DNA Replication in Mammalian Cells Damaged by Mutagens
Rapid inhibition of the overall rate of DNA synthesis in each cell, as measured by incorporation of 3H-thymidine. This occurs to a similar extent in nearly all cell types.
Subsequent recovery of normal rates of DNA synthesis. This recovery occurs at very different rates in different cell types1–3, and is not solely dependent on the capability of the cell type to carry out excision-repair3.
Reduction in the size of DNA labelled with a pulse of radioactive thymidine shortly after irradiation. This is again very dependent on cell type (e.g. refs. 4–5). It could result from (a) blocking of the progression of the growing forks by damage in the parental DNA, (b) the production of gaps in the daughter strands in the region of the damage (or possibly elsewhere) without the progression of the forks being halted.
Subsequent increase in size of the initially small DNA labelled soon after irradiation. This implies that the hypothetical blocks are not permanent or that the gaps are sealed.
Recovery of the ability to synthesize normal-sized DNA as observed by pulse labelling with 3H-thymidine at later times after irradiation.
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- 9.R. Hand, Hum. Genet., 37., 55–64 (1977).Google Scholar
- 15.J. M. Clarkson and R. R. Hewitt, Biophys. J. 16, 1155–1164 (1976).Google Scholar
- 16.A. R. Lehmann, J. Mol. Biol. 66, 319–337 (1972).Google Scholar
- 17.M. R. James, M.Sc. Thesis, University of Queensland (1979).Google Scholar
- 20.J. J. Roberts, Advances Radiat. Biol. 7, 211–436 (1978).Google Scholar
- 24.A. R. Lehmann and L. Mayne. This volume.Google Scholar
- 27.W. K. Kaufmann, J. E.. Cleaver and R. B. Painter, Biochim. Biophys. Acta 608 (1980).Google Scholar
- 28.L. J. Tolmach and R. W. Jones, Radiation Res, 69, 117–133 (1977).Google Scholar