PET9
S. cerevisiae
ADP/ATP carrier protein PET9
What the model saw
Gene: PET9 Organism: Saccharomyces cerevisiae Known functions: ADP/ATP carrier protein PET9. ATP:ADP antiporter activity. cardiolipin binding.
View unredacted entry
ADP/ATP carrier protein PET9. ATP:ADP antiporter activity. cardiolipin binding.
Solver output
PET9 encodes the major mitochondrial ADP/ATP carrier (AAC2) in S. cerevisiae, which catalyzes the exchange of cytosolic ADP for matrix ATP across the inner mitochondrial membrane. This antiporter activity is essential for oxidative phosphorylation efficiency, as it couples mitochondrial ATP synthesis to cytosolic energy demands. Its cardiolipin binding is critical for proper insertion and function within the inner mitochondrial membrane, since cardiolipin stabilizes the carrier and supports the mitochondrial membrane potential. Efficient ADP/ATP exchange sustains mitochondrial respiration and reduces reliance on fermentation, which is associated with healthier aging in yeast. Loss of PET9 function impairs mitochondrial ATP export, collapses respiratory capacity, and accelerates aging phenotypes, consistent with its pro-longevity role.
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 for PET9 with high confidence (0.78). The mechanistic reasoning is excellent: it correctly identifies PET9 as encoding the major mitochondrial ADP/ATP carrier (AAC2), explains its role in oxidative phosphorylation, discusses cardiolipin binding for membrane stability, and correctly reasons that loss of function impairs mitochondrial ATP export and accelerates aging. The mechanism class "mitochondrial_dysfunction" is appropriate since loss of PET9 leads to mitochondrial dysfunction. The reasoning is detailed, accurate, and well-grounded in yeast biology.
Raw API responses
solver
{
"reasoning": "PET9 encodes the major mitochondrial ADP/ATP carrier (AAC2) in S. cerevisiae, which catalyzes the exchange of cytosolic ADP for matrix ATP across the inner mitochondrial membrane. This antiporter activity is essential for oxidative phosphorylation efficiency, as it couples mitochondrial ATP synthesis to cytosolic energy demands. Its cardiolipin binding is critical for proper insertion and function within the inner mitochondrial membrane, since cardiolipin stabilizes the carrier and supports the mitochondrial membrane potential. Efficient ADP/ATP exchange sustains mitochondrial respiration and reduces reliance on fermentation, which is associated with healthier aging in yeast. Loss of PET9 function impairs mitochondrial ATP export, collapses respiratory capacity, and accelerates aging phenotypes, consistent with its pro-longevity role.",
"confidence": 0.78,
"key_pathways": [
"oxidative phosphorylation / ADP-ATP exchange",
"mitochondrial inner membrane transport",
"cardiolipin-dependent mitochondrial membrane integrity"
],
"mechanism_class": "mitochondrial_dysfunction",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly predicted pro_longevity for PET9 with high confidence (0.78). The mechanistic reasoning is excellent: it correctly identifies PET9 as encoding the major mitochondrial ADP/ATP carrier (AAC2), explains its role in oxidative phosphorylation, discusses cardiolipin binding for membrane stability, and correctly reasons that loss of function impairs mitochondrial ATP export and accelerates aging. The mechanism class \"mitochondrial_dysfunction\" is appropriate since loss of PET9 leads to mitochondrial dysfunction. The reasoning is detailed, accurate, and well-grounded in yeast biology.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}