A CDC25 phosphatase is essential for animal development as a cell cycle regulator by removing inhibitory phosphates from the cyclin-dependent kinase. However, we found that expression of CDC-25.2 remained in the somatic tissues at the post-developmental stage, suggesting a non-canonical role of CDC-25.2. At the adult stage,
cdc-25.2(
g52) mutant increased production of intracellular reactive oxygen species (ROS) and germ cell apoptosis (GA) which were suppressed by antioxidant, N-acetyl-L-cysteine treatment. These results suggest that GA was induced by intracellular ROS produced in the
cdc-25.2(
g52) mutants. Furthermore, we found that intestine-specific
cdc-25.2 RNAi induced both the high levels of mitochondrial ROS production and GA, and intestine-specific overexpression of
cdc-25.2 in
cdc-25.2(
g52) mutants suppressed mitochondrial ROS production and GA. Therefore, these findings indicate that CDC-25.2 in the intestine is required for the control of GA by modulating ROS production. Interestingly, this process was somatic CEP-1 dependent because depletion of
cep-1 in the soma by soma-biased RNAi did not increase both levels of ROS production and GA in the
cdc-25.2(
g52) mutants. Based on these findings, we suggest a non-canonical role of
cdc-25.2 in the intestine, that is,
cdc-25.2 controls mitochondrial oxidative stress in the soma to protect cell death in the germ line in which somatic CEP-1 activity is required. This study was supported by NRF2018R1A2B6007915 and NRF2021R1A2C1011658.