asg-2
C. elegans
putative ATP synthase subunit g 2, mitochondrial
What the model saw
Gene: asg-2 Organism: Caenorhabditis elegans Known functions: putative ATP synthase subunit g 2, mitochondrial. proton transmembrane transporter activity. proton-transporting ATP synthase activity, rotational mechanism.
View unredacted entry
putative ATP synthase subunit g 2, mitochondrial. proton transmembrane transporter activity. proton-transporting ATP synthase activity, rotational mechanism.
Solver output
asg-2 encodes a putative subunit g of the mitochondrial ATP synthase (Complex V), which is a structural component of the F0 subunit involved in proton translocation across the inner mitochondrial membrane via a rotational mechanism. Proper ATP synthase function is essential for efficient oxidative phosphorylation and maintenance of the mitochondrial membrane potential. Loss or impairment of ATP synthase subunits in C. elegans (e.g., asb-2/atp-3 related subunits) typically disrupts mitochondrial bioenergetics, leading to reduced ATP production and mitochondrial dysfunction—a recognized hallmark of aging. Functional ATP synthase activity supports cellular energy homeostasis, which is critical for organismal healthspan and longevity. In C. elegans, mild mitochondrial perturbations can sometimes extend lifespan via mitohormesis, but the primary role of this subunit in sustaining normal Complex V assembly and proton-coupled ATP synthesis places its normal function in the pro-longevity category by preventing mitochondrial dysfunction.
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 predicted pro_longevity but the ground truth is anti_longevity. The model's reasoning is internally inconsistent - it acknowledges that mild mitochondrial perturbations can extend lifespan via mitohormesis in C. elegans, but then dismisses this in favor of a pro_longevity classification. In fact, asg-2 is anti_longevity, meaning its normal function promotes aging (or its loss extends lifespan). This is consistent with the well-known phenomenon in C. elegans where knockdown of mitochondrial electron transport chain/ATP synthase components (like isp-1, clk-1, nuo-6, and various ATP synthase subunits) extends lifespan through mitohormesis or reduced metabolic rate. The model failed to correctly apply this known C. elegans biology despite mentioning it. The confidence of 0.72 for the wrong answer is notable.
Raw API responses
solver
{
"reasoning": "asg-2 encodes a putative subunit g of the mitochondrial ATP synthase (Complex V), which is a structural component of the F0 subunit involved in proton translocation across the inner mitochondrial membrane via a rotational mechanism. Proper ATP synthase function is essential for efficient oxidative phosphorylation and maintenance of the mitochondrial membrane potential. Loss or impairment of ATP synthase subunits in C. elegans (e.g., asb-2/atp-3 related subunits) typically disrupts mitochondrial bioenergetics, leading to reduced ATP production and mitochondrial dysfunction—a recognized hallmark of aging. Functional ATP synthase activity supports cellular energy homeostasis, which is critical for organismal healthspan and longevity. In C. elegans, mild mitochondrial perturbations can sometimes extend lifespan via mitohormesis, but the primary role of this subunit in sustaining normal Complex V assembly and proton-coupled ATP synthesis places its normal function in the pro-longevity category by preventing mitochondrial dysfunction.",
"confidence": 0.72,
"key_pathways": [
"oxidative phosphorylation / Complex V (ATP synthase)",
"mitochondrial proton gradient maintenance",
"mitochondrial energy homeostasis"
],
"mechanism_class": "mitochondrial_dysfunction",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model predicted pro_longevity but the ground truth is anti_longevity. The model's reasoning is internally inconsistent - it acknowledges that mild mitochondrial perturbations can extend lifespan via mitohormesis in C. elegans, but then dismisses this in favor of a pro_longevity classification. In fact, asg-2 is anti_longevity, meaning its normal function promotes aging (or its loss extends lifespan). This is consistent with the well-known phenomenon in C. elegans where knockdown of mitochondrial electron transport chain/ATP synthase components (like isp-1, clk-1, nuo-6, and various ATP synthase subunits) extends lifespan through mitohormesis or reduced metabolic rate. The model failed to correctly apply this known C. elegans biology despite mentioning it. The confidence of 0.72 for the wrong answer is notable.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}