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Biomedical subjects

E C Pollard

Publications and source records attributed to E C Pollard.

At least 19 recordsLinked to original sources
PubMed1986

The influence of repair systems on the presence of sensitive and resistant fractions in the relation of survival of colony-forming ability in Escherichia coli to UV exposure.

In the experimentally observed relationship between survival of colony-forming ability and the amount of exposure to ultraviolet light, two characteristics are generally found. First, sensitive and resistant components often show. Second, there is often a shouldered character to the survival. We present evidence that the first is largely due to the presence of active replication forks in the genome, and that the second is related to the operation of the recombinational repair system. We are able to describe our data in terms of a superposition of single and multiple-hit fractions and to show that the latter are greatly increased, in excision-repair-competent strains, by prevention of protein synthesis for 1 h prior to irradiation. Applying this analysis and treatment to a number of mutant strains enables us to make suggestions as to the interaction between recombinational and excision repair.

DNA Repair↗
PubMed1981

Induced radioresistance: an aspect of induced repair.

Irradiation of Escherichia coli cells with UV or X-rays followed by incubation under conditions in which protein synthesis can occur results in a population of cells that is resistant to X-rays; however, this resistance develops only if the cells are recA+ and lexA+, a fact that associates the phenomenon with induced (S.O.S.) repair. By observing separately the component of a culture that is resistant and the component that retains its normal growth, the fraction of induced and uninduced cells for a dose of UV or X-rays can be estimated. Such estimates show that the dose-response for UV induction of resistant cells agrees with that of the recA gene product. Thus induced radioresistance is considered to be due to the changes in the cell occasioned by the derepression of recA and lexA. These changes are expected to be involved with the synapsis of homologous genomes that is necessary for the use of a second genome to repair damage occurring in both strands of a duplex at the same base, as exemplified by a double-strand break or an interstrand crosslink. This consideration is additionally supported by the increased resistance of cells grown to contain multiple genomes in the same envelope, an increased resistance not found in recA- or lexA- cells. The condition of a completed chromosome is also resistant, again not in recA- or lexA- cells. We suggest that cell killing by X-rays is due to the double-strand breaks which are not repaired by molecular synapsis before the arrival of the replication polymerase at the break.

DNA Repair↗
PubMed1978

Relative rates of repair of single-strand breaks and postirradiation DNA degradation in normal and induced cells of Escherichia coli.

Labeled DNA from irradiated Excherichia coli cells has been studied on an alkaline sucrose gradient without acid precipitation of the DNA. This enables the observation of both DNA repair and DNA degradation. The use of a predose of ultraviolet light (UV) causes induction of an inhibitor of postirradiation DNA degradation in lex+ strains. The effect of this induction on both the repair of single-strand breaks and DNA degradation has been followed in strains WU3610 (uvr+) and WU3610-89 (uvr-). The repair process is more rapid than the degradation, and when degradation is inhibited more repair is apparent. Cells that are lex- (Bs-1 and AB2474) cannot be induced for inhibition of degradation. Nevertheless, by observation at short times repair can be seen clearly. This repaired DNA is degraded, suggesting that the signal for DNA degradation is not a single-strand break.

Centrifugation, Density Gradient↗
PubMed1978

Induced radioresistance in four strains of Escherichia coli, two with lambda lysogens.

Cells of E. coli that are recA+ and lex+ show a phenomenon of induced radioresistance. A preexposure to ultraviolet light, or ionizing radiation followed by incubation to allow protein synthesis, followed by treatment with rifampin to prevent further induction, renders the cells resistant to further doses of radiation. When this is attempted with lambda lysogens of the same strains, no radioresistance is seen, even though the preexposure is too small to induce lambda itself. If the lysogens are ind-, namely lambda C1857, about the normal radioresistance can be developed by pretreatment. These findings suggest that the lambda repressors can bind to single-strand breaks caused by the inducing agent and can modify the course of induction.

Coliphages↗
PubMed1977

Inositol-less death in yeast results in a simultaneous increase in intracellular viscosity.

Inositol auxotrophs of yeast developing on isositol-deficient medium continue protein synthesis for 4-6 h, lose viability rapidly after 6 h, and show an increase in cytoplasmic viscosity as measured by spin label rotational motion. Cycloheximide prevents the rapid loss of cell viability, stops protein synthesis, and simultaneously prevents an increase in cytoplasmic viscosity. From these observations, we infer that intracellular translational diffusion is upset as a consequence of inositol starvation. Cell death may be caused by a modified intracellular diffusion environment.

Cell Survival↗
PubMed1977

Action of hydrogen peroxide on degradation of DNA after irradiation in Escherichia coli.

Hydrogen peroxide (H2O2), which produces breaks in cellular DNA, has not hitherto been shown to cause degradation of DNA. In this investigation it is shown that if transcription is blocked with rifampin, treatment with H2O2 causes degradation of DNA to nearly the same extent as does gamma-radiation. Further, if cells are given a treatment with H2O2 and incubated for 50 min, the amount of degradation in a second treatment is markedly less. This is attributed to the induction of the inhibitor of post-irradiation degradation of DNA (prd) by the first treatment. There is thus a double action of H2O2: first, to induce inhibition, and second, to cause degradation of DNA to begin in non-induced cells. The genetic dependence of induction by H2O2 mimics that of ionizing radiation. Accordingly, the induction process does not occur in recA- and lex- cells, because they are not inducible and is absent in recB- cells because they lack exonuclease V, the major component of prd. Potassium iodide (KI), an OH radical scavenger, negates the action of peroxide on DNA. The results obtained in this study suggest a possible theory for the evolution of radiation response systems

DNA, Bacterial↗
PubMed1977

Ultraviolet induction of prophage lambda during inhibition of deoxyribonucleic acid synthesis by hydroxyurea.

Hydroxyurea inhibited synthesis of certain deoxyribonucleic acid (DNA) precursors and causes the cessation of DNA synthesis. It did not cause induction of lambda. Superinfection of an irradiated lysogen with lambdaind- could prevent induction, but the percentage of cells protected decreased as the time between irradiation and superinfection increased. The presence of hydroxyurea did not increase the time during which cells could be rescued by superinfection. The accumulation of DNA precursors after ultraviolet or ionizing radiation was not necessary for the induction of lambda prophage to occur.

Cobalt Radioisotopes↗
PubMed1975

Induction of radioresistance in Escherichia coli.

The effect of prior treatment by inducing agents on the radioresistance of cells of Escherichia coli has been studied. In order to separate the induction process from the radiation-damage process, cells were first treated with inducing agents such as ultraviolet light, ionizing radiation, or nalidixic acid, allowed to become induced by incubation for 50 min and then given rifampin to prevent further induction. They were then tested for radiation sensitivity. It was found that all strains tested except recA-, lex-, and recB showed very apparent protection. Induction by UV had the most effect and by nalidixic acid the least. The time course of development of protection was observed in one case: it is 50% established in 15 min. The absence of effect in recA- and lex- is explainable by the fact that these cells cannot be induced, for example, for prophage or the inducible inhibitor of post-irradiation DNA degradation. We suggest that the inducible inhibitor of postirradiation DNA degradation is one factor in a recovery system possessed by E. coli cells.

Cell Division↗
PubMed1974

Repair of radiation-induced strand breaks as related to the inducible inhibitor of postirradiation DNA degradation.

The repair of radiation-produced single-strand breaks observed under alkaline conditions is very apparent in cells which possess an inducible inhibitor of postirradiation DNA degradation. Previous induction of the inhibitor with ultraviolet light increases the amount of repair. In those cells which are genetically not inducible there is no increase following ultraviolet irradiation.

Centrifugation, Density Gradient↗
PubMed1974

Involvement of recA and exr genes in the in vivo inhibition of the recBC nuclease.

When Escherichia coli cells are gamma irradiated they degrade their deoxyribonucleic acid (DNA). The DNA of previously gamma-irradiated T4 phage is also degraded in infected cells. The amount of degradation is not only dependent on the dose but also on the genotype of the cell. The amount of degradation is less in cells carrying a recB or a recC mutation, suggesting that most of the DNA degradation is due to the recB(+) and recC(+) gene product (exonuclease V). In some strains a previous dose of ultraviolet (UV) light followed by incubation renders the cells resistant to DNA degradation after gamma irradiation. We have shown this inhibition to take place for infecting T4 phage also. By using six strains of E. coli selected for mutations in the genes recA, exr (or lex), and uvrB, we have been able to show that the preliminary UV treatment produces no change in recA and exr cells for both endogenous DNA degradation and the degradation of infecting irradiated T4 phage DNA, i.e., inhibition was not detected in these strains. On the other hand, wild-type cells and strains carrying mutations of uvrB show inhibition in both types of experiments. Because the recA gene product and the exr(+) (lex(+)) gene product are necessary for the induction of prophage, it is possible that the phenomenon of inducible inhibition requires recA(+) and exr(+) presence. One interpretation of these results is that an inducible inhibitor may be controlled by the exr gene.

Carbon Radioisotopes↗