Superoxide dismutase (SOD) is an enzyme that catalytically removes the superoxide radical (.O2-) and protects organisms from oxidative damage during normal aging. We previously found a functional compensation by the
sod-5 gene in the deletion mutants of
sod-1 gene encoding a Cu/Zn SOD in the nematode Caenorhabditis elegans (C. elegans). Here, we examined whether levels of
sod-1 gene expression alternatively are increased in the deletion mutant of
sod-5 gene also encoding other Cu/Zn SOD. As a result, not
sod-1 gene, but
sod-2 gene encoding an Mn SOD was induced several fold in the mutant. Likewise, we detected about induction of
sod-2 gene expression in a
sod-1;
sod-5 double mutant. It is well known that the
sod-3 and
sod-5 genes are controlled via the insulin/insulin-like growth factor-1 (Ins/IGF-1) signaling pathway, which regulates longevity and stress resistance of C. elegans. The mammalian forkhead transcription factor FOXO ortholog, DAF-16, is located downstream on the Ins/IGF-1 signaling pathway. There are the DAF-16 consensus binding element (DBE) sequences, which bind the DAF-16 transcription factor, in each promoter region of
sod-2,
sod-3 and
sod-5 genes on the DDBJ/GenBank/EMBL International Nucleotide Sequence Database. DBE in the promoter region of
sod-2 gene seemed to barely function using a
daf-16 gene null mutant,
daf-16(mgDf50) strain, from a previous report. However, we propose that
sod-2 gene is also the target of DAF-16 transcription factor, and is associated with normal aging in C. elegans under intracellular stressful condition such as the
sod-1 and
sod-5 genes deletion mutant.