ATP2
S. cerevisiae
F1F0 ATP synthase subunit beta
What the model saw
Gene: ATP2 Organism: Saccharomyces cerevisiae Known functions: F1F0 ATP synthase subunit beta. ATP binding. ATP hydrolysis activity. protein binding. proton-transporting ATP synthase activity, rotational mechanism. proton-transporting ATPase activity, rotational mechanism.
View unredacted entry
F1F0 ATP synthase subunit beta. ATP binding. ATP hydrolysis activity. protein binding. proton-transporting ATP synthase activity, rotational mechanism. proton-transporting ATPase activity, rotational mechanism.
Solver output
ATP2 encodes the beta subunit of the mitochondrial F1F0 ATP synthase, which is the catalytic core responsible for oxidative phosphorylation-coupled ATP synthesis via the rotational mechanism. Proper mitochondrial ATP synthesis is essential for maintaining cellular energy homeostasis and membrane potential; loss of this function leads to mitochondrial dysfunction, a canonical hallmark of aging. In yeast, functional ATP synthase is required to maintain mitochondrial membrane potential (ΔΨm) and cristae structure, both of which are critical for mitochondrial quality and longevity. Disruption of ATP2 forces cells into fermentative metabolism, impairs mitochondrial biogenesis signaling, and accelerates aging phenotypes. Additionally, the proton-transporting ATPase activity of this complex is central to coupling the electron transport chain to ATP production, and its integrity is tightly linked to reduced ROS generation and extended replicative and chronological lifespan in S. cerevisiae.
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 ATP2 in S. cerevisiae with high confidence (0.88). The mechanistic reasoning is sound: ATP2 encodes the beta subunit of F1F0 ATP synthase, and its role in mitochondrial energy homeostasis, membrane potential maintenance, and ROS regulation is well-established. The reasoning that disruption leads to mitochondrial dysfunction and accelerated aging is consistent with the literature. The model slightly overstates certainty in some claims (e.g., "accelerates aging phenotypes" from ATP2 disruption is plausible but could be more nuanced), but overall the reasoning is solid and well-aligned with the ground truth.
Raw API responses
solver
{
"reasoning": "ATP2 encodes the beta subunit of the mitochondrial F1F0 ATP synthase, which is the catalytic core responsible for oxidative phosphorylation-coupled ATP synthesis via the rotational mechanism. Proper mitochondrial ATP synthesis is essential for maintaining cellular energy homeostasis and membrane potential; loss of this function leads to mitochondrial dysfunction, a canonical hallmark of aging. In yeast, functional ATP synthase is required to maintain mitochondrial membrane potential (ΔΨm) and cristae structure, both of which are critical for mitochondrial quality and longevity. Disruption of ATP2 forces cells into fermentative metabolism, impairs mitochondrial biogenesis signaling, and accelerates aging phenotypes. Additionally, the proton-transporting ATPase activity of this complex is central to coupling the electron transport chain to ATP production, and its integrity is tightly linked to reduced ROS generation and extended replicative and chronological lifespan in S. cerevisiae.",
"confidence": 0.88,
"key_pathways": [
"oxidative phosphorylation / F1F0 ATP synthase rotational catalysis",
"mitochondrial membrane potential maintenance",
"mitochondrial energy homeostasis and ROS regulation"
],
"mechanism_class": "mitochondrial_dysfunction",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly predicted pro_longevity for ATP2 in S. cerevisiae with high confidence (0.88). The mechanistic reasoning is sound: ATP2 encodes the beta subunit of F1F0 ATP synthase, and its role in mitochondrial energy homeostasis, membrane potential maintenance, and ROS regulation is well-established. The reasoning that disruption leads to mitochondrial dysfunction and accelerated aging is consistent with the literature. The model slightly overstates certainty in some claims (e.g., \"accelerates aging phenotypes\" from ATP2 disruption is plausible but could be more nuanced), but overall the reasoning is solid and well-aligned with the ground truth.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}