f11g11.13
C. elegans
arginine kinase
What the model saw
Gene: F11G11.13 Organism: Caenorhabditis elegans Known functions: arginine kinase. ATP binding. arginine kinase activity. catalytic activity. kinase activity. phosphotransferase activity, nitrogenous group as acceptor. transferase activity, transferring phosphorus-containing groups.
View unredacted entry
arginine kinase. ATP binding. arginine kinase activity. catalytic activity. kinase activity. phosphotransferase activity, nitrogenous group as acceptor. transferase activity, transferring phosphorus-containing groups.
Solver output
Arginine kinase catalyzes the reversible phosphorylation of arginine to phosphoarginine using ATP, serving as the invertebrate functional analog of creatine kinase in vertebrates. This reaction buffers cellular ATP levels during periods of high energy demand, maintaining the ATP/ADP ratio and supporting energy homeostasis. In C. elegans, robust phosphagen kinase activity helps sustain mitochondrial energy output and prevents energetic collapse under stress, which is closely tied to metabolic sensing pathways (AMPK, mTOR) that are central regulators of longevity. By maintaining cellular energy charge, arginine kinase supports the organism's ability to mount stress responses and avoid the energetic deficits that accelerate aging. Loss of this buffering capacity would be expected to impair energy homeostasis and reduce lifespan, making the normal function pro-longevity.
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 plausible in general terms (arginine kinase buffers ATP, supports energy homeostasis), but it incorrectly concludes that this makes the gene pro-longevity. In C. elegans, F11G11.13 (arginine kinase) is actually anti-longevity, meaning its loss or reduction extends lifespan. The model's logic that "loss of buffering capacity would reduce lifespan" is backwards from the actual experimental finding. The model showed moderate confidence (0.65) but was still clearly wrong on both the answer and the mechanistic interpretation of the gene's role in longevity.
Raw API responses
solver
{
"reasoning": "Arginine kinase catalyzes the reversible phosphorylation of arginine to phosphoarginine using ATP, serving as the invertebrate functional analog of creatine kinase in vertebrates. This reaction buffers cellular ATP levels during periods of high energy demand, maintaining the ATP/ADP ratio and supporting energy homeostasis. In C. elegans, robust phosphagen kinase activity helps sustain mitochondrial energy output and prevents energetic collapse under stress, which is closely tied to metabolic sensing pathways (AMPK, mTOR) that are central regulators of longevity. By maintaining cellular energy charge, arginine kinase supports the organism's ability to mount stress responses and avoid the energetic deficits that accelerate aging. Loss of this buffering capacity would be expected to impair energy homeostasis and reduce lifespan, making the normal function pro-longevity.",
"confidence": 0.65,
"key_pathways": [
"phosphagen energy buffering (phosphoarginine/arginine cycle)",
"AMPK-mediated energy sensing",
"mitochondrial ATP homeostasis"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model predicted pro_longevity but the ground truth is anti_longevity. The model's reasoning is plausible in general terms (arginine kinase buffers ATP, supports energy homeostasis), but it incorrectly concludes that this makes the gene pro-longevity. In C. elegans, F11G11.13 (arginine kinase) is actually anti-longevity, meaning its loss or reduction extends lifespan. The model's logic that \"loss of buffering capacity would reduce lifespan\" is backwards from the actual experimental finding. The model showed moderate confidence (0.65) but was still clearly wrong on both the answer and the mechanistic interpretation of the gene's role in longevity.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}