Inhibition of DNA synthesis and cell division in Salmonella typhimurium by azide

1974 ◽  
Vol 135 (4) ◽  
pp. 339-348 ◽  
Author(s):  
Z. Cieśla ◽  
Krystyna Mardarowicz ◽  
T. Klopotowski
1989 ◽  
Vol 139 (2) ◽  
pp. 269-274 ◽  
Author(s):  
Heideh Fattaey ◽  
Terry C. Johnson ◽  
Hsin-Hwei Chou

1972 ◽  
Vol 18 (2) ◽  
pp. 145-151 ◽  
Author(s):  
M. V. O'Shaughnessy ◽  
S. H. S. Lee ◽  
K. R. Rozee

Using monodispersed cell suspensions, interferon preparations were shown to have both a lethal and a growth-depression effect in the same concentration range as that required for antiviral activity. In addition, synchronized cells treated with interferon respond by delaying their normal uptake of thymidine during S phase until after a period during which new protein is synthesized. Puromycin added during this period prevents both the synthesis of this protein and the subsequent synthesis of DNA.


1969 ◽  
Vol 14 (2) ◽  
pp. 111-119 ◽  
Author(s):  
Michael H. L. Green ◽  
John Donch ◽  
Young S. Chung ◽  
Joseph Greenberg

The effect of nalidixic acid, a specific inhibitor of DNA synthesis, onEscherichia colistrain B (lon) and its u.v.-sensitive derivatives is examined. Strain B itself is sensitive to nalidixic acid, whereas its u.v.-resistant derivative B/r is resistant.It is shown that in allexr Astrains, in which u.v.-induced filamentation is suppressed, resistance to nalidixic acid is increased. Amongexr Astrains, Bs4 is exceptionally resistant to nalidixic acid. This is because nalidixic acid kills only growing cells and strain Bs4, atryauxotroph, may grow poorly under the conditions used to test nalidixic acid.Theuvrgenes of the HCR strains Bs1, Bs8 and Bs12 do not suppress u.v.-induced filamentation nor do they affect the response to nalidixic acid. Theuvrgene of strain Bs3 is unusual in increasing the tendency to filament and also sensitivity to nalidixic acid.Strains Bs1, Bs3 and Bs8 are all doubly mutated from strain B, the second mutation (notuvr) being responsible for their increased resistance to nalidixic acid as well as partially or completely suppressing filamentation.It is concluded that the cell division mechanism of (lon) strain B is sensitive to inhibition of DNA synthesis. Mutations which suppress the tendency of strain B to filament reduce its sensitivity to inhibition of DNA synthesis.


1968 ◽  
Vol 53 (2-3) ◽  
pp. 506-518 ◽  
Author(s):  
A. Toliver ◽  
E.H. Simon ◽  
P.T. Gilham

1966 ◽  
Vol 22 (5) ◽  
pp. 294-295 ◽  
Author(s):  
H. Rothstein ◽  
J. Fortin ◽  
D. Sonneborn

1955 ◽  
Vol 1 (5) ◽  
pp. 399-419 ◽  
Author(s):  
George Setterfield ◽  
Robert E. Duncan

At a concentration of 9.6 x 10–5 M, 2,6-diaminopurine (DAP) completely inhibited cell enlargement, cell division, and DNA synthesis (determined by microphotometric measurement of Feulgen dye) in Vicia faba roots. Inhibition of cell enlargement was partially reversed by adenine, guanine, xanthine, adenosine, and desoxyadenosine. Guanine and the nucleosides gave the greatest reversal, suggesting that one point of DAP action upon cell enlargement is a disruption of nucleoside or nucleotide metabolism, possibly during pentosenucleic acid synthesis. DAP inhibited cell division by preventing onset of prophase. At the concentrations used it had no significant effect on the rate or appearance of mitoses in progress. Inhibition of entrance into prophase was not directly due to inhibition of DNA synthesis since approximately half of the inhibited nuclei had the doubled (4C) amount of DNA. Adenine competitively reversed DAP inhibition of cell division, giving an inhibition index of about 0.5. Guanine gave a slight reversal while xanthine, hypoxanthine, adenosine, and desoxyadenosine were inactive. A basic need for free adenine for the onset of mitosis was suggested by this reversal pattern. Meristems treated with DAP contained almost no nuclei with intermediate amounts of DNA, indicating that DAP prevented the onset of DNA synthesis while allowing that underway to reach completion. The inhibition of DNA synthesis was reversed by adenine, adenosine, and desoxyadenosine although synthesis appeared to proceed at a slower rate in reversals than in controls. Inhibition of DNA synthesis by DAP is probably through nucleoside or nucleotide metabolism. A small general depression of DNA content of nuclei in the reversal treatments was observed. This deviation from DNA "constancy" cannot be adequately explained at present although it may be a result of direct incorporation of DAP into DNA. The possible purine precursor, 4-amino-5-imidazolecarboxamide gave no reversal of DAP inhibition of cell elongation and cell division and only a slight possible reversal of inhibition of DNA synthesis.


1972 ◽  
Vol 18 (5) ◽  
pp. 671-681 ◽  
Author(s):  
Michael L. Murray ◽  
Philip E. Hartman

Salmonella typhimurium derepressed for the histidine biosynthetic enzymes form wrinkled colonies at 37 °C on media containing a high (2%) content of metabolizable carbon source. "Wrinkledness" reflects accumulation of multinucleate filamentous cells caused by impaired cell division. At 42 °C, DNA synthesis and nuclear division are impaired. Addition of methionine at 42 °C permits DNA synthesis, nuclear division, and, under some conditions, cell division. However, multinucleate filaments are formed both on high and on low carbon source at 42 °C. The filaments contain nuclei that are peculiarly hypersensitive to inactivation with ultraviolet (uv.) light.Overproduction of both the hisH and hisF gene products is required for these pleiotropic effects of derepression. The hisH and hisF proteins, and even some of their enzymologically inactive forms, may cooperate to inhibit cell division by direct interaction with (a) sensitive cellular site(s).


1975 ◽  
Vol 142 (4) ◽  
pp. 960-973 ◽  
Author(s):  
J Nedrud ◽  
M Touton ◽  
W R Clark

The requirement for cell division and expression of new genes was examined in the primary and secondary mouse mixed leukocyte culture (MLC). Hydroxyurea (HU) was used to block DNA synthesis and cell division, and 5-bromo-2'-deoxyuridine (BUdR) was used to probe for the expression of new cell-specific genes. In the primary MLC, inhibition of DNA synthesis and cell division by HU almost totally suppressed the generation of initial, target-specific cytotoxicity. When HU was washed out of the cultures, cytotoxicity was generated after a lag time approximately equal to the period of treatment with HU. The rate of development and maximal value of cytotoxicity in HU-reversed cultures was identical to untreated controls, suggesting that the inhibition was not due to a nonspecific lethal effect of the drug. Development of initial cytotoxicity in primary MLC was similarly suppressed by levels of BUdR 25 to 75-fold below the levels of this drug having nonspecific mutagenic effects in lymphocytes, indicating that development of cytotoxicity was also dependent on the expression of a new genetic program. In the secondary MLC, regeneration of both DNA synthesis and cytotoxicity was apparent 12-15 h after re-exposure to initial stimulating antigen. In this reaction, however, generation of cytotoxicity was insensitive to both HU and BUdR. Thus, the cytotoxic program developed in the primary MLC appears to be genetically stable through the production of effector memory cells, and into regeneration of fully cytotoxic memory cells in secondary MLC.


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