SOD2
S. cerevisiae
superoxide dismutase SOD2
What the model saw
Gene: SOD2 Organism: Saccharomyces cerevisiae Known functions: superoxide dismutase SOD2. manganese ion binding. metal ion binding. superoxide dismutase activity.
View unredacted entry
superoxide dismutase SOD2. manganese ion binding. metal ion binding. superoxide dismutase activity.
Solver output
SOD2 encodes the mitochondrial manganese superoxide dismutase, which catalyzes the dismutation of superoxide radicals (O2•⁻) into hydrogen peroxide and molecular oxygen within the mitochondrial matrix. By neutralizing superoxide — a primary reactive oxygen species (ROS) generated as a byproduct of the electron transport chain — SOD2 directly prevents oxidative damage to mitochondrial DNA, proteins, and lipids. Reduced mitochondrial ROS accumulation preserves electron transport chain integrity and mitochondrial membrane potential, delaying age-associated mitochondrial dysfunction. In yeast, loss of SOD2 leads to shortened chronological and replicative lifespan, while overexpression extends lifespan, consistent with its pro-longevity role. This places SOD2 squarely within the mitochondrial dysfunction hallmark of aging, acting as a key antioxidant defense at the source of ROS production.
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 SOD2 as pro_longevity with high confidence (0.92). The mechanistic reasoning is excellent and accurate: SOD2 encodes mitochondrial manganese superoxide dismutase, which neutralizes superoxide radicals in the mitochondrial matrix, preventing oxidative damage and preserving mitochondrial function. The model correctly notes that loss of SOD2 shortens lifespan in yeast while overexpression extends it. The mechanism class of mitochondrial_dysfunction is appropriate, and the key pathways identified are all relevant. This is a well-reasoned, accurate prediction.
Raw API responses
solver
{
"reasoning": "SOD2 encodes the mitochondrial manganese superoxide dismutase, which catalyzes the dismutation of superoxide radicals (O2•⁻) into hydrogen peroxide and molecular oxygen within the mitochondrial matrix. By neutralizing superoxide — a primary reactive oxygen species (ROS) generated as a byproduct of the electron transport chain — SOD2 directly prevents oxidative damage to mitochondrial DNA, proteins, and lipids. Reduced mitochondrial ROS accumulation preserves electron transport chain integrity and mitochondrial membrane potential, delaying age-associated mitochondrial dysfunction. In yeast, loss of SOD2 leads to shortened chronological and replicative lifespan, while overexpression extends lifespan, consistent with its pro-longevity role. This places SOD2 squarely within the mitochondrial dysfunction hallmark of aging, acting as a key antioxidant defense at the source of ROS production.",
"confidence": 0.92,
"key_pathways": [
"mitochondrial ROS detoxification",
"superoxide dismutation",
"oxidative stress response"
],
"mechanism_class": "mitochondrial_dysfunction",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly predicted SOD2 as pro_longevity with high confidence (0.92). The mechanistic reasoning is excellent and accurate: SOD2 encodes mitochondrial manganese superoxide dismutase, which neutralizes superoxide radicals in the mitochondrial matrix, preventing oxidative damage and preserving mitochondrial function. The model correctly notes that loss of SOD2 shortens lifespan in yeast while overexpression extends it. The mechanism class of mitochondrial_dysfunction is appropriate, and the key pathways identified are all relevant. This is a well-reasoned, accurate prediction.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}