Abstract
Reactive oxygen species are continuously generated in living cells. They interact with DNA, which produce a wide variety of base damage and cause mutations. Bacteria and eukaryotes have evolved DNA repair systems to maintain the genetic stability and to prevent mutations. Many enzymes are involved in the base excision repair pathways in E. coli and eukaryotes. For instance, MutT dephosphorylates 8-oxo-dGTP and prevents the incorporation of 8-oxodGTP produced in nucleotide pool. 8-oxoG mispairs with A and causes G:C to T:A transversions. E. coli Nth has glycosylase activity that recognizes and excises thymine glycol (Tg). Tg blocks DNA replication in vitro. The phenotypes of DNA repair defective mutant are well studied in E. coli and S. cerevisiae, while little in multicellular organisms. In humans, the defect of nucleotide excision repair results in serious hereditary diseases. In order to investigate the effect of DNA repair deficiency in multicellular organisms, we first identified the homologs of E. coli MutT and Nth in C. elegans. [J Radiat Res 44:411 (2003)]
