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Effects of inhibitors of nucleic acid and protein synthesis on growth and aggregation of the cellular slime mold Dictyostelium discoideum.
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Experimental chemoprophylaxis against schistosomiasis. I. Introduction and rationale.
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Nucleolar necklaces in chick embryo fibroblast cells. II. Microscope observations of the effect of adenosine analogues on nucleolar necklace formation.
The round nucleoli of chick embryo fibroblast cells, when exposed to adenosine (2 mM)or to a number of adenosine analogues, lose material and unravel over a period of several hours to become beaded strands, 20 mu M in length, termed nucleolar necklaces (NN). Light microscope observations on this process are described. Biochemical experiments have revealed that most of these analogues interfere with both messenger RNA synthesis and ribosome synthesis, causing extensive degradation of the preribosome species containing 32S RNA although most of the preribosomes containing 18S RNA survive. We suggest that it is the depletion from the nucleolus of the adhesive 32S and 28S RNA preribosomes which allows the remaining nucleolar apparatus to spread apart into the NN configuration. Also required for the maintenance of the NN structure is the synthesis of some ribosomal RNA (rRNA) possibly present as rRNA "feathers" on the DNA. The addition of inhibitors of rRNA synthesis such as actinomycin D to the NN-containing cells causes loss of rRNA. Then a contraction and collapse of the NN structure into small dense spheres is observed.
Rifampicin-resistant bacteriophage PBS2 infection and RNA polymerase in Bacillus subtilis.
Bacteriophage PBS2 replication is unaffected by rifampicin and other rifamycin derivatives, which are potent inhibitors of Bacillus subtilis RNA synthesis. Extracts of gently-lysed infected cells contain a DNA-dependent RNA polymerase activity which is specific for uracil-containing PBS2 DNA. The PBS2-induced RNA polymerase is insensitive to rifamycin derivatives which inhibit the host's RNA polymerase.
Variation in G1 transit time relative to the cycloheximide and actinomycin D drug restriction points.
The transit time distribution at various points in the cell cycle of synchronized Chinese hamster ovary cells was determined from the mitotic index, [3H]thymidine labeling index and increase in cell number monitored at regular intervals after mitotic selection. Variation in G1 transit time compared with that for the total cell cycle indicates that variation in cell cycle transit time occurs mainly during G1 phase. The cycloheximide (5.0 microgram/ml) and actinomycin D (3.0 microgram/ml) restriction points occur 0.2 and 1.7 hr prior to entry into S phase, respectively. The transit time distributions are further characterized by the moments of the distributions. The variance (2nd moment about the mean) of the transit time distribution at the actinomycin D restriction point is similar to the variance of the transit time distribution at the G1/S border, thus variation in cell cycle transit time originates earlier than 1.7 hr prior to entry into S phase (i.e., the first 3/4 of G1). If G1 transit time variability and cell cycle control are related, then the results presented here indicate that the major regulatory events do not occur during late G1 phase.
Bilharziasis of the cervix uteri.
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Preliminary studies on porphylaxis, drug resistance, and synergism in experimental schistosomiasis.
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Hycanthone: a frameshift mutagen.
Rapid spot-test screening of antischistosomal agents reveals that hycanthone is a potent frameshift mutagen while the closely related compound, miracil D, is nonmutagenic in Salmonella. Both hycanthone and miracil D are frameshift mutagens for T4 bacteriophage during growth in Escherichia coli.
Comparative ability of hycanthone and miracil D to interact with DNA.
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Miracil D: inhibition of deoxyribonucleic acid polymerase-deficient Escherichia coli.
Miracil D preferentially inhibited the growth of a deoxyribonucleic acid (DNA) polymerase-deficient Escherichia coli strain. This is taken to indicate that miracil D is capable of altering the DNA of living cells and that it may thereby be a potential mutagen and carcinogen.
Stereospecific sulfur oxidation of 7-methylthioxanthone-2-carboxylic acid by Calonectria decora.
Thin-layer chromatography was used to determine the ability of three microorganisms capable of sulfur oxygenation, including Aspergillus niger, Streptomyces armentosus subsp. armentosus, and Calonectria decora, to oxidize 7-methylthioxanthone-2-carboxylic acid to the corresponding sulfoxide in growing cultures. In addition, optical rotary dispersion, circular dichroism, and nuclear magnetic resonance analysis in the presence of chiral shift reagent were used variously to access reaction stereoselectivity, absolute configuration, and optical purity of isolated products. The data indicated that C. decora produced the sulfoxide in high yield (69%) and optical purity (97%), most probably in the S-configuration.
Effect of miracil D on marker frequency ratio and cytotoxicity in Bacillus subtilis.
When Miracil D was added to mid-log phase Bacillus subtilis cells, the rate of growth decreased immediately, and the turbidity of the culture began to decrease within 15 to 20 min after addition of the drug. At this stage, ghostlike cells were observed under phase-contrast microscopy. The viable count also began to decrease rapidly after 15 min in the presence of the drug, and within 60 min there was a 10,000-fold reduction in viability. Incorporation of (3)H-thymidine into deoxyribonucleic acid (DNA) proceeded normally up to 20 min of exposure to the drug, after which incorporation ceased. Cells which were prelabeled with (3)H-thymidine and exposed to the drug released labeled DNA into the medium after 15 to 20 min. Results of transformation analyses with donor DNA from cells grown in the presence of Miracil show a decrease with time in the ratio of origin markers to terminus markers. Electron micrographs of sectioned cells grown for 5, 10, and 15 min in the presence of Miracil D show profound cytotoxic effects. The most striking aspect of such cells is the very condensed appearance of the nucleoid. In those cells about to divide, the nucleoid appears not to be properly separating, being strung out in the region of the developing septum. Finally, the mesosome is very poorly defined or entirely absent in Miracil-treated cells.
Use of miracil D to suppress bacterial ribonucleic acid and protein synthesis during bacteriophage MS2 infection.
Under certain culture conditions, Miracil (35 mug/ml) halts the growth of uninfected Escherichia coli. Cellular ribonucleic acid (RNA) synthesis is almost completely suppressed, whereas deoxyribonucleic acid and protein synthesis are inhibited to a lesser extent. When the drug is added to host bacteria prior to infection with bacteriophage MS2, the phage adsorb to the cells, but penetration of the viral RNA is inhibited. Penetration may be achieved without further viral development by infection in the presence of chloramphenicol. If the bacteria are infected with MS2 in the presence of chloramphenicol, subsequently washed to remove the chloramphenicol, and then treated with Miracil at any time between 0 and 20 min postinfection, a second viral function is inhibited and the yield of progeny phage is reduced. Addition of the drug after 20 min postinfection does not inhibit the infection process. When Miracil is present from early times in infection, only a limited synthesis of both double- and single-stranded virus-specific RNA is observed. The viral RNA species thus produced do not appear to differ from those made in the absence of the drug. A comparison of the activities of the viral RNA synthetase produced during the course of infection in the presence and in the absence of Miracil suggests that a possible cause of the inhibition is the synthesis of an unstable enzyme in the presence of the drug.
"Nilodin" in treatment of Schistosoma haematobium.
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High-resolution nuclear magnetic resonance studies of double helical polynucleotides.
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