Messenger RNA Synthesis in Mumps-Virus-Infected Cells

1980 ◽  
Vol 8 (4) ◽  
pp. 441-442
Author(s):  
BERT K. RIMA ◽  
SAMUEL J. MARTIN
Keyword(s):  
Messenger Rna ◽  
Rna Synthesis ◽  
Mumps Virus ◽  
Infected Cells

RNA synthesis in polyoma virus-infected cells. I. Pattern of formation of polyribosome-associated messenger RNA during productive infection

1970 ◽  
Vol 48 (10) ◽  
pp. 1104-1112 ◽  
Author(s):  
William P. Cheevers ◽  
Rose Sheinin
Keyword(s):  
Dna Replication ◽  
Messenger Rna ◽  
Rna Synthesis ◽  
Polyoma Virus ◽  
Productive Infection ◽  
Mrna Synthesis ◽  
Viral Dna ◽  
Experimental Conditions ◽  
Embryo Cells ◽  
Infected Cells

Experimental conditions have been established for selective measurement of the synthesis of mRNA in mouse embryo cells. Using such conditions, it was found that productive infection of these cells by polyoma virus resulted in stimulation of mRNA synthesis. The pattern of induction of mRNA synthesis was biphasic, characterized by distinct "early" and "late" periods, as denoted by the time of initiation of progeny viral DNA replication. The formation of "early" mRNA was first detected at 9–11 h postinfection, 6 h prior to the time of onset of virus-induced synthesis of cell DNA and 9 h prior to initiation of polyoma DNA replication. The initiation of synthesis of "late" mRNA was approximately coincident with the onset of formation of viral DNA. Most of the newly synthesized "early" and "late" mRNA was of relatively small size (8–12 S) and was associated with polyribosomes which sedimented at less than 180 S. The proportion of the total "late" mRNA which was virus-specific was three times higher than that of the total "early" mRNA; however, the mRNA synthesized both "early" and "late" was predominantly cell-specific.

Studies of two temperature-sensitive mutants of Mengo virus

1979 ◽  
Vol 57 (6) ◽  
pp. 902-913 ◽  
Author(s):  
Patrick W. K. Lee ◽  
John S. Colter
Keyword(s):  
Rna Synthesis ◽  
Viral Rna ◽  
Temperature Sensitive ◽  
Supporting Evidence ◽  
Structural Polypeptide ◽  
Infected Cells ◽  
Mengo Virus ◽  
In Vitro Stability

Studies of the synthesis of viral ribonucleates and polypeptides in cells infected with two RNA−ts mutants of Mengo virus (ts 135 and ts 520) have shown that when ts 135 infected cells are shifted from the permissive (33 °C) to the nonpermissive (39 °C) temperature: (i) the synthesis of all three species of viral RNA (single stranded, replicative form, and replicative intermediate) is inhibited to about the same extent, and (ii) the posttranslational cleavage of structural polypeptide precursors A and B is partially blocked. Investigations of the in vivo and in vitro stability of the viral RNA replicase suggest that the RNA− phentotype reflects a temperature-sensitive defect in the enzyme. The second defect does not appear to result from the inhibition of viral RNA synthesis at 39 °C, since normal cleavage of polypeptides A and B occurs in wt Mengo-infected cells in which viral RNA synthesis is blocked by cordycepin, and at the nonpermissive temperature in ts 520 infected cells. Considered in toto, the evidence suggests that ts 135 is a double mutant.Subviral (53 S) particles have been shown to accumulate in ts 520 (but not ts 135) infected cells when cultures are shifted from 33 to 39 °C. This observation provides supporting evidence for the proposal that this recently discovered particle is an intermediate in the assembly pathway of Mengo virions.

scholarly journals Role for nsP2 Proteins in the Cessation of Alphavirus Minus-Strand Synthesis by Host Cells

2006 ◽  
Vol 80 (1) ◽  
pp. 360-371 ◽  
Author(s):  
Dorothea L. Sawicki ◽  
Silvia Perri ◽  
John M. Polo ◽  
Stanley G. Sawicki
Keyword(s):  
Host Response ◽  
Rna Synthesis ◽  
Late Phase ◽  
Host Cells ◽  
Minus Strand ◽  
Wild Type ◽  
Persistent Infections ◽  
Infected Cells ◽  
Replicative Intermediates ◽  
Transcription Complexes

ABSTRACT In order to establish nonlytic persistent infections (PI) of BHK cells, replicons derived from Sindbis (SIN) and Semliki Forest (SFV) viruses have mutations in nsP2. Five different nsP2 PI replicons were compared to wild-type (wt) SIN, SFV, and wt nsPs SIN replicons. Replicon PI BHK21 cells had viral RNA synthesis rates that were less than 5% of those of the wt virus and ∼10% or less of those of SIN wt replicon-infected cells, and, in contrast to wt virus and replicons containing wt nsP2, all showed a phenotype of continuous minus-strand synthesis and of unstable, mature replication/transcription complexes (RC+) that are active in plus-strand synthesis. Minus-strand synthesis and incorporation of [3H]uridine into replicative intermediates differed among PI replicons, depending on the location of the mutation in nsP2. Minus-strand synthesis by PI cells appeared normal; it was dependent on continuous P123 and P1234 polyprotein synthesis and ceased when protein synthesis was inhibited. The failure by the PI replicons to shut off minus-strand synthesis was not due to some defect in the PI cells but rather was due to the loss of some function in the mutated nsP2. This was demonstrated by showing that superinfection of PI cells with wt SFV triggered the shutdown of minus-strand synthesis, which we believe is a host response to infection with alphaviruses. Together, the results indicate alphavirus nsP2 functions to engage the host response to infection and activate a switch from the early-to-late phase. The loss of this function leads to continuous viral minus-strand synthesis and the production of unstable RC+.

Effect of Interferon on RNA Synthesis in Sindbis Virus Infected Cells

1966 ◽  
Vol 121 (2) ◽  
pp. 630-632 ◽  
Author(s):  
H. B. Levy ◽  
L. F. Snellbaker ◽  
S. Baron
Keyword(s):  
Sindbis Virus ◽  
Rna Synthesis ◽  
Infected Cells

scholarly journals Control of adenovirus early gene expression: posttranscriptional control mediated by both viral and cellular gene products.

1981 ◽  
Vol 1 (9) ◽  
pp. 807-813 ◽  
Author(s):  
M G Katze ◽  
H Persson ◽  
L Philipson
Keyword(s):  
Gene Product ◽  
Messenger Rna ◽  
Adenovirus Type ◽  
Negative Regulator ◽  
Early Gene ◽  
In Vitro Translation ◽  
Mapping Technique ◽  
Cellular Gene ◽  
Infected Cells ◽  
Adenovirus Type 5

An adenovirus type 5 host range mutant (hr-1) located in region E1A and phenotypically defective in expressing viral messenger ribonucleic acid (RNA) from other early regions (Berk et al., Cell 17:935-944, 1979) was analyzed for accumulation of viral RNA in the presence of protein synthesis inhibitors. Nuclear RNA was transcribed from all early regions at the same rate, regardless of whether the drug was present or absent. As expected, low or undetectable levels of RNA were found in the cytoplasm of hr-1-infected cells compared with the wild-type adenovirus type 5 in the absence of drug. When anisomycin was added 30 min before hr-1 infection, cytoplasmic RNA was abundant from early regions E3 and E4 when assayed by filter hybridization. In accordance, early regions E3 and E4 viral messenger RNA species were detected by the S1 endonuclease mapping technique only in hr-1-infected cells that were treated with the drug. Similar results were obtained by in vitro translation studies. Together, these results suggest that this adenovirus type 5 mutant lacks a viral gene product necessary for accumulation of viral messenger RNA, but not for transcription. It is proposed that a cellular gene product serves as a negative regulator of viral messenger RNA accumulation at the posttranscriptional level.

scholarly journals MESSENGER RNA SYNTHESIS BY A "COATED" VIRAL GENOME

1967 ◽  
Vol 57 (2) ◽  
pp. 314-320 ◽  
Author(s):  
J. R. Kates ◽  
B. R. McAuslan
Keyword(s):  
Viral Genome ◽  
Messenger Rna ◽  
Rna Synthesis

Induction of implantation in the rat by intraparametrial injection of uterine RNA from oestrogen-treated animals

1982 ◽  
Vol 93 (3) ◽  
pp. 397-NP ◽  
Author(s):  
B. Lejeune ◽  
F. Puissant ◽  
M. Camus ◽  
F. Leroy
Keyword(s):  
Messenger Rna ◽  
Rna Synthesis ◽  
Ovariectomized Rats ◽  
Pregnant Rats ◽  
Rnase Digestion

Crude RNA preparations from uteri of oestradiol-treated rats induced the implantation of delayed blastocysts when injected into the parametrium of ovariectomized pregnant rats. Treatment of donor animals with labelled oestradiol showed that this effect could not be due to contamination of the RNA extracts by oestradiol. RNase digestion of these extracts suppressed their capacity to induce implantation. Purified poly (A)-rich RNA from oestrogen-treated uteri failed to elicit implantation although it was capable of increasing epithelial height when repeatedly injected into uterine horns of ovariectomized rats. These results suggest that uterine RNA synthesis might somehow mediate the effects of oestrogen in causing implantation and that RNAs other than messenger RNA might be involved.

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