ANALYSIS OF REPAIR OF CYCLOBUTANE PYRIMIDINE DIMERS AND PYRIMIDINE-6-4-PYRIMIDONE PHOTOPRODUCTS IN TRANSCRIPTIONALLY ACTIVE AND INACTIVE GENES IN CHINESE-HAMSTER CELLS

Irradiation of cells with short wave ultraviolet light (W-C) induces b oth cyclobutane pyrimidine dimers (CPD) as well as pyrimidine 6-4 pyri midone photoproducts (6-4 PP). We have focused on the removal of both types of DNA photolesions from the transcriptionally active adenine ph osphoribosyltransferase (APRT) and hypoxanthine-guanine phosphoribosyl transferase (HPRT) genes and the inactive c-mos gene, Induction levels of both CPD and 6-4 PP were similar for all three genes analyzed, wit h the induction of 6-4 PP being about 3-fold lower than of CPD, Repair of CPD was analyzed using the CPD-specific enzyme T4 endonuclease V; repair of 6-4 PP was examined employing Escherichia coil UVrABC excinu clease. Unlike the HPRT gene, in which CPD were removed selectively fr om the transcribed strand, both strands of the 16-kilobase fragment en compassing the 2.6-kilobase APRT gene were repaired efficiently. This suggests the existence of multiple transcription units in the APRT reg ion including transcription units running in the opposite direction of the APRT gene. Only a marginal part of the CPD was removed from the i nactive c-mos gene after 24 h. In all three genes investigated, 6-4 PP were repaired more rapidly than CPD and, as demonstrated for the HPRT and APRT genes, without strand specificity, The difference in the rep air phenotype of CPD between the HPRT gene and the APRT gene coincides with differences between both genes with regard to the DNA strand dis tribution of previously published UV-induced mutations,