[en] A partial release of K-specific restriction of phage lambda grown in Escherichia coli C was observed when E. coli K strains AB1157 (having wild-type repair of uv-produced DNA damage) and AB1886 (uvrA) were irradiated with uv light before infection. The effect occurred in AB1886 at lower uv fluences than it did in AB1157. Little or no release of restriction was observed when AB2463 (recA) or AB2494 (lex-1) was used. Such release of restriction appears to be another of the uv-induced phenomena associated with ''SOS'' repair

[en] Caffeine is shown to block repair of ultraviolet-irradiated adenovirus 2 when the irradiated virus infects normal human fibroblasts from a xeroderma pigmentosum (XP) variant. Such blockage is not observed when the irradiated virus infects XP fibroblasts belonging to XP complementation group A. Thus normal and XP variant cells have a caffeine-sensitive repair process. This may be either excision or an excision dependent repair process because fibroblasts belonging to XP complementation group A are believed to lack the excision repair process

[en] Among the progeny produced by UV-irradiated adenovirus 5ts2 when infecting either A498 (human kidney tumor) or CRL1187 (normal human fibroblast) strains at 32⁰C were a certain number (UV-fluence dependent) of revertants able to grow at 39⁰C. Within experimental error, the induced reversion frequency was independent of whether or not the cells received UV (5 J/m²) 20 h prior to infection, indicating that induced error-prone repair was not observed in these experiments. (author)

No abstract available

[en] Over a period of 5 years, 29 experiments were performed in which survival curves of UV-irradiated adenovirus were determined using fibroblast strains from 10 normal persons and from 7 persons having Cockayne's syndrome. In all of these, the survival of UV-irradiated adenovirus 5 was less when assayed using monolayers of fibroblasts from Cockayne's syndrome patients than from normal persons. Survival curves using normal fibroblasts were, within error, straight lines on a log survival vs. linear fluence plot. Survival curves obtained using Cockayne's syndrome fibroblasts showed 2 components: an initial sensitive component, reflecting the behavior of approx. 75% of the infected cells, followed by a component having normal sensitivity. In the 28 experiments that were considered reliable, 58 curves were done using Cockayne's fibroblasts, 41 using normal human fibroblasts. Although experimental variation was encountered, there was no individual case in which sensitivity as measured using Cockayne's was equal to (or less than) the sensitivity measured using normal fibroblasts. (author)

[en] Inhibitors of (a) DNA topoisomerases (novobiocin and nalidixic acid) and of (b) eukaryotic DNA polymerases α (cytosine arabinoside) and β (dideoxythymidine) blocked different steps of DNA repair, demonstrated by the effects of the inhibitors on the relaxation of supercoiled DNA nucleoids following treatment of human cell cultures with ultraviolet light (1-3 J/m²) or MNNG (5 or 20 μM) and the subsequent restoration of the supercoiled nucleoids during repair incubation. Inhibition of repair by novobiocin was partially reversible; upon its removal from the culture medium, the nucleoid DNA of repairing cells became relaxed. The DNA polymerase inhibitors allowed the initial relaxation of DNA after treatment of the cells with ultraviolet or MNNG but delayed the regeneration of rapidly-sedimenting (supercoiled) nucleoid DNA for 2-4 h. Dideoxythymidine (1 mM) was more effective than cytosine arabinoside (1 μM) in producing this delay, but neither inhibitor by itself blocked repair permanently. Incubation of ultraviolet-irradiated cells with 1 μM cytosine arabinoside plus 1 mM dideoxythymidine blocked the completion of repair for 24 h, whereas incubation with 10 μM cytosine arabinoside or 5 mM dideoxythymidine produced only temporary repair delays of 2-4 h. Thus, it is likely that the two DNA polymerase inhibitors act upon separate targets and that both targets are involved in repair. (Auth.)

[en] Adenovirus-2 is damaged by treatment with psoralen plus near-ultraviolet (UV) light as shown by reduced ability to infect human fibroblasts. The apparent sensitivity of the virus to this treatment depended upon the strain of cells used. The virus was 3-4 times more sensitive to the treatment when infecting xeroderma pigmentosum (XP complementation groups A or D) fibroblasts than when infecting normal fibroblasts. DNA extracted from virus preparations that had undergone such treatment was analyzed for treatment-induced crosslinks by gel electrophoresis and sedimentation in alkaline sucrose gradients. The fraction of adenovirus DNA molecules remaining non-crosslinked after treatment was found to correlate with the survival of the virus in normal fibroblasts. This result showed that the psoralen plus near-UV treatment gave rise to non-crosslink lesions (presumably psoralen-DNA mono-adducts), that were repairable by normal but not by XP fibroblasts, and suggested the possibility that normal fibroblasts cannot repair this type of crosslink in the DNA of an infecting adenovirion

[en] The effects of hydroxyurea on plaque formation by UV-irradiated and MNNG-treated adenovirus 5 were investigated. Hydroxyurea blocked the recovery of UV-irradiated viruses in all cases studied, but the effect was less when fibroblasts from a patient with xeroderma pigmentosum were used. This fact supports the notion that hydroxyurea blocks excision repair of UV-produced damage. The recovery of MNNG-treated viruses was not blocked by hydroxyurea when viruses were used to infect normal human fibroblasts, but was blocked if the cell strain used as viral host were deficient in repair of O⁶-methylguanine. To account for these data, we propose that hydroxyurea blocks repair in which DNA polymerases play a role, but does not block repair in which DNA polymerases are not required. (orig.)

[en] Studies of physically or chemically induced mutability (or revertibility) of viruses have aided the understanding of repair processes both in bacteria and in mammalian cells. Others first showed that UV-irradiated lambda phage underwent far more mutagenesis when infecting UV-irradiated E. coli host cells than when infecting non-irradiated hosts. This finding was indispensable to the concept of S.O.S. or error-prone repair and was, at least in part, responsible for the current interest in the biological and biochemical functions of the E. coli recA gene product and the regulatory system of which it is a part. Work along similar lines in mammalian cells, represents the extension of such research to mammalian cells. Systematic studies of UV-produced mutagenesis or reversion among nuclear-replicating double-stranded DNA mammalian viruses have been reported in SV40, their herpes viruses and adenoviruses. In this chapter the authors describe their methods for adenovirus 5

[en] Effects of the introduction of the Simian virus 40 T-antigen (SV40 T-Ag) gene to cultured human cells were examined in relation to radiosensitivity. Two relatively radioresistant tumor cell lines (T98 and G361) became significantly radiosensitive after the introduction of SV40 T-Ag, whereas radiosensitive tumor cell lines did not show a change in radiosensitivity. In contrast, a human fibroblast cell line became radioresistant after SV40 T-Ag introduction. T98 cells which have a mutation at codon 237 in the p53 gene were unable to form a complex between p53 protein and SV40 T-Ag, whereas G361, which became radiosensitive by a SV40 T-Ag introduction, formed the complex. This indicates that the status of p53 is independent of the change in radiosensitivity in the cell lines studied. (author)