| Pathway | Key components | Role of SOD-2 | Biological outcome | Evidence |
|---|---|---|---|---|
| Mitochondrial superoxide detoxification | Mitochondrial electron transport chain; superoxide (O2•−); Mn cofactor; SOD-2 in mitochondrial matrix; H2O2/O2 products | Primary mitochondrial Mn-superoxide dismutase that converts superoxide to hydrogen peroxide and oxygen; active dimeric enzyme with mitochondrial transit peptide and matrix localization | Limits mitochondrial superoxide burden and contributes to basal antioxidant defense; loss increases oxidative stress sensitivity and oxidative damage even when lifespan is not shortened | (pqac-00000000, pqac-00000001, pqac-00000008, pqac-00000014) |
| RAS-dependent ROS signaling (RDRS) | Mitochondrial superoxide; SOD-2; cytosolic SOD-1; H2O2; LET-60/RAS C118 redox switch | Loss of SOD-2 raises mitochondrial superoxide; longevity signal requires downstream conversion by SOD-1 to H2O2, which oxidizes LET-60/RAS and activates RDRS | Global transcriptional remodeling and lifespan extension from mitochondrial ROS signaling rather than simple detoxification | (pqac-00000018, pqac-00000027) |
| p38 MAPK/SKN-1/Nrf2 regulation of sod-2 | p38 MAPK pathway; SKN-1/Nrf2; sod-2 promoter | sod-2 is regulated predominantly by SKN-1 rather than DAF-16 under stress-responsive conditions, especially in molecular compensation among sod mutants | Supports stress adaptation and longevity-associated redox homeostasis under intracellular oxidative stress | (pqac-00000019, pqac-00000020, pqac-00000044) |
| Insulin/IGF-1 signaling (IIS) via DAF-2/DAF-16 | DAF-2 insulin/IGF-1 receptor; DAF-16/FoxO; MnSOD genes sod-2 and sod-3 | sod-2 is part of the MnSOD antioxidant network linked to longevity signaling, but unlike sod-3 it is not strongly induced in daf-2 mutants and appears less directly controlled by DAF-16 | Contributes to oxidative stress resistance framework of IIS, while sod-3 is the more prominent dauer/DAF-16-responsive MnSOD output | (pqac-00000021, pqac-00000022, pqac-00000042, pqac-00000045) |
| Mitochondrial unfolded protein response (UPRmt) / mitochondrial dysfunction programs | Mitochondrial stress; mitochondrial proteostasis pathways; respiratory dysfunction; stress-response genes including SOD enzymes | SOD-2 is repeatedly discussed as part of mitochondrial stress-response programs and as a mitochondrial redox effector whose loss phenocopies long-lived mitochondrial mutants with reduced respiration | Links mitochondrial dysfunction to compensatory stress programs and altered lifespan trajectories | (pqac-00000007, pqac-00000010, pqac-00000023) |
| Complex I ROS signaling and hypoxic avoidance behavior | Complex I-derived ROS; SOD-2/SOD-3; H2O2; redox-sensitive thiol switch on NDUF-2.1-related pathway; locomotory/hypoxia avoidance circuitry | SOD-2 is required to convert complex I-derived superoxide into H2O2 that mediates behavioral signaling; loss of sod-2 abolishes ROS-triggered avoidance/photolocomotory responses | Enables mitochondrial ROS to function as a signal for hypoxic avoidance and acute behavioral adaptation | (pqac-00000029, pqac-00000030) |
| Sperm activation via H2O2 signaling | SOD-2; SOD-1; H2O2; Pronase-responsive sperm activation; pseudopod extension machinery | SOD-2-generated H2O2 acts as a positive signaling molecule required for sperm activation and pseudopod extension; exogenous H2O2 rescues activation defects in sod-1;sod-2 mutants | Promotes normal sperm motility/activation and supports fertility/brood size | (pqac-00000015, pqac-00000016, pqac-00000017) |


*Table: This table summarizes the main signaling and biochemical pathways involving C. elegans SOD-2, emphasizing where it acts as a detoxifying enzyme versus a redox-signaling mediator. It is useful for functional annotation because it connects SOD-2 to localization, pathway context, and experimentally observed organismal outcomes.*