tax-4
C. elegans
Cyclic nucleotide-gated channel
What the model saw
Gene: tax-4 Organism: Caenorhabditis elegans Known functions: Cyclic nucleotide-gated channel. cGMP binding. identical protein binding. intracellularly cAMP-activated cation channel activity. intracellularly cGMP-activated cation channel activity. intracellularly cyclic nucleotide-activated monoatomic cation channel activity. monoatomic ion channel activity. voltage-gated potassium channel activity.
View unredacted entry
Cyclic nucleotide-gated channel. cGMP binding. identical protein binding. intracellularly cAMP-activated cation channel activity. intracellularly cGMP-activated cation channel activity. intracellularly cyclic nucleotide-activated monoatomic cation channel activity. monoatomic ion channel activity. voltage-gated potassium channel activity.
Solver output
TAX-4 is the alpha subunit of the cyclic nucleotide-gated (CNG) channel in C. elegans sensory neurons, particularly the AFD thermosensory and ASJ/ASI chemosensory neurons. Its cGMP-activated cation channel activity is essential for sensory signal transduction that modulates neuroendocrine signaling, including the insulin/IGF-1-like signaling (IIS) pathway. Loss of tax-4 function impairs sensory neuron activity, which reduces DAF-28/insulin secretion from sensory neurons, thereby lowering IIS and promoting nuclear localization of DAF-16/FOXO transcription factor — a well-established pro-longevity mechanism in C. elegans. Additionally, tax-4 mutants show extended lifespan through thermosensory neuron-mediated modulation of the IIS axis, placing it upstream of the canonical nutrient/insulin sensing pathway that governs aging rate.
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 internally coherent — it correctly identifies that tax-4 loss reduces IIS signaling and activates DAF-16/FOXO, which would extend lifespan. However, the ground truth classifies tax-4 as anti_longevity, meaning loss of tax-4 actually shortens lifespan or tax-4 activity promotes longevity. The model's mechanistic reasoning about the IIS pathway is plausible but leads to the wrong conclusion about the direction of effect. The model was fairly confident (0.72) in the wrong direction. The mechanism described (reduced IIS → DAF-16 activation → extended lifespan) would predict pro_longevity for loss-of-function, but the actual classification is anti_longevity, suggesting the real biology is more complex or different from what the model described. The reasoning quality is moderate — it shows good knowledge of C. elegans biology but arrives at the wrong answer.
Raw API responses
solver
{
"reasoning": "TAX-4 is the alpha subunit of the cyclic nucleotide-gated (CNG) channel in C. elegans sensory neurons, particularly the AFD thermosensory and ASJ/ASI chemosensory neurons. Its cGMP-activated cation channel activity is essential for sensory signal transduction that modulates neuroendocrine signaling, including the insulin/IGF-1-like signaling (IIS) pathway. Loss of tax-4 function impairs sensory neuron activity, which reduces DAF-28/insulin secretion from sensory neurons, thereby lowering IIS and promoting nuclear localization of DAF-16/FOXO transcription factor — a well-established pro-longevity mechanism in C. elegans. Additionally, tax-4 mutants show extended lifespan through thermosensory neuron-mediated modulation of the IIS axis, placing it upstream of the canonical nutrient/insulin sensing pathway that governs aging rate.",
"confidence": 0.72,
"key_pathways": [
"insulin/IGF-1 signaling (IIS) / DAF-16 FOXO pathway",
"cGMP-mediated sensory neuron signaling",
"neuroendocrine regulation of lifespan"
],
"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 internally coherent — it correctly identifies that tax-4 loss reduces IIS signaling and activates DAF-16/FOXO, which would extend lifespan. However, the ground truth classifies tax-4 as anti_longevity, meaning loss of tax-4 actually shortens lifespan or tax-4 activity promotes longevity. The model's mechanistic reasoning about the IIS pathway is plausible but leads to the wrong conclusion about the direction of effect. The model was fairly confident (0.72) in the wrong direction. The mechanism described (reduced IIS → DAF-16 activation → extended lifespan) would predict pro_longevity for loss-of-function, but the actual classification is anti_longevity, suggesting the real biology is more complex or different from what the model described. The reasoning quality is moderate — it shows good knowledge of C. elegans biology but arrives at the wrong answer.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 3,
"ground_truth_questionable": false
}