Base excision repair (BER) plays an important role in repairing small base damage in DNA and maintaining genome stability. In the BER pathway, damaged bases are removed by DNA glycosylases, and then resulting apurinic/apyrimidinic (AP) sites or 3'-a,b unsaturated aldehydes are processed by AP endonucleases. Unrepaired DNA damage may cause mutation or cell death. It is also thought that accumulation of DNA damage is related to aging. In C. elegans, two DNA glycosylases (NTH-1 and UNG-1) and two AP endonucleases (EXO-3 and APN-1) have already been identified. In addition, their enzymatic activities have also been characterized. However, comprehensive study of these genes has not been accomplished yet. We do not yet fully understand their relationship and roles in C. elegans.
Our purpose is to investigate how these BER genes functions in C. elegans and whether they are related to the aging process of C. elegans. In this study, we examined a variety of mutants deficient in BER genes. We found that mutation in
exo-3, one of the AP endonucleases in C. elegans, results in decreased self-brood size. The
exo-3 mutant also showed extended lifespan. These results suggest that mutation in the
exo-3 gene is harmful for maintaining the group, even if it may be beneficial for individual worms.