We have used a non-replicating recombinant adenovirus, Ad5MCMVlacZ, which expresses the β-galactosidase reporter gene, to examine both constitutive and inducible repair of UV-damaged DNA in repair proficient CHO-AA8 Chinese hamster ovary cells and in mutant CHO-UV61 cells which are deficient in the transcription-coupled repair (TCR) pathway of nucleotide excision repair. Host cell reactivation (HCR) of β-galactosidase activity for UV-irradiated Ad5MCMVlacZ was significantly reduced in non-irradiated CHO-UV61 cells compared to that in non-irradiated CHO-AA8 cells suggesting that repair in the transcribed strand of the UV-damaged reporter gene in untreated cells utilizes TCR. Prior UV-irradiation of cells with low UV fluences resulted in a transient enhancement of HCR for expression of the UV-damaged reporter gene in CHO-AA8 cells but not in TCR deficient CHO-UV61 cells. These results suggest the presence of an inducible DNA pathway in CHO cells that results from an enhancement of TCR or a mechanism that involves the TCR pathway.

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