sod-1
C. elegans
Superoxide dismutase
What the model saw
Gene: sod-1 Organism: Caenorhabditis elegans Known functions: Superoxide dismutase. copper ion binding. metal ion binding. protein homodimerization activity. superoxide dismutase activity.
View unredacted entry
Superoxide dismutase. copper ion binding. metal ion binding. protein homodimerization activity. superoxide dismutase activity.
Solver output
SOD-1 is the cytoplasmic Cu/Zn superoxide dismutase in C. elegans, catalyzing the dismutation of superoxide radicals (O₂•⁻) into hydrogen peroxide and molecular oxygen. By neutralizing superoxide — a primary reactive oxygen species (ROS) generated as a byproduct of mitochondrial electron transport — SOD-1 directly limits oxidative damage to proteins, lipids, and nucleic acids. Reduced oxidative stress is a well-established correlate of extended lifespan in C. elegans, and overexpression of SOD-1 has been associated with lifespan extension in multiple model organisms. The copper ion binding and homodimerization activities are essential for its catalytic mechanism, consistent with its canonical antioxidant role. This places sod-1 squarely within the mitochondrial dysfunction/ROS hallmark of aging, acting as a pro-longevity factor by buffering mitochondria-derived oxidative stress.
GenAge curators classify each gene's normal function as promoting (Pro-Longevity) or opposing (Anti-Longevity) longevity, based on synthesis across studies. Loss-of-function effects can vary from this depending on the manipulation.
Advisor judgment
The model predicted pro_longevity with 0.85 confidence, but the ground truth is anti_longevity. In C. elegans, sod-1 loss-of-function studies have shown that SOD-1 is not simply a pro-longevity factor. Research (notably by Van Raamsdonk & Hekimi and others) has demonstrated that sod-1 mutants can have normal or even extended lifespan, challenging the free radical theory of aging in C. elegans. The model relied on the classical assumption that antioxidant enzymes = pro-longevity, which does not hold for sod-1 in C. elegans. The model's reasoning is based on a general/textbook understanding that doesn't account for the C. elegans-specific experimental evidence showing sod-1 is anti-longevity (i.e., its presence/overexpression does not extend lifespan and may actually limit it). The mechanism class of 'mitochondrial_dysfunction' is also somewhat misapplied — SOD-1 is cytoplasmic Cu/Zn SOD, not primarily mitochondrial (that would be SOD-2/MnSOD). The model was highly confident in an incorrect answer with flawed reasoning.
Raw API responses
solver
{
"reasoning": "SOD-1 is the cytoplasmic Cu/Zn superoxide dismutase in C. elegans, catalyzing the dismutation of superoxide radicals (O₂•⁻) into hydrogen peroxide and molecular oxygen. By neutralizing superoxide — a primary reactive oxygen species (ROS) generated as a byproduct of mitochondrial electron transport — SOD-1 directly limits oxidative damage to proteins, lipids, and nucleic acids. Reduced oxidative stress is a well-established correlate of extended lifespan in C. elegans, and overexpression of SOD-1 has been associated with lifespan extension in multiple model organisms. The copper ion binding and homodimerization activities are essential for its catalytic mechanism, consistent with its canonical antioxidant role. This places sod-1 squarely within the mitochondrial dysfunction/ROS hallmark of aging, acting as a pro-longevity factor by buffering mitochondria-derived oxidative stress.",
"confidence": 0.85,
"key_pathways": [
"ROS detoxification / superoxide dismutation",
"mitochondrial oxidative stress response",
"insulin/IGF-1 longevity pathway (DAF-16 target gene regulation)"
],
"mechanism_class": "mitochondrial_dysfunction",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model predicted pro_longevity with 0.85 confidence, but the ground truth is anti_longevity. In C. elegans, sod-1 loss-of-function studies have shown that SOD-1 is not simply a pro-longevity factor. Research (notably by Van Raamsdonk & Hekimi and others) has demonstrated that sod-1 mutants can have normal or even extended lifespan, challenging the free radical theory of aging in C. elegans. The model relied on the classical assumption that antioxidant enzymes = pro-longevity, which does not hold for sod-1 in C. elegans. The model's reasoning is based on a general/textbook understanding that doesn't account for the C. elegans-specific experimental evidence showing sod-1 is anti-longevity (i.e., its presence/overexpression does not extend lifespan and may actually limit it). The mechanism class of 'mitochondrial_dysfunction' is also somewhat misapplied — SOD-1 is cytoplasmic Cu/Zn SOD, not primarily mitochondrial (that would be SOD-2/MnSOD). The model was highly confident in an incorrect answer with flawed reasoning.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": true
}