Abstract
Base excision repair (BER) is one of the pathways to avoid mutations in living cells. Damaged bases are excised by DNA glycosylases and then AP lyases nick DNA, followed by repair synthesis and rejoining by DNA polymerases and DNA ligases. Increased frequency of mutations in BER-defective mutants in E. coli and S. cerevisiae indicates that BER plays an important role in the cells. However, the effects of BER deficiency in multicellular organisms are yet unknown. In human, defect of nucleotide excision repair results in serious hereditary diseases, while no desease has been found to relate to BER deficiency. So we investigated the influence of BER deficiency in multicellular organsim using C. elegans. Recently, we identified the uracil DNA glycosylase homolog gene (Ceung) in C. elegans, and clarified the glysocylase activity of purified recombinant CeUNG. In this study, we examined the phenotypic properties of C. elegans defective in UNG activity using RNAi. [J Radiat Res 44:409 (2003)]
