asg-1
C. elegans
putative ATP synthase subunit g 1, mitochondrial
What the model saw
Gene: asg-1 Organism: Caenorhabditis elegans Known functions: putative ATP synthase subunit g 1, mitochondrial. proton transmembrane transporter activity. proton-transporting ATP synthase activity, rotational mechanism.
View unredacted entry
putative ATP synthase subunit g 1, mitochondrial. proton transmembrane transporter activity. proton-transporting ATP synthase activity, rotational mechanism.
Solver output
asg-1 encodes a putative subunit g of the mitochondrial ATP synthase (Complex V), which is a structural component of the F0 rotor ring that couples proton translocation across the inner mitochondrial membrane to ATP synthesis via the rotational mechanism. Proper ATP synthase function is essential for maintaining mitochondrial membrane potential and efficient oxidative phosphorylation. In C. elegans, mild impairment of mitochondrial function (e.g., via partial ETC knockdown) can paradoxically extend lifespan through mitohormesis, but the core structural subunits of ATP synthase are generally required for normal mitochondrial bioenergetics. Loss of ATP synthase subunit g disrupts the integrity of the F0 complex, impairing proton-coupled ATP synthesis and potentially collapsing membrane potential, which is associated with reduced healthspan. The normal function of asg-1 therefore supports mitochondrial energy homeostasis, placing it in the pro-longevity category as its presence sustains the mitochondrial function required for healthy aging rather than driving pathological ROS or senescence signaling.
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 acknowledged the mitohormesis phenomenon (where mild mitochondrial impairment can extend lifespan in C. elegans) but then dismissed it, concluding that asg-1 must be pro_longevity because it supports mitochondrial function. In reality, asg-1 is anti_longevity, meaning its loss (knockdown/knockout) extends lifespan - consistent with the well-documented mitohormesis effect in C. elegans where reducing ATP synthase activity extends lifespan. The model's mechanistic reasoning was actually partially correct in identifying the mitohormesis pathway but then incorrectly concluded the gene was pro_longevity. The model had moderate confidence (0.62) but still got the answer wrong. The reasoning quality is moderate - it correctly identified the relevant biology but drew the wrong conclusion.
Raw API responses
solver
{
"reasoning": "asg-1 encodes a putative subunit g of the mitochondrial ATP synthase (Complex V), which is a structural component of the F0 rotor ring that couples proton translocation across the inner mitochondrial membrane to ATP synthesis via the rotational mechanism. Proper ATP synthase function is essential for maintaining mitochondrial membrane potential and efficient oxidative phosphorylation. In C. elegans, mild impairment of mitochondrial function (e.g., via partial ETC knockdown) can paradoxically extend lifespan through mitohormesis, but the core structural subunits of ATP synthase are generally required for normal mitochondrial bioenergetics. Loss of ATP synthase subunit g disrupts the integrity of the F0 complex, impairing proton-coupled ATP synthesis and potentially collapsing membrane potential, which is associated with reduced healthspan. The normal function of asg-1 therefore supports mitochondrial energy homeostasis, placing it in the pro-longevity category as its presence sustains the mitochondrial function required for healthy aging rather than driving pathological ROS or senescence signaling.",
"confidence": 0.62,
"key_pathways": [
"oxidative phosphorylation / ATP synthesis (Complex V)",
"mitochondrial proton gradient maintenance",
"mitochondrial membrane potential regulation"
],
"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 acknowledged the mitohormesis phenomenon (where mild mitochondrial impairment can extend lifespan in C. elegans) but then dismissed it, concluding that asg-1 must be pro_longevity because it supports mitochondrial function. In reality, asg-1 is anti_longevity, meaning its loss (knockdown/knockout) extends lifespan - consistent with the well-documented mitohormesis effect in C. elegans where reducing ATP synthase activity extends lifespan. The model's mechanistic reasoning was actually partially correct in identifying the mitohormesis pathway but then incorrectly concluded the gene was pro_longevity. The model had moderate confidence (0.62) but still got the answer wrong. The reasoning quality is moderate - it correctly identified the relevant biology but drew the wrong conclusion.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 3,
"ground_truth_questionable": false
}