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Biomedical subjects

S Person

Publications and source records attributed to S Person.

At least 73 records · Page 4Linked to original sources
PubMed1976

Effects of 2-deoxyglucose, glucosamine, and mannose on cell fusion and the glycoproteins of herpes simplex virus.

2-Deoxyglucose and glucosamine were found to inhibit cell fusion caused by a syncytial mutant of herpes simplex virus and to inhibit the glycosylation of viral glycoproteins in the infected cells. The inhibition of fusion and the inhibition of glycosylation caused by 2-deoxyglucose were substantially prevented when mannose was also present during infection. When glycosylation was inhibited, three new bands were found in major glycoprotein region on sodium dodecyl sulfate-polyacrylamide gels. These bands may be precursors to the normal glycoproteins. The correlation between fusion and glycosylation in the presence of 2-deoxyglucose, glucosamine, and mannose suggests that the cells cannot fuse if their glycoproteins have a considerably reduced carbohydrate content.

Cell Fusion↗
PubMed1975

Kinetics of cell fusion induced by a syncytia-producing mutant of herpes simplex virus type I.

We have isolated a number of plaque-morphology mutants from a strain of herpes simplex virus type I which, unlike the wild type, cause extensive cell fusion during a productive viral infection. After the onset of fusion, there is an exponential decrease in the number of single cells as a function of time after infection. At a multiplicity of infection (MOI) of 3.8 plaque-forming units per cell, fusion begins 5.3 h after infection with the number of single cells decreasing to 10% of the original number 10.2 h after infection. As the MOI is gradually increased from 0.4 to 8, the onset of fusion occurs earlier during infection. However, when the MOI is increased from 8 to 86, the onset of fusion does not occur any earlier. The rate of fusion is independent of the MOI for an MOI greater than 1. The rate of fusion varies linearly with initial cell density up to 3.5 X 10(4) cells/cm2 and is independent of initial cell density at higher cell concentrations. To assay cell fusion we have developed a smiple quantitative assay using a Coulter counter to measure the number of single cells as a function of time after infection. Data obtained using a Coulter counter are similar to those obtained with a microscope assay.

Cell Count↗
PubMed1974

Ultraviolet mutagenesis and its repair in an Escherichia coli strain containing a nonsense codon.

Ultraviolet mutagenesis and its repair were studied mainly in WU36-10-89, a uvr(-) strain of Escherichia coli containing a UAG mutation in a gene for leucine biosynthesis. Following ultraviolet (UV) irradiation revertants appearing with or without direct photoreactivation (PR) were classified according to the presence and type of suppressor they contained. We find UV mutation production to be quite specific. An analysis of revertants produced by UV indicates they are formed mainly from GC --> AT and that the miscoding is due to a cytosine residue at the site of mutation in a cytosine-thymine (CT) dimer. We propose that the dimer serves as template during some aspects of repair replication and at the time of replication the C in the dimer directs the insertion of A in the complementary strand. We also note that C --> A and T -->G changes caused by a CT dimer occur much less frequently.

Base Sequence↗
PubMed1969

Cytosine to thymine transitions from decay of cytosine-5-3H in bacteriophage S13.

Decay of cytosine-5-(3)H incorporated into bacteriophage S13 DNA causes a molectular rearrangement of the cytosine molecutle undergoing the decay. The molecular rearrangement produces a cytosine to thyimine coding change with at efficiency approaching one. Decay of either thymidine-(methyl)-(3)H or cytosine-6-(3)H is less than 1 percent as effective in calusing either cytosine to thymine or thymine to cytosine transitions.

Centrifugation, Density Gradient↗
PubMed1968

Calculated energy deposits from the decay of tritium and other radioisotopes incorporated into bacteria.

Transmutation of the radioisotope tritium occurs with the production of a low energy electron, having a range in biological material similar to the dimensions of a bacterium. A computer program was written to determine the radiation dose distributions which may be expected within a bacterium as a result of tritium decay, when the isotope has been incorporated into specific regions of the bacterium. A nonspherical model bacterium was used, represented by a cylinder with hemispherical ends. The energy distributions resulting from a wide variety of simulated labeled regions were determined; the results suggested that the nuclear region of a bacterium receives on the average significantly different per decay doses, if the labeled regions were those conceivably produced by the incorporation of thymidine-(3)H, uracil-(3)H, or (3)H-amino acids. Energy distributions in the model bacterium were also calculated for the decay of incorporated (14)carbon, (35)sulfur, and (32)phosphorous.

Amino Acids↗
PubMed1968

The mechanism of inactivation of T4 bacteriophage by tritium decay.

Coliphage T4 was used as a model system to study the mechanism of biological inactivation produced by tritium decay. Experimentally, tritiated precursors were incorporated into phage DNA (thymidine-(3)H) or into phage protein ((3)H-amino acids). The ratio of killing efficiencies for decays originating in phage DNA to those originating in phage protein was 2.6. Inactivation by decays from labeled amino acids was assumed to occur exclusively from beta-particle irradiation of phage DNA. If decays originating in DNA are due solely to irradiation of DNA, then the killing efficiencies reflect the energy transfer paths in phage DNA for decays originating in phage DNA and in the protein coat. The energy transfer paths were determined for the two cases with the help of a computer and found to be very nearly equal to the experimentally determined ratio (2.6). The killing efficiencies for decays originating in phage DNA were 0.12 and for decays originating in protein 0.046.

Amino Acids↗
PubMed1968

Nonsense suppression in a multiauxotrophic derivative of Escherichia coli 15T-: identification and consequences of an amber triplet in the deoxyribomutase gene.

Previously, arginine revertants of Escherichia coli WWU, a derivative of E. coli 15T(-), have been subdivided by two independent methods: (i) the streak morphology on nutrient agar, and (ii) the pattern of phage growth using amber and ochre mutants of bacteriophage T4. In the first assay, revertants were subdivided into two classes according to the appearance of streaks after incubation on nutrient agar, a thick, even line of growth defining normal revertants and a thin, irregular line defining aberrant revertants. In the second assay, revertants were classified by the suppressors they contained. The present work demonstrates that revertants containing an amber suppressor show the aberrant morphology and are also able to catabolize thymidine for energy and carbon. This is in contrast to the parent WWU containing no suppressor, which shows a normal morphology and cannot utilize thymidine as an energy source. Revertants containing no suppressor, isolated specifically for their ability to catabolize thymidine, show an aberrant morphology. Together, these results indicate that the aberrant morphology results from suppression of an amber triplet in a gene of the thymidine catabolic pathway. Enzyme assays show the amber triplet to be in the gene specifying deoxyribomutase. It is suggested that the aberrant arginine revertants are analogous to high thymine-requiring mutants and that, in general, high and low thymine-requiring mutants differ from one another in their ability to catabolize deoxyribose-1-phosphate.

Arginine↗