Inducible DNA polymerase in cultured rat fibroblasts treated with skin carcinogen mitomycin C

Abstract

DNA polymerases are involved in the filling of excision [ 1,2] and postreplication [3,4] single-strand gaps in DNA in ultraviolet-irradiated bacteria. Gapfilling with the constitutive DNA polymerase is an error-free process that cannot be the source of ultraviolet-induced mutations [ 51. It has been reported that heat treatment of tif strain of E. coli causes the appearance of a mutagenic DNA polymerase responsible for the fixation of premutational lesions during heat-induced ‘SOS repair’ [6] . An inducibility has been shown for minor branch of postreplication repair in E. coli [7] , Micrococcus luteus [8] and in human fibroblasts [9] . The question remains: Is inducible repair in mammalian cells coupled with the induction of a DNA polymerase with a reduced fidelity in repair replication? Mitomycin C (MMC) studied extensively for its mutagenic [lo] and carcinogenic [ 111 properties can induce in E. cob the synthesis of X protein [ 121. This property usually correlates with the ability of a chemical to induce SOS repair [5] . In connection with the question above the observation of an increased DNA polymerase activity in extracts from MMC-treated mammalian cells [ 13,141 is of interest. We therefore investigated the origin and reaction properties of the DNA polymerase in cells affected by MMC.