Abstract
The role of the pyrimidine dimer in cell killing, DNA synthesis and repair has been studied by utilizing the light-requiring DNA-repair mechanism of photo-reactivation in UV-irradiated chicken-embryo fibroblasts. Survival, as measured by colony-forming ability at 41 degrees C, is increased in cells left in the light. The initial inhibition of DNA synthesis by UV is much less in light-treated cells, and levels reach that of unirradiated controls much faster than when the cells are left in the dark. The number of endonuclease-sensitive sites (dimers) measured by an assay with a crude extract from M. luteus, rapidly decreases as the cells are allowed to photoreactivate. However, in the dark, significant amounts of repair also occur, but at a much lower rate and with a lag phase of several dark- and light-treated cells, confirming the finding that some amount of excision repair occurs that is light-independent. When survival is examined as a function of the number of dimers present, the dimers, not the non-dimer products, appear to be responsible for cell killing. In this study, the removal of dimers in vivo by photoreactivation has made it possible to demonstrate directly that dimers are primarily responsible for the deleterious effects of UV on DNA synthesis and survival.
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