Sod2
D. melanogaster
Superoxide dismutase 2 (Mn)
What the model saw
Gene: Sod2 Organism: Drosophila melanogaster Known functions: Superoxide dismutase 2 (Mn). superoxide dismutase 2 (Mn). antioxidant activity. manganese ion binding. metal ion binding. superoxide dismutase activity.
View unredacted entry
Superoxide dismutase 2 (Mn). superoxide dismutase 2 (Mn). antioxidant activity. manganese ion binding. metal ion binding. superoxide dismutase activity.
Solver output
Sod2 encodes the mitochondrial manganese superoxide dismutase (MnSOD), which catalyzes the dismutation of superoxide radicals (O₂•⁻) generated by the mitochondrial electron transport chain into hydrogen peroxide and molecular oxygen. By neutralizing mitochondrial superoxide, Sod2 directly limits oxidative damage to mitochondrial DNA, proteins, and lipids — a key driver of mitochondrial dysfunction and aging. In Drosophila, loss-of-function mutations in Sod2 dramatically shorten lifespan and increase oxidative stress, while overexpression studies have demonstrated lifespan extension, consistent with the mitochondrial free radical theory of aging. This places Sod2 squarely in the mitochondrial ROS detoxification pathway as a pro-longevity factor.
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 pro_longevity with high confidence (0.95). The mechanistic reasoning is accurate and detailed: Sod2 encodes mitochondrial MnSOD, which neutralizes superoxide radicals from the electron transport chain, reducing oxidative damage. The model correctly notes that loss-of-function shortens lifespan and overexpression extends lifespan in Drosophila, consistent with the free radical theory of aging. The mechanism class (mitochondrial_dysfunction) and key pathways are all appropriate and well-reasoned.
Raw API responses
solver
{
"reasoning": "Sod2 encodes the mitochondrial manganese superoxide dismutase (MnSOD), which catalyzes the dismutation of superoxide radicals (O₂•⁻) generated by the mitochondrial electron transport chain into hydrogen peroxide and molecular oxygen. By neutralizing mitochondrial superoxide, Sod2 directly limits oxidative damage to mitochondrial DNA, proteins, and lipids — a key driver of mitochondrial dysfunction and aging. In Drosophila, loss-of-function mutations in Sod2 dramatically shorten lifespan and increase oxidative stress, while overexpression studies have demonstrated lifespan extension, consistent with the mitochondrial free radical theory of aging. This places Sod2 squarely in the mitochondrial ROS detoxification pathway as a pro-longevity factor.",
"confidence": 0.95,
"key_pathways": [
"mitochondrial ROS detoxification",
"superoxide dismutase antioxidant defense",
"mitochondrial electron transport chain oxidative stress response"
],
"mechanism_class": "mitochondrial_dysfunction",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly predicted pro_longevity with high confidence (0.95). The mechanistic reasoning is accurate and detailed: Sod2 encodes mitochondrial MnSOD, which neutralizes superoxide radicals from the electron transport chain, reducing oxidative damage. The model correctly notes that loss-of-function shortens lifespan and overexpression extends lifespan in Drosophila, consistent with the free radical theory of aging. The mechanism class (mitochondrial_dysfunction) and key pathways are all appropriate and well-reasoned.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}