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K C Smith

Publications and source records attributed to K C Smith.

At least 163 records · Page 9Linked to original sources
PubMed1982

Effects of the ssb-1 and ssb-113 mutations on survival and DNA repair in UV-irradiated delta uvrB strains of Escherichia coli K-12.

The molecular defect in DNA repair caused by ssb mutations (single-strand binding protein) was studied by analyzing DNA synthesis and DNA double-strand break production in UV-irradiated Escherichia coli delta uvrB strains. The presence of the ssb-113 mutation produced a large inhibition of DNA synthesis and led to the formation of double-strand breaks, whereas the ssb-1 mutation produced much less inhibition of DNA synthesis and fewer double-strand breaks. We suggest that the single-strand binding protein plays an important role in the replication of damaged DNA, and that it functions by protecting single-stranded parental DNa opposite daughter-strand gaps from nuclease attack.

Cell Survival↗
PubMed1981

Effect of recB21, uvrD3, lexA101 and recF143 mutations on ultraviolet radiation sensitivity and genetic recombination in delta uvrB strains of Escherichia coli K-12.

The interaction of the recB21, uvrD3, lexA101, and recF143 mutations on UV radiation sensitization and genetic recombination was studied in isogenic strains containing all possible combinations of these mutations in a delta uvrB genetic background. The relative UV radiation sensitivities of the multiply mutant strains in the delta uvrB background were: recF recB lexA greater than recF recB uvrD lexA, recF recB uvrD greater than recA greater than recF uvrD lexA greater than recF recB, recF uvrD greater than recF lexA greater than recB uvrD lexA greater than recB uvrD greater than recB lexA, lexA uvrD greater than recB greater than lexA, uvrD greater than recF; three of these strains were more UV radiation sensitive than the uvrB recA strain. There was no correlation between the degree of radiation sensitivity and the degree of deficiency in genetic recombination. An analysis of the survival curves revealed that the recF mutation interacts synergistically with the recB, uvrD, and lexA mutations in UV radiation sensitization, while the recB, uvrD, and lexA mutations appear to interact additively with each other. We interpret these data to suggest that there are two major independent pathways for postreplication repair; one is dependent on the recF gene, and the other is dependent on the recB, uvrD, and lexA genes.

DNA Repair↗
PubMed1981

The effects of lexA101, recB21, recF143 and uvrD3 mutations on liquid-holding recovery in ultraviolet-irradiated Escherichia coli K12 recA56.

Using an Escherichia coli K12 recA strain, we have tested the effects of incorporating additional mutations affecting deoxyribonucleic acid (DNA) repair on ultraviolet-radiation sensitivity and on the expression of liquid-holding recovery (LHR). (This laboratory had previously shown that a mutation at uvrA, uvrB or uvrC blocked LHR in a recA strain.) In the recA56 background, an additional lexA101 mutation had no effect on UV-radiation sensitivity or LHR. The addition of a recB21 mutation to recA56 did not alter UV-radiation sensitivity, but greatly increased the rate of LHR. The recB gene product (exonuclease V) appears to act as a competitive inhibitor both of excision repair and of photoreactivation under liquid-holding (LH) conditions. The uvrD3 mutation increased the radiation sensitivity of a recA strain, and almost completely blocked LHR. The recA uvrD strain showed more DNA degradation and DNA double-strand breaks during LH than did the recA strain. The recF143 mutation increased both UV-radiation sensitivity and LHR in a recA strain, suggesting that the recF gene product may also function in recA-independent pathways of DNA repair.

DNA Repair↗
PubMed1981

Effect of the uvrD3 mutation on ultraviolet radiation-induced DNA-repair replication in Escherichia coli K12.

Ultraviolet-radiation-induced DNA-repair replication was measured in wild-type, polA1, uvrD3, and polA1 uvrD3 strains of Escherichia coli K12. A large stimulation of repair replication was observed in the uvrD3 strain, compared to the wild-type and polA1 strains. This enhanced repair replication was reduced in the polA1 uvrD3 strain. Therefore, uvrD3 mutation appears to affect the amount of repair replication performed by DNA polymerase I. In the polA1 strain, there also appears to be an effect of the uvrD3 mutation on the amount of repair replication performed by DNA polymerase III (and/or II). The enhanced repair replication observed for the uvrD3 strains appears to be in response to the enhanced DNA degradation observed for these strains.

DNA Repair↗
PubMed1981

Enhancement of viral RNA-induced interferon production of L cells treated with insulin and amphotericin B methyl ester.

A study was initiated to develop a more efficient method of producing high-titered L cell interferon. The induction of interferon by viral infectious RNA could be augmented by pretreating the cell cultures with insulin and infecting in the presence of Amphotericin B methyl ester (AmBME). L cells were treated for 24 hr with different concentrations of insulin and then challenged with MM virus RNA suspended in a balanced salt solution with and without AmBME. The fluids were collected 48 hr after infection and assayed for interferon activity. Interferon production was markedly increased in insulin-treated cultures and that the increase was dose-dependent.

Amphotericin B↗
PubMed1981

Much of spontaneous mutagenesis in Escherichia coli is due to error-prone DNA repair: implications for spontaneous carcinogenesis.

The role of DNA repair genes (uvrA, uvrB, uvrD, recA, recB, lexA, and umuC) in spontaneous mutation rate per bacterium per cell division (micro) was determined for the reversion of UAA (his-4 and trpE65), UAG (lacZ53), and frameshift (trpE9777) mutations, and for the occurrence of forward mutations to valine resistance. Rich growth medium enhanced micro in a wildtype strain but not in a uvrB5 strain. In minimal growth medium, the uvrA and uvrB strains had the largest micro (1.9-6.2-fold greater than that for isogenic wild-type strains, depending on the mutation assay). The uvrB strains carrying lexA, recA, umuC, or both the uvrD and rec B mutations (in combination), i.e., mutations that inhibit error-prone DNA repair, had the lowest micro values (approximately 10-fold less than the uvrB strain). Teh recA and lexA mutations also reduced micro (by approximately 2-fold) in uvr+ strains. The genetic control of the error prone repair-dependent sector of spontaneous mutagenesis was shown to be qualitatively similar to the genetic control for u.v. radiation mutagenesis. The umuC mutation, which drastically reduced spontaneous mutagensis, had no effect on genetic recombination. It is proposed that the low level of spontaneous mutagenesis observed in the recA, lexA, umuC, and the uvrD recB strains is due to errors made during DNA replication, while the enhanced level of spontaneous mutagenesis observed in the wild type, and especially in the uvrA and uvrB strains, is due to excisable lesions that are produced in the DNA by normal metabolic reactions, and that such unexcised lesions induce mutations via error-prone DNA repair. These results are discussed in terms of their relevance to spontaneous carcinogenesis.

Culture Media↗
PubMed1981

Photobiology and photomedicine: the future is bright.

Important events since 1966 that have helped to advance photobiology in general and photomedicine in particular are reviewed. More formal courses on photobiology are needed so that future photobiologists and photodermatologists will not have to be self-taught about the properties and action of light. The effectiveness of current phototherapies and their future improvement are discussed. Some of the areas of photobiology what will impact on photomedicine in the years to come are ultraviolet (UV) radiation effects on the immune system, the light activation of enzymes as a potential new type of photothoerapy, the development of new photosensitizers for phototherapy, the effects of near-UV radiation on cellular membranes, and, of course, the role of DNA damage and repair in mutagenesis and carcinogenesis. The future is bright for photomedicine.

Carcinogens↗
PubMed1980

Cerenkov ultraviolet radiation (137Cs gamma-rays) and direct excitation (137Cs gamma-rays and 50 kVp X-rays) produce photoreactivable damage in Escherichia coli.

The mechanism of formation of photoreactivable damage in deoxyribonucleic acid (DNA) by ionizing radiation in a dark repair deficient strain of Escherichia coli (uvrA recA) has been investigated. By altering the ratio of damage produced directly (by ionization) to that formed indirectly (by Cerenkov ultraviolet (U.V.) radiation by 137Cs gamma-rays, it has been demonstrated that the major portion of the photoreactivable damage is produced by Cerenkov U.V. radiation. The amount of photoreactivable damage produced by 50 kVp X-rays, which cannot generate Cerenkov radiation, is similar to that component of photoreactivable damage produced by 137Cs gamma-rays that is not attributed to Cerenkov radiation. It is suggested that the second mechanism of formation of photoreactivable damage in DNA by ionizing radiation is the direct excitation of DNA. The possible role of Cerenkov U.V. radiation in ionizing radiation mutagenesis is discussed.

Animals↗
PubMed1980

Involvement of genes uvrD and recB in separate mutagenic deoxyribonucleic acid repair pathways in Escherichia coli K-12 uvrB5 and B/r uvrA155.

We compared the ultraviolet radiation-induced reversion of nonsense (lacZ53) and missense (leuB19) mutations in uvrB5, uvrB5 uvrD3, uvrB5 recB21, and uvrB5 uvrD3 recB21 strains of Escherichia coli K-12. Nonsense (trpE65) reversion was also compared in similar derivatives of E. coli B/r uvrA155. The uvrD mutation reduced mutagenesis in very case, but had its main effect in cells ultraviolet irradiated with low fluences (< 0.6 J m-2). The effect of the recB mutation varied; it decreased Leu and Trp reversion, but had little effect on Lac reversion. The effect of the uvrD recB combination was a gross reduction in mutagenesis. Only in the case of Lac reversion was appreciable mutagenesis detected (at fluences > 0.3 J m-2). These results indicate that separate uvrD- and recB-controlled pathways exist for ultraviolet radiation mutagenesis.

DNA Repair↗
PubMed1979

Radioprotection by DMSO of mammalian cells exposed to X-rays and to heavy charged-particle beams.

Populations of G1-phase Chinese hamster cells in stirred suspensions containing various concentrations of DMSO were irradiated with 250 kV X-rays or various heavy charged-particle beams. Chemical radioprotection of cell inactivation was observed for all LET values studied. When cell survival data were resolved into linear and quadratic components, the extent and concentration dependence of DMSO protection were found to be different for the two mechanisms. The chemical kinetics of radioprotection for single-events were similar for LET values up to those which gave the maximum RBE. DMSO protected to a lesser extent against energetic argon ions at an median LET of approximately 220 keV/micron. These data could indicate the contribution of indirect action by hydroxyl radicals and hydrogen atoms to cell inactivation by single-hit and double-hit mechanisms for various radiation qualities. The decrease in RBE observed at very high LET may result, in part, from reduced yields of water radicals at 10(-9)-10(-8) s resulting from radical recombination mechanisms within the charged particle tracks.

Animals↗
PubMed1979

Multiple, independent components of ultraviolet radiation mutagenesis in Escherichia coli K-12 uvrB5.

Reversion systems involving the lacZ53(amber) and leuB19)missense) mutations were developed to study the mutant frequency response of Escherichia coli K-12 uvrB5 (SR250) to ultraviolet radiation (254 nm). A one-hit mutant frequency response was discernible at ultraviolet radiation fluences below approximately 0.5 J m-2. At higher fluences the overall mutant frequency response could be resolved into one-hit and two-hit components. A new interpretation of the published data on E. coli K-12 indicates that SR250 is not unique in this respect. In addition, the Lac reversion system showed enhanced mutagenesis after ultraviolet radiation fluences of approximately 1 to 3 J m-2, whereas the Leu reversion system did not. We conclude that the complex ultraviolet radiation mutant frequency response curves for E. coli K-12 uvrB5 were the result of three independent mutagenic processes for Lac reversion and two for Leu reversion.

Escherichia coli↗
PubMed1978

The involvement of DNA polymerase I in the postreplication repair of ultraviolet radiation-induced damage in Escherichia coli K-12.

A deficiency in DNA polymerase I increased the ultraviolet (UV) radiation sensitivity of a uvrA strain of Escherichia coli K-12 when plated on minimal growth medium. The slope of the survival curve for the uvrA polA strain was 2.0-times greater than that for the uvrA strain. The fluence-dependent yield of unrepaired deoxyribonucleic acid (DNA) parental-strand breaks following UV irradiation and incubation in minimal growth medium was similar in both strains. However, the fluence-dependent yield of unrepaired DNA daughter-strand gaps observed following UV irradiation was 1.8-fold greater in the uvrA polA strain than in the uvrA strain. These results suggest that DNA polymerase I is involved in the filling of at least some daughter-strand gaps during postreplication repair. Also, the uvrA polA strain was sensitized by a post-UV treatment with chloramphenicol (CAP) to a similar extent as was the uvrA strain, indicating that DNA polymerase I is not involved in the CAP-inhibitable pathway of postreplication repair.

DNA Polymerase I↗