DNA repair after ultraviolet irradiation of ICR 2A frog cells. Pyrimidine dimers are long acting blocks to nascent DNA synthesis

Rosenstein, Barry S.; Setlow, R. B.

doi:10.1016/s0006-3495(80)85050-8

Cited by 43 publications

(14 citation statements)

References 19 publications

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“…2). This is similar to results reported by Rosenstein and Setlow (1980) who found that when ICR 2A cells were exposed to PRL after UV irradiation, the size of the nascent DNA synthesized was nearly the same as in unirradiated cells and there was an increase in total DNA synthesis, although there was still a depression in thymidine incorporation. The photoreactivable sector for ICR 2A cells for DNA synthesis was 0.58 and for survival was 0.69.…”

Section: Resultssupporting

confidence: 91%

“…In contrast, when wildtype AA8 Chinese hamster ovary (CHO) cells were exposed to 6.5 Jim', incorporation dropped slowly for the first 1-2 h after exposure, and then recovered with the rate of thymidine incorporation reaching control levels 5 h after exposure (Griffiths and Ling, 1984). The IAL-PID2 results are similar to those with frog ICR 2A cells, where the amount of label incorporated into DNA remained depressed several days after exposure to 7.5 Jim2 (Rosenstein and Setlow, 1980). Exposure to PRL decreased the extent of this depression in insect cells (Fig.…”

Section: Resultsmentioning

confidence: 75%

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Effects of Ultraviolet Light on Thymidine Incorporation and Dna Chain Elongation in Photoreactivable Insect Cells

1989

Photochem & Photobiology

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An insect cell line, IAL-PID2, was exposed to UV and analyzed for its ability to incorporate [3H]-thymidine and to elongate replicon-sized DNA fragments. After exposure to 5 or 10 J/m2 UV, the cells exhibited a rapid and prolonged depression in the rate of thymidine incorporation. Photoreactivation reduced this depression but did not entirely reverse it. For exposures of 5 J/m2 or above, full recovery did not occur until 18 h after exposure. The blockage of fork progression after UV exposure was fluence-dependent, with replication segments after exposure to 20 J/m2 being shorter than those observed after exposure to 10 J/m2. Immediately after exposure to either 10 or 20 J/m2, photoreactivation reversed blockage of fork progression, indicating that the (5-6) cyclobutyl pyrimidine dimer is responsible for blockage. This also indicates that blockage of fork progression may not be the only factor responsible for the prolonged depression seen in thymidine incorporation. Three hours after exposure to either 10 or 20 J/m2, replication segments were still significantly shorter than control segments. Photoreactivation completely reversed blockage after exposure to 10 J/m2, but did not completely reverse blockage after exposure to 20 J/m2, indicating that at such fluences, other lesions may play a role in UV-induced blockage of fork progression.

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Section: Resultssupporting

confidence: 91%

Section: Resultsmentioning

confidence: 75%

Effects of Ultraviolet Light on Thymidine Incorporation and Dna Chain Elongation in Photoreactivable Insect Cells

1989

Photochem & Photobiology

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“…Studies of the biological effects of cyclobutane pyrimidine dimers, the predominant photoproducts induced in D N A by ultraviolet-C (UV-C) irradiation (240-290 nm), have been facilitated by the use of enzymes that specifically recognize this class of damage. In situ repair of cyclobutane dimers by enzymatic photoreactivation was observed to reduce both cell killing and mutation induction in various nonmammalian eukaryotes ( Lehmann and Stevens, 1975;Rosenstein and Setlow, 1980). In mammalian cells, recent host-cell reactivation (HCR)?…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Transient Gene Expression in Chinese, Hamster Ovary Cells by Triplet‐sensitized Uv‐b Irradiation of Transfected Dna

Mitchell

Adair

Nairn

1989

Photochem & Photobiology

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The biological effectiveness of thymine-thymine cyclobutane dimers specifically induced by photosensitized ultraviolet-B irradiation was analyzed by host-cell reactivation of triplet-sensitized, UV-B irradiated plasmid pRSV beta gal DNA transfected into normal and repair-deficient Chinese hamster ovary cells. For comparison, pRSV beta gal DNA was also UV-C irradiated and transfected into the same cell lines. Ultraviolet endonuclease-sensitive site induction was determined after UV-C irradiation or acetophenone-sensitized UV-B irradiation of plasmid pRSV beta gal DNA. These data were used to calculate the number of cyclobutane pyrimidine dimers required to inactivate expression of the lacZ reporter gene in each irradiation condition. Transfection with UV-C-irradiated plasmid DNA resulted in a significantly greater reduction of reporter gene expression than did transfection with acetophenone-sensitized UV-B-irradiated pRSV beta gal DNA at equivalent induction of enzyme-sensitive sites. Since only a fraction of the inhibition could be accounted for by noncyclobutane dimer photoproducts, these results suggest that cytosine-containing pyrimidine cyclobutane dimers may be more effective than thymine-thymine dimers in inhibiting transient gene expression as measured in such host-cell reactivation experiments in mammalian cells.

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“…Secondly these cells are highly proficient in the enzymatic photoreactivation of pyrimidine dimers (Freed et al . 1979, Rosenstein andSetlow 1980) . It is therefore possible to induce a population of DNA damage that is subsequently virtually free of pyrimidine dimers through exposure of these cells to sunlamp UV > 315 nm plus photoreactivating light (PRL) .…”

Section: Introductionmentioning

confidence: 99%

“…1985 . Approximately 80 per cent of the relatively small yield of dimers can then be specifically removed by treatment with PRL (Rosenstein and Setlow 1980) .…”

Section: Introductionmentioning

confidence: 99%

Inhibition and Recovery of Semiconservative DNA Synthesis in Normal and Solar UV Sensitive ICR 2A Frog Cell Lines Following the Induction of Non-dimer DNA Damage by Sunlamp UV > 315 nm

Rosenstein

1989

International Journal of Radiation Biology

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Cultures of the solar UV-sensitive cell lines, DRP 36 and DRP 153, and of the parental ICR 2A cell line, were exposed to 150 kJ/m2 of sunlamp UV greater than 315 nm plus photoreactivating light. This treatment resulted in the induction primarily of non-dimer DNA damage. Following either a 0, 3, 6, 12 or 24 h incubation, the cultures were pulse-labelled with [3H]thymidine, and the synthesis of different size classes of replicon intermediates measured using the alkaline step elution assay. For all three cell lines tested, an immediate depression of low molecular weight DNA synthesis was observed. This was followed by an inhibition of all size classes of replicon intermediates. Within 12 h following irradiation, recovery of DNA synthesis was observed, which was generally most apparent for low molecular weight DNA. The ICR 2A cells exhibited a nearly full recovery in all size classes of DNA synthesized by 24 h. However, a much smaller recovery of DNA synthesis was detected for the DRP 36 and DRP 153 cultures. This continued inhibition was primarily in the synthesis of full replicon size DNA, and was most pronounced for the DRP 36 cells. Hence, it appears that replicon chain elongation continues to be inhibited in these solar UV-sensitive cell lines long after irradiation.

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DNA repair after ultraviolet irradiation of ICR 2A frog cells. Pyrimidine dimers are long acting blocks to nascent DNA synthesis

Cited by 43 publications

References 19 publications

Effects of Ultraviolet Light on Thymidine Incorporation and Dna Chain Elongation in Photoreactivable Insect Cells

Effects of Ultraviolet Light on Thymidine Incorporation and Dna Chain Elongation in Photoreactivable Insect Cells

Inhibition of Transient Gene Expression in Chinese, Hamster Ovary Cells by Triplet‐sensitized Uv‐b Irradiation of Transfected Dna

Inhibition and Recovery of Semiconservative DNA Synthesis in Normal and Solar UV Sensitive ICR 2A Frog Cell Lines Following the Induction of Non-dimer DNA Damage by Sunlamp UV > 315 nm

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