daf-1
C. elegans
Cell surface receptor daf-1
What the model saw
Gene: daf-1 Organism: Caenorhabditis elegans Known functions: Cell surface receptor daf-1. ATP binding. activin binding. activin receptor activity, type I. protein binding. protein kinase activity. transforming growth factor beta receptor activity. transmembrane receptor protein serine/threonine kinase activity.
View unredacted entry
Cell surface receptor daf-1. ATP binding. activin binding. activin receptor activity, type I. protein binding. protein kinase activity. transforming growth factor beta receptor activity. transmembrane receptor protein serine/threonine kinase activity.
Solver output
DAF-1 is a type I TGF-β/activin receptor with transmembrane serine/threonine kinase activity that transduces TGF-β superfamily signals in C. elegans. In the context of the DAF-7/TGF-β pathway, DAF-1 (together with DAF-4) signals through SMAD proteins (DAF-8, DAF-14) to repress the transcription factor DAF-3, which otherwise promotes dauer formation and stress resistance. Active DAF-1 signaling suppresses dauer entry and the associated longevity program, meaning its normal function opposes the pro-longevity dauer/stress-resistance state. Loss-of-function mutations in daf-1 promote constitutive dauer formation and extended lifespan, consistent with an anti-longevity role for the wild-type gene. This pathway intersects with nutrient-sensing networks (including DAF-16/FOXO regulation) that are central hallmarks of aging regulation in C. elegans.
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 identifies daf-1 as anti_longevity with high confidence (0.82). The mechanistic reasoning is detailed and accurate: DAF-1 is a type I TGF-β/activin receptor that, when active, suppresses dauer formation and the associated longevity program. Loss-of-function mutations promote dauer and extended lifespan, making wild-type DAF-1 anti-longevity. The model correctly identifies the key pathway components (DAF-7, DAF-4, DAF-8, DAF-14, DAF-3). The mechanism_class of "deregulated_nutrient_sensing" is a reasonable categorization, though TGF-β signaling is more precisely categorized separately from nutrient sensing — however, the model does acknowledge the intersection with nutrient-sensing networks. Overall, the prediction and reasoning are excellent.
Raw API responses
solver
{
"reasoning": "DAF-1 is a type I TGF-β/activin receptor with transmembrane serine/threonine kinase activity that transduces TGF-β superfamily signals in C. elegans. In the context of the DAF-7/TGF-β pathway, DAF-1 (together with DAF-4) signals through SMAD proteins (DAF-8, DAF-14) to repress the transcription factor DAF-3, which otherwise promotes dauer formation and stress resistance. Active DAF-1 signaling suppresses dauer entry and the associated longevity program, meaning its normal function opposes the pro-longevity dauer/stress-resistance state. Loss-of-function mutations in daf-1 promote constitutive dauer formation and extended lifespan, consistent with an anti-longevity role for the wild-type gene. This pathway intersects with nutrient-sensing networks (including DAF-16/FOXO regulation) that are central hallmarks of aging regulation in C. elegans.",
"confidence": 0.82,
"key_pathways": [
"TGF-β/DAF-7 signaling pathway",
"DAF-3/SMAD transcriptional repression",
"Dauer formation and longevity regulation"
],
"mechanism_class": "deregulated_nutrient_sensing",
"longevity_influence": "anti_longevity"
}advisor
{
"notes": "The model correctly identifies daf-1 as anti_longevity with high confidence (0.82). The mechanistic reasoning is detailed and accurate: DAF-1 is a type I TGF-β/activin receptor that, when active, suppresses dauer formation and the associated longevity program. Loss-of-function mutations promote dauer and extended lifespan, making wild-type DAF-1 anti-longevity. The model correctly identifies the key pathway components (DAF-7, DAF-4, DAF-8, DAF-14, DAF-3). The mechanism_class of \"deregulated_nutrient_sensing\" is a reasonable categorization, though TGF-β signaling is more precisely categorized separately from nutrient sensing — however, the model does acknowledge the intersection with nutrient-sensing networks. Overall, the prediction and reasoning are excellent.",
"failure_mode": "correct",
"answer_correct": true,
"mechanism_correct": true,
"reasoning_quality": 5,
"ground_truth_questionable": false
}