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Biomedical subjects

K C Smith

Publications and source records attributed to K C Smith.

At least 199 records · Page 11Linked to original sources
PubMed1976

Genetic control of multiple pathways of post-replicational repair in uvrB strains of Escherichia coli K-12.

The effect of the recA, uvrD, exrA, and recB mutations and of post-irradiation treatment with chloramphenicol on the survival and post-replication repair after ultraviolet irradiation of uvrB strains of Escherichia coli K-12 was examined. Each of these mutations or treatments was found to decrease survival and the extent of repair. The interactions of the inhibitory effects of the uvrD, exaA, and recB mutations and chloramphenicol treatment were determined by examining the survival and repair characteristics of the several multiple mutants. The survival results suggest that the post-replication repair process in uvrB strains may be subdivided into at least five different branches. These include three branches that are blocked by the exrA, recB, or uvrD mutation, a fourth branch that is blocked by any of these mutations and is also sensitive to chloramphenicol treatment, and at least one additional branch that is not sensitive to either of these mutations or to chloramphenicol treatment. The extent of post-replicational repair observed with each of the strains is in general agreement with the pathways postulated on the basis of the survival data, although there are several apparent exceptions to this correlation.

Chloramphenicol↗
PubMed1976

Role of deoxyribonucleic acid polymerase III in the repair of single-strand breaks produced in Escherichia coli deoxyribonucleic acid by gamma radiation.

Cell survival, deoxyribonucleic acid (DNA) degradation, and the repair of DNA single-strand breaks were measured for Escherichia coli K-12 pol+, polA1, polC1026(ts), and polA1 polC1026(ts) cells after 137Cs gamma irradiation. The results indicate that DNA polymerase III is required for growth medium-dependent (type III) repair in polA+ or polA cells. In pol+ or polC cells, DNA polymerase I performs type II repair efficiently. The relative deficiencies of each of these strains in DNA repair generally correlate with their relative sensitivities to cell killing and with the extent of DNA degradation observed.

DNA Nucleotidyltransferases↗
PubMed1976

Effects of actinomycin D on cell cycle kinetics and the DNA of Chinese hamster and mouse mammary tumor cells cultivated in vitro.

Actinomycin D produces changes in the cell cycle kinetics of Chinese hamster (HA1) and mouse mammary tumor cells (EMT6) cultivated in vitro. There was a reduced rate of progression of the cells through S phase and a G2 arrest, the duration and degree of which were drug dose dependent. The lethal effects of the drug on the two cell lines were comparable. At the molecular level, DNA single-strand breaks (true breaks and/or alkali-labile bonds) appear initially. After drug removal, the extent of disappearance of these DNA strand breaks was drug dose dependent. Similar results were obtained for the two cell lines. However, at the lower drug concentration (0.1 mug/ml), although the DNA strand breaks appeared to disappear after drug free incubation, about 60% of this cell population was not viable.

Animals↗
PubMed1975

Dependence upon growth medium and the polA, polC, recA, recB, recC, and exrA genes of separate branches of the uvr Gene-dependent excision-repair process in Escherichia coli K12 cells.

The repair of single-strand breaks which arise in DNA during the uvr gene-dependent excision-repair process was examined in certain radiation-sensitive strains of Escherichia coli K12. The results suggest that the excision-repair process may be divided into two branches, one which is dependent on the presence of growth medium and also the rec+ exr+ genotype, and a second which can occur in buffer (growth medium independent) and is largely dependent on DNA polymerase I. DNA polymerase III appears to be involved in the growth-medium-dependent branch of excision repair, and also in the residual growth-medium-independent repair which occurs in polA1 cells. Chloramphenicol, dinitrophenol, and impurities present in some brands of agar all appear to inhibit the growth-medium-dependent branch of excision-repair. The similarities of the two branches of excision-repair to two known pathways for the repair of X-ray-induced DNA chain breaks are discussed.

Chloramphenicol↗
PubMed1975

Enzymatic induction of DNA double-strand breaks in gamma-irradiated Escherichia coli K-12.

The polA1 mutation increases the sensitivity of E. coli K-12 by killing by gamma-irradiation in air by a factor of 2.9 and increases the yield of DNA double-strand breaks by a factor of 2.5. These additional DNA double-strand breaks appear to be due to the action of nucleases in the polA1 strain rather than to the rejoining of radiation-induced double-strand breaks in the pol+ strain. This conclusion is based upon the observation that gamma-irradiation at 3 degrees did not affect the yield of DNA double-strand breaks in the pol+ strain, but decreased the yield in the polA1 strain by a factor of 2.2. Irradiation of the polA1 strain at 3 degrees followed by incubation at 3 degrees for 20 min before plating resulted in approximately a 1.5-fold increase in the D0. The yield of DNA double-strand breaks was reduced by a factor of 1.5. The pol+ strain, however, did not show the protective effect of the low temperature incubation upon either survival or DNA double-strand breakage. We suggest that the increased yield of DNA double-strand breaks in the polA1 strain may be the result of the unsuccessful exision repair of ionizing radiation-induced DNA base damage.

Cell Survival↗
PubMed1975

R.b.e. of 50 k Vp x-rays and 660 keV gamma-rays (137 Cs) with respect to the production of DNA damage, repair and cell-killing in Escherichia coli K-12.

We have compared the efficiency of cell-killing, DNA single-strand breakage and double-strand breakage in an Escherichia coli K-12 wild-type strain after irradiation with soft X-rays (50kVp) and hard gamma-rays (600 keV) under aerobic conditions. Irradiation with 50 kVP x-rays resulted in 1.47 times more cell killing than was observed with 137Cs gamma-rays based on a comparison of D0 values evaluated from the survival curves. DNA sedimentation studies showed that, although 50 kVp X-rays were 1-93 times more effective than 137Cs gamma-rays in producing DNA double-strand breaks, there was no sigificant difference between the two qualities of radiation with respect to the initial number of single-strand breaks produced. When the cells were irradiated and allowed to repair maximally in minimal medium, 1-57 times more unrepaired DNA single-strand breaks remained per krad after irradiation with 50 kVp X-rays than with 137Cs gamma-rays. The increased yield of DNA double-strand breaks resulting from 50 kVp X-radiation may account for most of these additional unrepaired single-strand breaks, since single- and double-strand breaks are indistinguishable on alkaline sucrose gradients. These results suggest that the greater r.b.e. of 50 kVp X-rays may be related to an increased effectiveness for producing DNA double-strand breaks compared with the higher energy 137Cs gamma-rays.

Cell Survival↗
PubMed1975

Enzymatic production of deoxyribonucleic acid double-strand breaks after ultraviolet irradiation of Escherichia coli K-12.

We have observed the enzymatic production of deoxyribonucleic acid (DNA) doublestrand breaks in Escherichia coli K12 after ultraviolet irradiation. Doublestrand breaks appeared in wild-type, polA1, recB21, recA, and exrA strains after incubation in minimal medium. THE UVRA6 strain showed no evidence of double-strand breakage under the same conditions. Our data suggest that uvr+ cells, which are proficient in the incision step of excision repair, accumulate double-strand breaks in their DNA as a result of the excision repair process, i.e., arising from closely matched incisions, excision gaps, or incisions and gaps on opposite strands of the DNA twin helix. Furthermore, strains deficient in excision repair subsequent to the incision step (i.e., polA, rec, exrA) showed more double-strand breaks than the wild type strain. The results raise the possibility that a significant fraction of the lethal events in ultraviolet-irradiated, repair-proficient (uvr+) cell may be enzymatically-induced DNA double-strand breaks.

Centrifugation, Density Gradient↗