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Updated: Aug 10, 2026
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Measuring DNA Damage and Repair in Mouse Splenocytes After Chronic In Vivo Exposure to Very Low Doses of Beta- and Gamma-Radiation
Published on: July 3, 2015
DNA synthesis in irradiated mammalian cells
1Laboratory of Radiobiology and Environmental Health, University of California, San Francisco 94143.
Journal of Cell Science. Supplement
|January 1, 1987
Summary
DNA damage in S phase mammalian cells inhibits DNA replicon initiation. Ultraviolet light (UV) triggers this inhibition via a rare DNA lesion, not single-strand breaks during repair.
Area of Science:
- Molecular Biology
- Cell Biology
- DNA Repair Mechanisms
Background:
- DNA damage in S phase mammalian cells triggers an immediate response: inhibition of DNA replicon initiation.
- Ionizing radiation induces single-strand breaks, which block initiation in adjacent replicons.
- Ultraviolet (UV) light also inhibits replicon initiation, but the specific trigger is less understood.
Purpose of the Study:
- To investigate the specific DNA lesion responsible for UV-induced inhibition of replicon initiation.
- To differentiate the mechanism of UV-induced inhibition from that caused by ionizing radiation.
- To explore the role of DNA repair pathways in UV-induced replicon inhibition.
Main Methods:
- Comparison of UV-induced replicon initiation inhibition in Chinese hamster cells with varying pyrimidine dimer excision capabilities.
- Analysis of UV sensitivity in human ataxia telangiectasia cells concerning replicon initiation inhibition.
- Correlation of DNA damage levels (pyrimidine dimers, single-strand breaks) with the extent of replicon initiation inhibition.
Main Results:
- UV-induced inhibition of replicon initiation is similar in cells proficient and deficient in pyrimidine dimer excision.
- Single-strand breaks formed during excision repair are not the primary stimulus for UV-induced inhibition.
- Human ataxia telangiectasia cells show reduced sensitivity to UV-induced replicon initiation inhibition.
Conclusions:
- A DNA lesion other than pyrimidine dimers or single-strand breaks formed during repair likely triggers UV-induced replicon initiation inhibition.
- The findings suggest a distinct mechanism for UV-induced DNA damage response compared to ionizing radiation.
- Further research is needed to identify the specific rare lesion responsible for UV-induced inhibition.
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