Abstract
We studied the repair of psoralen adducts in the pol I–transcribed ribosomal RNA (rRNA) genes of excision repair competent Chinese hamster ovary (CHO) cell lines, their UV sensitive mutant derivatives, and their UV resistant transformants, which express a human excision repair gene. In the parental cell line CHO‐AA8, both monoadducts and interstrand crosslinks are removed efficiently from the rRNA genes, whereas neither adduct is removed in the UV sensitive derivative UV5; removal of both adducts is restored in the UV resistant transformant CHO‐5T4 carrying the human excision repair gene ERCC‐2. In contrast, removal of psoralen adducts from the rRNA genes is not detected in another parental CHO cell line CHO‐9, neither in its UV sensitive derivative 43°3B, nor in its UV resistant transformant 83°G5 carrying the human excision repair gene ERCC‐1. In contrast to such intergenomic heterogeneity of repair, persistence of psoralen monoadducts during replication of the rRNA genes occurs equally well in all CHO cell lines tested. From these data, we conclude that: (1) The repair efficiency of DNA damage in the rRNA genes varies between established parental CHO cell lines; (2) the repair pathways of intrastrand adducts and interstrand crosslinks in mammalian cells share, at least, one gene product, i.e., the excision repair gene ERCC‐2; (3) replicational bypass of psoralen monoadducts at the CHO rRNA locus occurs similarly on both DNA strands.