The object of this research is to determine the role of thymine dimers, as opposed to other UV-induced lesions in DNA, in reducing the rate of DNA replication, cell killing and mutation induction. The importance of different DNA repair mechanisms for cellular recovery and their cell cycle dependence will be considered by comparing the response of Chinese hamster ovary cells, which are unable to excise thymine dimers, with the response of HeLa cells. Sensitivity to UV-irradiation (and other mutagens) is greatest in early S phase and this may be a consequence of the replication of damaged DNA. It is possible then, that if HeLa cells are held in G1 phase, such that thymine dimers are removed prior to S phase, the subsequent rate of DNA replication and survival would be increased. Mutation induction could then be estimated (as resistance to 6-thioguanine) in order to determine whether such repair mechanisms are error-prone. The fraction of thymine dimers/total DNA damage can also be varied by either incorporating bromouracil into the DNA, or by using a different wavelength of UV light (e.g., 313 nm). The effects of other types of DNA damage, and the capacity of each cell line for their repair, can then be determined. Thymine dimer induction and repair is estimated using a dimer-specific endonuclease and assaying molecular weight changes on alkaline sucrose gradients. Molecular weight determinations are also used to estimate single-strand breaks and alkaline-labile bands, the primary lesions following UV-irradiation of bromouracil-substituted DNA.