Werner's syndrome (WS) is an autosomal recessive disorder in humans characterized by the premature development of age-associated pathologies. WRN, the gene defective in WS, plays a key role in protecting the genome. The cell derived from WS patients show genomic instabilities such as sister chromatid exchange and telomere shortening. Caenorhabditis elegans (C. elegans) with a WRN-1 ortholog also exhibits a shorter life span. Our results showed
wrn-1 interacts with
mre-11 or
him-6 and affects during embryonic and larval development. When inhibiting the expression of
mre-11 or
him-6 in
wrn-1 (
gk99) by RNA interference (RNAi) resulted in a significant increase of embryonic lethality and the retarded larval development compared with control worms of N2 (RNAi) worms. In addition,
wrn-1 (
gk99):
him-6 (RNAi) or
wrn-1 (
gk99):
mre-11 (RNAi) worms displayed abnormal premeiotic nuclei and multiple chromosomal abnormalities in oocyte nuclei at the diakinesis stage. Furthermore, observation of embryo cell division showed the slower development. These results suggest that MRE-11 and HIM-6 may interact with WRN-1, which is involved in embryonic development.