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TIME COURSE OF PHOTOREACTIVATION OF UV‐INDUCED CHROMOSOMAL ABERRATIONS AND LETHAL DAMAGE IN INTERPHASE XENOPUS CELLS

Abstract— Sets of G1, S, and G2 phase Xenopus cells were exposed to 15.0 Jm−2 UV and their ability to photoreactivate the induced cell killing (loss of colony forming ability) and chromosomal aberrations was determined as a function of time following the UV exposure. Most of the lesions induced in G1 cells that lead to cell death were converted to a non‐photoreactivable state before the cells entered the S phase, while lesions leading to chromosomal aberrations were converted to a non‐photoreactivable state as the cells entered the S phase. In S phase cells the UV‐induced lesions leading to aberrations appeared to be converted to a non‐photoreactivable state at a much faster rate than those leading to cell death. A significant fraction of the lesions induced in G2 cells, that lead to cell death, were converted to a non‐photoreactivable state before the progeny of the exposed cells reached the next succeeding S phase. Few, if any, lesions were induced in G2 cells that were expressed as aberrations at the first mitosis following exposure. Some of the lesions induced in the G2 cells led to aberrations that were observable in the progeny that progressed to the second mitosis following exposure. These lesions were converted to a non‐photoreactivable state as the progeny of the exposed G2 cells progressed through the first S phase following exposure. These results suggest that the intracellular mechanism which expresses photoreactivable UV‐induced lesions as cell death is not identical to the mechanism which expresses such lesions as chromosomal aberrations, and the two mechanisms operate with different efficiencies in different phases of the cell cycle.