Abstract
DNA repair is essential to genome integrity. Base excision repair (BER) is responsible to repair the small, non-helix-distorting base lesions including those induced by oxidative stress. Previous studies have suggested that repair of oxidative DNA damage depends on DNA replication. Inhibition of DNA synthesis by hydorxyurea and ara-C abolishes repair of 8-oxoguanine, a typical base lesion caused by oxidative stress. In this study, the dependence of repair of oxidative DNA damage on DNA replication is re-examined by the strategy knockdown of cdc45, the DNA helicase activator essential for DNA replication. The data of cdc45 knockdown confirm that DNA replication is essential for repair of oxidative DNA damage. In addition, knockdown of geminin, which inhibits initiation of DNA replication, was also tested. Surprisingly, the cells with geminin knockdown showed reduction of DNA replication and delay of repair of oxidative DNA damage. This effect will be discussed.