gcy-6
C. elegans
Receptor-type guanylate cyclase gcy-6
What the model saw
Gene: gcy-6 Organism: Caenorhabditis elegans Known functions: Receptor-type guanylate cyclase gcy-6. ATP binding. guanylate cyclase activity. peptide receptor activity. phosphorus-oxygen lyase activity. protein kinase activity.
View unredacted entry
Receptor-type guanylate cyclase gcy-6. ATP binding. guanylate cyclase activity. peptide receptor activity. phosphorus-oxygen lyase activity. protein kinase activity.
Solver output
GCY-6 is a receptor-type guanylate cyclase that synthesizes cGMP upon peptide ligand binding, directly coupling extracellular signals to intracellular second-messenger production. In C. elegans, cGMP signaling in sensory neurons (particularly chemosensory neurons) modulates the activity of cGMP-gated channels and downstream kinases (PKG/EGL-4), which intersect with the insulin/IGF-1 signaling pathway to regulate DAF-16/FOXO nuclear localization and stress responses. Receptor guanylate cyclases in C. elegans sensory neurons are well-established modulators of lifespan through neuroendocrine control of DAF-2/insulin signaling; loss or gain of function in this class of receptors can shift the balance of pro-longevity DAF-16 activity. The peptide receptor and protein kinase activities further suggest integration into nutrient/hormonal sensing circuits that govern metabolic rate and stress resistance, canonical determinants of C. elegans longevity. The pro-longevity prediction is based on the general role of cGMP/PKG signaling in sensory neurons promoting DAF-16 activity and lifespan extension when insulin-like signaling is attenuated.
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 about cGMP signaling and sensory neuron-mediated lifespan regulation is plausible in general terms for the guanylate cyclase family, but it incorrectly applied this to gcy-6 specifically. The model acknowledged that receptor guanylate cyclases can shift lifespan in either direction but then defaulted to pro_longevity without sufficient justification for this specific gene. The mechanistic reasoning is generic and not specific to gcy-6's actual role. The confidence of 0.62 is moderate but still represents a wrong prediction. The model failed to identify that gcy-6 acts as an anti-longevity gene, likely because it over-generalized from the broader cGMP/PKG/DAF-16 framework without accounting for the specific neuroendocrine context of gcy-6.
Raw API responses
solver
{
"reasoning": "GCY-6 is a receptor-type guanylate cyclase that synthesizes cGMP upon peptide ligand binding, directly coupling extracellular signals to intracellular second-messenger production. In C. elegans, cGMP signaling in sensory neurons (particularly chemosensory neurons) modulates the activity of cGMP-gated channels and downstream kinases (PKG/EGL-4), which intersect with the insulin/IGF-1 signaling pathway to regulate DAF-16/FOXO nuclear localization and stress responses. Receptor guanylate cyclases in C. elegans sensory neurons are well-established modulators of lifespan through neuroendocrine control of DAF-2/insulin signaling; loss or gain of function in this class of receptors can shift the balance of pro-longevity DAF-16 activity. The peptide receptor and protein kinase activities further suggest integration into nutrient/hormonal sensing circuits that govern metabolic rate and stress resistance, canonical determinants of C. elegans longevity. The pro-longevity prediction is based on the general role of cGMP/PKG signaling in sensory neurons promoting DAF-16 activity and lifespan extension when insulin-like signaling is attenuated.",
"confidence": 0.62,
"key_pathways": [
"cGMP second-messenger signaling",
"insulin/IGF-1 (DAF-2/DAF-16) neuroendocrine axis",
"sensory neuron-mediated lifespan regulation"
],
"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 about cGMP signaling and sensory neuron-mediated lifespan regulation is plausible in general terms for the guanylate cyclase family, but it incorrectly applied this to gcy-6 specifically. The model acknowledged that receptor guanylate cyclases can shift lifespan in either direction but then defaulted to pro_longevity without sufficient justification for this specific gene. The mechanistic reasoning is generic and not specific to gcy-6's actual role. The confidence of 0.62 is moderate but still represents a wrong prediction. The model failed to identify that gcy-6 acts as an anti-longevity gene, likely because it over-generalized from the broader cGMP/PKG/DAF-16 framework without accounting for the specific neuroendocrine context of gcy-6.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}