cup-4
C. elegans
Acetylcholine receptor-like protein cup-4
What the model saw
Gene: cup-4 Organism: Caenorhabditis elegans Known functions: Acetylcholine receptor-like protein cup-4. acetylcholine receptor activity. 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-like protein cup-4. acetylcholine receptor activity. 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
CUP-4 is a C. elegans acetylcholine-gated cation channel (nicotinic acetylcholine receptor-like) expressed in coelomocytes, where it mediates fluid-phase endocytosis. Proper coelomocyte function is required for clearance of extracellular debris and signaling molecules; loss of cup-4 impairs endocytic uptake in coelomocytes, which disrupts intercellular communication and waste clearance. Acetylcholine signaling through nicotinic receptors in C. elegans is also linked to neuronal regulation of lifespan via neuroendocrine pathways. Intact cholinergic receptor activity at coelomocytes supports systemic homeostasis, and disruption of cup-4 has been associated with reduced organismal fitness. Thus, the normal function of CUP-4 in maintaining coelomocyte-mediated clearance and cholinergic intercellular signaling is predicted to be 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 correctly predicted pro_longevity for cup-4. The mechanistic reasoning is solid and well-grounded: CUP-4 is indeed an acetylcholine receptor-like protein expressed in coelomocytes that mediates fluid-phase endocytosis, and loss of cup-4 impairs coelomocyte endocytic function. The model correctly identifies coelomocyte-mediated clearance as the key mechanism. The mechanism class "altered_intercellular_communication" is reasonable given the receptor/signaling context. The reasoning is slightly speculative in places (e.g., linking to neuroendocrine pathways), but the core mechanistic explanation about coelomocyte endocytosis is accurate. Confidence of 0.62 is appropriately calibrated.
Raw API responses
solver
{
"reasoning": "CUP-4 is a C. elegans acetylcholine-gated cation channel (nicotinic acetylcholine receptor-like) expressed in coelomocytes, where it mediates fluid-phase endocytosis. Proper coelomocyte function is required for clearance of extracellular debris and signaling molecules; loss of cup-4 impairs endocytic uptake in coelomocytes, which disrupts intercellular communication and waste clearance. Acetylcholine signaling through nicotinic receptors in C. elegans is also linked to neuronal regulation of lifespan via neuroendocrine pathways. Intact cholinergic receptor activity at coelomocytes supports systemic homeostasis, and disruption of cup-4 has been associated with reduced organismal fitness. Thus, the normal function of CUP-4 in maintaining coelomocyte-mediated clearance and cholinergic intercellular signaling is predicted to be pro-longevity.",
"confidence": 0.62,
"key_pathways": [
"cholinergic/nicotinic acetylcholine receptor signaling",
"coelomocyte-mediated endocytosis and extracellular clearance",
"neuroendocrine regulation of lifespan"
],
"mechanism_class": "altered_intercellular_communication",
"longevity_influence": "pro_longevity"
}advisor
{
"notes": "The model correctly predicted pro_longevity for cup-4. The mechanistic reasoning is solid and well-grounded: CUP-4 is indeed an acetylcholine receptor-like protein expressed in coelomocytes that mediates fluid-phase endocytosis, and loss of cup-4 impairs coelomocyte endocytic function. The model correctly identifies coelomocyte-mediated clearance as the key mechanism. The mechanism class \"altered_intercellular_communication\" is reasonable given the receptor/signaling context. The reasoning is slightly speculative in places (e.g., linking to neuroendocrine pathways), but the core mechanistic explanation about coelomocyte endocytosis is accurate. Confidence of 0.62 is appropriately calibrated.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 4,
"ground_truth_questionable": false
}