Base excision repair (BER) is a repair pathway for relatively small damaged bases in DNA, and consists of various kinds of enzymes, such as DNA glycosylases and AP endonucleases. The molecular mechanism of BER has been elucidated so well, but its physiological roles in multicellular organisms are not fully understood. In this study, we investigated the relationship between DNA glycosylases and AP endonucleases in animal development and morphogenesis, using Caenorhabditis elegans (C. elegans). In C. elegans, two DNA glycosylases,
nth-1 and
ung-1, which remove oxidative pyrimidines and uracil respectively, and two AP endonucleases,
apn-1 and
exo-3, are conserved. We found that the
exo-3 mutant showed developmental delay, and increased number of protruding vulva (pvl) under
dut-1 RNAi, while the
apn-1 mutant did not show either of them. The developmental delay was dependent on not
ung-1 but
nth-1 under normal conditions. However, when worms were treated with sodium bisulfite (NaHSO3), which causes excessive uracil in DNA, the phenotype depended on
ung-1. On the other hand, the pvl relied on
ung-1, and was enhanced under additional oxidative stress conditions, such as
ndx-1 RNAi,
ndx-2 RNAi, or methyl viologen treatment. The enhancement of the pvl did not depend on
nth-1. Moreover, both of these two phenotypes in the
exo-3 mutant, developmental delay and increased number of pvl, were rescued by the lack of
chk-2. These results suggest that deficient repair of AP sites has an adverse effect on development and morphogenesis through removing base damages such as oxidative base damages and uracils from genome and subsequently checkpoint activation.