Abstract
Repair rates of both pyrimidine-pyrimidone (6-4) photoproducts and cyclobutane pyrimidine dimers have been measured in the UV-sensitive mutants of Saccharomyces cerevisiae: rad1 to rad12 and rad14 to rad24. A dot blot immunoassay for UV photoproducts was used which measures lesions in the genome as a whole and which distinguishes 6-4 photoproducts from cyclobutane dimers. The principal findings are: (1) Wild-type yeast cells, like normal mammalian cells, repair 6-4 photoproducts more rapidly than cyclobutane domers. (2) All mutants that are defective in repair are defective in repair of both lesions. (3) The most sensitive alleles of rad1, rad2, rad3, rad4 and rad10 show no repair of either lesion. (4) Leaky alleles of rad1, rad3 and rad4 show a very marked difference in repair rates of the two lesions, rather like the human XPA revertant cell line XP129 and the Chinese hamster mutants UV61 and V-H1. (5) No mutant repairs cyclobutane dimers more rapidly than 6-4 photoproducts.
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