Quantitative measurement of translesion replication in human cells: evidence for bypass of abasic sites by a replicative DNA polymerase.

ABSTRACT: Mutations in oncogenes and tumor suppressor genes are critical in the development of cancer. A major pathway for the formation of mutations is the replication of unrepaired DNA lesions. To better understand the mechanism of translesion replication (TLR) in mammals, a quantitative assay for TLR in cultured cells was developed. The assay is based on the transient transfection of cultured cells with a gapped plasmid, carrying a site-specific lesion in the gap region. Filling in of the gap by TLR is assayed in a subsequent bioassay, by the ability of the plasmid extracted from the cells, to transform an Escherichia coli indicator strain. Using this method it was found that TLR through a synthetic abasic site in the adenocarcinoma H1299, the osteogenic sarcoma Saos-2, the prostate carcinoma PC3

SUBMITTER: Avkin S 

PROVIDER: S-EPMC122598 | biostudies-literature | 2002 Mar

REPOSITORIES: biostudies-literature