des-2
C. elegans
Acetylcholine receptor DES-2-like protein;Acetylcholine receptor subunit alpha-type des-2
What the model saw
Gene: des-2 Organism: Caenorhabditis elegans Known functions: Acetylcholine receptor DES-2-like protein;Acetylcholine receptor subunit alpha-type des-2. acetylcholine-gated monoatomic cation-selective channel activity. extracellular ligand-gated monoatomic ion channel activity. monoatomic ion channel activity. neurotransmitter receptor activity. transmembrane signaling receptor activity.
View unredacted entry
Acetylcholine receptor DES-2-like protein;Acetylcholine receptor subunit alpha-type des-2. acetylcholine-gated monoatomic cation-selective channel activity. extracellular ligand-gated monoatomic ion channel activity. monoatomic ion channel activity. neurotransmitter receptor activity. transmembrane signaling receptor activity.
Solver output
DES-2 is an alpha-type nicotinic acetylcholine receptor (nAChR) subunit that forms ligand-gated cation channels activated by acetylcholine. In C. elegans, cholinergic signaling through nAChRs primarily governs neuromuscular and neuronal communication rather than directly regulating canonical longevity pathways such as insulin/IGF-1, TOR, or dietary restriction. While altered intercellular communication is a hallmark of aging, the specific role of this ionotropic receptor subunit in modulating lifespan is not well-established. Nicotinic receptor signaling could theoretically influence longevity indirectly via neuronal circuits that regulate metabolism or stress responses, but the direction of effect is not predictable from molecular function annotations alone. The lack of a clear mechanistic link to pro- or anti-longevity pathways makes a confident directional prediction unreliable.
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 "unclear" while the ground truth is "anti_longevity." The model correctly identified DES-2 as a nicotinic acetylcholine receptor subunit and noted cholinergic signaling pathways, but failed to make a directional prediction. The model's uncertainty is understandable given the limited functional annotation provided, but it still got the answer wrong. The mechanism class of "altered_intercellular_communication" is plausible but not specifically validated. The model's reasoning is coherent but overly cautious, resulting in a missed prediction. This is a case of appropriate uncertainty rather than confident wrongness, but the answer is still incorrect.
Raw API responses
solver
{
"reasoning": "DES-2 is an alpha-type nicotinic acetylcholine receptor (nAChR) subunit that forms ligand-gated cation channels activated by acetylcholine. In C. elegans, cholinergic signaling through nAChRs primarily governs neuromuscular and neuronal communication rather than directly regulating canonical longevity pathways such as insulin/IGF-1, TOR, or dietary restriction. While altered intercellular communication is a hallmark of aging, the specific role of this ionotropic receptor subunit in modulating lifespan is not well-established. Nicotinic receptor signaling could theoretically influence longevity indirectly via neuronal circuits that regulate metabolism or stress responses, but the direction of effect is not predictable from molecular function annotations alone. The lack of a clear mechanistic link to pro- or anti-longevity pathways makes a confident directional prediction unreliable.",
"confidence": 0.38,
"key_pathways": [
"nicotinic acetylcholine receptor signaling",
"cholinergic neurotransmission",
"ligand-gated ion channel activity"
],
"mechanism_class": "altered_intercellular_communication",
"longevity_influence": "unclear"
}advisor
{
"notes": "The model predicted \"unclear\" while the ground truth is \"anti_longevity.\" The model correctly identified DES-2 as a nicotinic acetylcholine receptor subunit and noted cholinergic signaling pathways, but failed to make a directional prediction. The model's uncertainty is understandable given the limited functional annotation provided, but it still got the answer wrong. The mechanism class of \"altered_intercellular_communication\" is plausible but not specifically validated. The model's reasoning is coherent but overly cautious, resulting in a missed prediction. This is a case of appropriate uncertainty rather than confident wrongness, but the answer is still incorrect.",
"failure_mode": "appropriately_uncertain",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}