Specific stimulation of ribosomal RNA synthesis in E. coli by a protein factor

1980 ◽  
Vol 177 (2) ◽  
pp. 291-295 ◽  
Author(s):  
Ben A. Oostra ◽  
AB Geert ◽  
Max Gruber



1971 ◽  
Vol 234 (47) ◽  
pp. 97-97 ◽  
Keyword(s):  


1970 ◽  
Vol 48 (1) ◽  
pp. 47-54 ◽  
Author(s):  
S. J. Igarashi ◽  
J. F. Elliott ◽  
R. P. Bissonnette

A temperature-sensitive mutant of RNA bacteriophage R17, ts24, which contains a ts-mutation in the RNA-replicating function, was used to analyze the effects of RNA phage infection on host E. coli cell metabolism in the presence and absence of phage RNA synthesis. The principal conclusions from these studies are as follows. (1) Host ribosomal RNA synthesis is inhibited by infection with R17 whether or not phage-specific RNA synthesis takes place. (2) Immediately following infection, overall protein synthesis is reduced to 10–20% of the level of synthesis occurring in noninfected cultures. (3) Phage RNA remains intact in the host cell for at least 90 min after infection. Based on these observations, a mechanism for the specific inhibition of ribosomal RNA by R17 infection was discussed.



1989 ◽  
Vol 264 (1) ◽  
pp. 101-106 ◽  
Author(s):  
R M Palmer ◽  
G P Campbell ◽  
P F Whitelaw ◽  
D S Brown ◽  
P A Bain ◽  
...  

Insulin stimulated total RNA accretion and the incorporation of [3H]uridine into RNA in L6 skeletal-muscle myoblasts. Incorporation of uridine into the rRNA was measured after either separation of 18 S and 28 S rRNA species by agarose-gel electrophoresis or separation of dissociated 40 S and 60 S ribosomal subunits on sucrose density gradients. Both methods showed a stimulation by insulin of uridine incorporation into the RNA of the two subunits. Two non-steroidal anti-inflammatory drugs, indomethacin and ibuprofen, which inhibit the metabolism of arachidonic acid by the cyclo-oxygenase pathway, inhibited the insulin-induced accretion of total cellular RNA and the incorporation of uridine into the RNA of both ribosomal subunits. The effect of insulin was observed both by using a tracer dose of [3H]uridine (5 microM) and in the presence of a high concentration (1 mM) of uridine to minimize possible changes in intracellular precursor pools. Neither insulin nor indomethacin was found to affect the incorporation of uridine into the total intracellular nucleotide pool, or the conversion of uridine into UTP. The ability of inhibitors of arachidonic acid metabolism to prevent insulin-induced increases in RNA metabolism suggests that a prostaglandin or other eicosanoid is involved in the signal mechanism whereby insulin stimulates RNA synthesis.



1974 ◽  
Vol 60 (1) ◽  
pp. 54-64 ◽  
Author(s):  
Joel B. Baseman ◽  
Domenic Paolini ◽  
Harold Amos

After the addition of insulin to monolayers of chick fibroblasts previously incubated in serum-free medium, the rates of protein and RNA synthesis increase continuously during the first 8–10 h. Little stimulation of DNA synthesis or mitosis results with the addition of insulin alone in contrast to the addition of fresh serum which stimulates both markedly. The stimulation in RNA synthesis does not result from expansion of the nucleotide pool but is correlated with increases in RNA polymerase activity. All major classes of RNA are stimulated; processing of preribosomal RNA to 28S and 18S and the association of this mature RNA with ribosomes appear to occur normally. The kinetics of stimulation of 5S RNA differ from those of the synthesis of 4S and of ribosomal RNA. Insulin and serum appear to affect the synthesis or stability of certain transcripts differentially.





1993 ◽  
pp. 119-130 ◽  
Author(s):  
Rolf Wagner ◽  
Günter Theißen ◽  
Martin Zacharias


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