Sequences within the spacer region of yeast rRNA cistrons stimulate synthesis of the major 35S rRNA precursor in vivo 10- to 30-fold (E. A. Elion and J. R. Warner, Cell 39:663-673, 1984). Spacer sequences that mediate this stimulatory activity are located approximately 2.2 kilobases upstream from sequences that encode the 5' terminus of the 35S rRNA precursor. By utilizing a centromere-containing plasmid carrying a 35S rRNA minigene, a 160-base-pair region of spacer rDNA was identified by deletion mapping that is required for efficient stimulation of 35S rRNA synthesis in vivo. A 22-base-pair sequence, previously shown to support RNA polymerase I-dependent selective initiation of transcription in vitro, was located 15 base pairs upstream from the 3' boundary of the stimulatory region. A 77-base pair region of spacer DNA that mediates transcriptional terminator activity in vivo was identified immediately downstream from the 5' boundary of the stimulatory region. Deletion mutations extending downstream from the 5' boundary of the 160-base-pair stimulatory region simultaneously interfere with terminator activity and stimulation of 35S rRNA synthesis from the minigene. The terminator region supported termination of transcripts initiated by RNA polymerase I in vivo. The organization of sequences that support terminator and promoter activities within the 160-base-pair stimulatory region is similar to the organization of rDNA gene promoters in higher organisms. Possible mechanisms for spacer-sequence-dependent stimulation of yeast 35S rRNA synthesis in vivo are discussed.

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