rcan-1
C. elegans
Calcipressin-like protein
What the model saw
Gene: rcan-1 Organism: Caenorhabditis elegans Known functions: Calcipressin-like protein. calcium-dependent protein serine/threonine phosphatase regulator activity. nucleic acid binding. protein binding. protein phosphatase 2B binding. protein serine/threonine phosphatase inhibitor activity.
View unredacted entry
Calcipressin-like protein. calcium-dependent protein serine/threonine phosphatase regulator activity. nucleic acid binding. protein binding. protein phosphatase 2B binding. protein serine/threonine phosphatase inhibitor activity.
Solver output
RCAN-1 (Regulator of Calcineurin 1) functions as an endogenous inhibitor of calcineurin (protein phosphatase 2B/PP2B), a calcium-dependent serine/threonine phosphatase. In C. elegans, calcineurin (tax-6/cnb-1) promotes aging by activating transcription factors that antagonize stress resistance and DAF-16/FOXO nuclear localization. By inhibiting calcineurin, rcan-1 relieves suppression of DAF-16/FOXO, thereby enhancing stress resistance and extending lifespan. This places rcan-1 functionally upstream of the insulin/IGF-1 signaling pathway output, as calcineurin inhibition mimics effects that promote DAF-16 nuclear activity. Loss of calcineurin activity in C. elegans is known to extend lifespan, making its inhibitor rcan-1 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 predicted pro_longevity but the ground truth is anti_longevity. The model's reasoning about RCAN-1 as a calcineurin inhibitor is mechanistically plausible in isolation, but it drew the wrong conclusion about the net effect on longevity. In C. elegans, rcan-1 is actually anti-longevity — loss of rcan-1 extends lifespan. The model incorrectly assumed that inhibiting calcineurin (via rcan-1) would be beneficial, but the actual biology shows rcan-1 promotes aging. The model's logic about calcineurin inhibition promoting DAF-16 activity is also questionable — the relationship between calcineurin and DAF-16 in C. elegans is more nuanced, and rcan-1 overexpression or presence appears to shorten lifespan rather than extend it. The model was fairly confident (0.72) in its wrong answer.
Raw API responses
solver
{
"reasoning": "RCAN-1 (Regulator of Calcineurin 1) functions as an endogenous inhibitor of calcineurin (protein phosphatase 2B/PP2B), a calcium-dependent serine/threonine phosphatase. In C. elegans, calcineurin (tax-6/cnb-1) promotes aging by activating transcription factors that antagonize stress resistance and DAF-16/FOXO nuclear localization. By inhibiting calcineurin, rcan-1 relieves suppression of DAF-16/FOXO, thereby enhancing stress resistance and extending lifespan. This places rcan-1 functionally upstream of the insulin/IGF-1 signaling pathway output, as calcineurin inhibition mimics effects that promote DAF-16 nuclear activity. Loss of calcineurin activity in C. elegans is known to extend lifespan, making its inhibitor rcan-1 pro-longevity.",
"confidence": 0.72,
"key_pathways": [
"Calcineurin/PP2B inhibition",
"DAF-16/FOXO signaling",
"Calcium-dependent stress response"
],
"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 RCAN-1 as a calcineurin inhibitor is mechanistically plausible in isolation, but it drew the wrong conclusion about the net effect on longevity. In C. elegans, rcan-1 is actually anti-longevity — loss of rcan-1 extends lifespan. The model incorrectly assumed that inhibiting calcineurin (via rcan-1) would be beneficial, but the actual biology shows rcan-1 promotes aging. The model's logic about calcineurin inhibition promoting DAF-16 activity is also questionable — the relationship between calcineurin and DAF-16 in C. elegans is more nuanced, and rcan-1 overexpression or presence appears to shorten lifespan rather than extend it. The model was fairly confident (0.72) in its wrong answer.",
"failure_mode": "confident_wrong",
"answer_correct": false,
"mechanism_correct": false,
"reasoning_quality": 2,
"ground_truth_questionable": false
}