SOD1
S. cerevisiae
superoxide dismutase SOD1
What the model saw
Gene: SOD1 Organism: Saccharomyces cerevisiae Known functions: superoxide dismutase SOD1. copper ion binding. metal ion binding. oxidoreductase activity, acting on a sulfur group of donors, oxygen as acceptor. protein binding. superoxide dismutase activity. zinc ion binding.
View unredacted entry
superoxide dismutase SOD1. copper ion binding. metal ion binding. oxidoreductase activity, acting on a sulfur group of donors, oxygen as acceptor. protein binding. superoxide dismutase activity. zinc ion binding.
Solver output
SOD1 encodes the cytosolic Cu/Zn superoxide dismutase, which catalyzes 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 respiration—SOD1 directly limits oxidative damage to proteins, lipids, and DNA. In S. cerevisiae, sod1Δ mutants exhibit dramatically shortened chronological and replicative lifespan, hypersensitivity to oxidative stress, and elevated mitochondrial dysfunction, while SOD1 overexpression extends lifespan. This places SOD1 squarely in the mitochondrial ROS detoxification axis, counteracting the accumulation of oxidative damage that drives aging. Its copper and zinc ion binding are essential for catalytic activity, and its protein-binding capacity may also support redox signaling networks that further buffer 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 correctly predicted SOD1 as pro_longevity in S. cerevisiae with high confidence (0.93). The mechanistic reasoning is accurate and detailed: SOD1 encodes Cu/Zn superoxide dismutase that neutralizes superoxide radicals, sod1Δ mutants show shortened lifespan, and overexpression extends lifespan. The mechanism class "mitochondrial_dysfunction" is slightly imprecise (SOD1 is primarily cytosolic, not mitochondrial — that's SOD2/MnSOD), but the broader reasoning about ROS detoxification and oxidative stress is correct. The model does acknowledge SOD1 is cytosolic in the text, so the mechanism_class label is a minor categorization issue rather than a fundamental error. Overall, the prediction and reasoning are excellent.
Raw API responses
solver
{
"reasoning": "SOD1 encodes the cytosolic Cu/Zn superoxide dismutase, which catalyzes 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 respiration—SOD1 directly limits oxidative damage to proteins, lipids, and DNA. In S. cerevisiae, sod1Δ mutants exhibit dramatically shortened chronological and replicative lifespan, hypersensitivity to oxidative stress, and elevated mitochondrial dysfunction, while SOD1 overexpression extends lifespan. This places SOD1 squarely in the mitochondrial ROS detoxification axis, counteracting the accumulation of oxidative damage that drives aging. Its copper and zinc ion binding are essential for catalytic activity, and its protein-binding capacity may also support redox signaling networks that further buffer oxidative stress.",
"confidence": 0.93,
"key_pathways": [
"superoxide dismutation / ROS detoxification",
"mitochondrial oxidative stress response",
"redox homeostasis"
],
"mechanism_class": "mitochondrial_dysfunction",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly predicted SOD1 as pro_longevity in S. cerevisiae with high confidence (0.93). The mechanistic reasoning is accurate and detailed: SOD1 encodes Cu/Zn superoxide dismutase that neutralizes superoxide radicals, sod1Δ mutants show shortened lifespan, and overexpression extends lifespan. The mechanism class \"mitochondrial_dysfunction\" is slightly imprecise (SOD1 is primarily cytosolic, not mitochondrial — that's SOD2/MnSOD), but the broader reasoning about ROS detoxification and oxidative stress is correct. The model does acknowledge SOD1 is cytosolic in the text, so the mechanism_class label is a minor categorization issue rather than a fundamental error. Overall, the prediction and reasoning are excellent.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}